Stemi
ST-elevation myocardial infarction (STEMI) is an acute complete coronary artery occlusion causing transmural myocardial ischemia, identified by persistent ST-segment elevation on electrocardiogram and requiring emergent reperfusion therapy.
STEMI stands for ST-Elevation Myocardial Infarction. Let's break the name down:
- ST-Elevation → refers to the characteristic ECG finding where the ST segment is raised above the baseline, indicating transmural (full-thickness) myocardial ischaemia
- Myocardial → "myo" = muscle, "cardial" = heart → heart muscle
- Infarction → tissue death (necrosis) due to prolonged ischaemia
STEMI is a clinical syndrome defined by symptoms of acute myocardial ischaemia in the presence of persistent new ST-elevation on ECG, with subsequent rise of cardiac biomarkers of myocardial necrosis [1]. It sits within the broader spectrum of Acute Coronary Syndrome (ACS), which includes:
| ACS Subtype | ST-Elevation on ECG | Troponin Rise | Underlying Pathology |
|---|---|---|---|
| STEMI | Yes (persistent ≥ 20 min) | Yes | Complete coronary occlusion |
| NSTEMI | No (may have ST depression/T-wave changes) | Yes | Partial/intermittent occlusion |
| Unstable Angina (UA) | No | No | Partial/intermittent occlusion without necrosis |
The key distinction is that STEMI represents acute, complete thrombotic occlusion of a coronary artery, leading to transmural ischaemia and necrosis [1][2]. This is a time-critical emergency — "time is myocardium."
Terminology recap from lecture slides [2]:
- Stable angina: ischaemia due to fixed stenosis
- Unstable angina: ischaemia due to dynamic obstruction
- Myocardial infarction: myocardial necrosis due to acute occlusion
Universal Classification of MI (5th Universal Definition, 2018)
- Type 1 MI: Spontaneous MI due to atherosclerotic plaque rupture, erosion, fissuring, or dissection → intraluminal thrombus → this is the classic STEMI
- Type 2 MI: MI secondary to oxygen supply-demand mismatch (e.g., coronary spasm, anaemia, hypotension, tachyarrhythmia) — NOT due to plaque rupture
- Type 3 MI: MI resulting in death when biomarkers are unavailable (cardiac death with ischaemic symptoms/ECG changes but death before blood drawn)
- Type 4a/4b/4c MI: MI related to PCI (4a = periprocedural, 4b = stent thrombosis, 4c = restenosis)
- Type 5 MI: MI related to CABG
STEMI is almost always Type 1 MI.
Epidemiology
- Incidence: In Western countries, the incidence of STEMI has been declining over the past two decades (likely due to better primary prevention, statin use, smoking cessation campaigns), while NSTEMI incidence has been relatively stable or increasing
- Annual incidence of STEMI in Europe: approximately 40–60 per 100,000 population
- In the United States: approximately 250,000 STEMI presentations per year
- In-hospital mortality for STEMI has dropped significantly with primary PCI, now approximately 4–6% in centres with modern reperfusion strategies, but 30-day mortality remains around 7–8%
- Coronary artery disease (CAD) is the 3rd leading cause of death in Hong Kong (after malignant neoplasms and pneumonia)
- Ischaemic heart disease accounts for approximately 12–15% of all deaths in HK [2]
- The Hong Kong population has a rising prevalence of metabolic risk factors (diabetes, hypertension, obesity) partially offset by declining smoking rates
- The door-to-balloon time in Hong Kong's public hospitals has improved significantly with the establishment of a 24/7 primary PCI service network across Hospital Authority clusters
- Mean age of presentation is typically 60–70 years, with a male predominance (M:F ≈ 3:1)
- Sex: Men are affected significantly more often than women, especially before age 55. Post-menopausal women lose the protective effect of oestrogen on the endothelium and lipid profile
- Age: Risk increases exponentially after age 45 in men and 55 in women
- Ethnicity: South Asians have higher rates of premature CAD compared to East Asians, but CAD is rapidly rising in Chinese populations with Westernisation of diet and lifestyle
Risk Factors
Risk factors for STEMI are essentially the risk factors for atherosclerotic cardiovascular disease (ASCVD), since STEMI arises from atherosclerotic plaque rupture [2][3].
| Factor | Explanation |
|---|---|
| Advanced age | Cumulative exposure to risk factors; age-related endothelial dysfunction and arterial stiffening |
| Male sex | Oestrogen in premenopausal women is protective (↑HDL, ↓LDL, vasodilatory via NO); after menopause, female risk approaches male risk |
| Family history of premature CVD | 1st-degree male relative < 55 yrs or female relative < 65 yrs; implies genetic susceptibility to atherogenesis (e.g., familial hypercholesterolaemia, polymorphisms affecting LDL receptor, lipoprotein(a)) |
| Previous vascular event | Prior MI, stroke, or PVD indicates established atherosclerosis with ongoing plaque burden |
| Factor | Mechanism of Atherogenesis |
|---|---|
| Cigarette smoking | Endothelial injury via free radicals → ↑LDL oxidation, ↓NO bioavailability, ↑platelet activation, ↑fibrinogen → prothrombotic state |
| Hypertension | Mechanical shear stress on endothelium → endothelial dysfunction → facilitates lipid infiltration and plaque growth; also promotes LVH (↑O₂ demand) |
| Dyslipidaemia (↑LDL, ↓HDL) | LDL particles infiltrate the intima and undergo oxidation → trigger macrophage uptake → foam cell formation → fatty streak → plaque. HDL performs reverse cholesterol transport (protective). Target LDL < 1.4 mmol/L in very high-risk patients (ESC 2019/2024) |
| Diabetes mellitus | Hyperglycaemia → advanced glycation end products (AGEs) → endothelial dysfunction; insulin resistance → ↑FFA → oxidative stress; DM also promotes a prothrombotic state (↑PAI-1, ↑fibrinogen). DM is a coronary heart disease risk equivalent [3] |
| Abdominal obesity | Central adiposity → ↑FFA release, ↑inflammatory adipokines (TNF-α, IL-6), ↓adiponectin → insulin resistance → metabolic syndrome [3] |
| Physical inactivity | ↓AMPK activation → ↓glucose uptake, ↓FFA metabolism → insulin resistance; ↓endothelial shear-mediated NO production |
| Diet | High saturated fat, trans fat, refined carbohydrates → dyslipidaemia; high sodium → HTN |
- Cocaine use: Causes coronary vasospasm + ↑sympathetic drive (↑HR, ↑BP → ↑O₂ demand) + direct endothelial toxicity + prothrombotic state → can cause STEMI even in young patients with normal coronaries
- Chronic kidney disease (CKD): Accelerated atherosclerosis, uraemic toxins damage endothelium, disordered calcium-phosphate metabolism → vascular calcification
- Autoimmune/inflammatory conditions (SLE, RA): Chronic systemic inflammation accelerates atherogenesis
- Obstructive sleep apnoea: Intermittent hypoxia → sympathetic activation → endothelial dysfunction
- Oral contraceptive pills and HRT: Mildly ↑thrombotic risk
High Yield — ASCVD Risk Assessment
Formal ASCVD risk assessment is indicated if ≥40 years old with ≥1 ASCVD risk factor [3]. Tools include the Framingham Risk Score, SCORE2, ACC/AHA ASCVD calculator, and the Chinese Multiprovincial Cohort Study (CMCS) for the Chinese population. Risk assessment guides the intensity of primary prevention (especially statin therapy and BP targets).
Anatomy and Function
Coronary Artery Anatomy
Understanding coronary anatomy is crucial because the territory of infarction and its complications are directly determined by which artery is occluded.
The heart is supplied by two coronary arteries arising from the aortic sinuses of Valsalva (just above the aortic valve):
- Arises from the left coronary sinus
- Left Main Stem (LMS): short trunk (0.5–2 cm) that bifurcates into:
- Left Anterior Descending (LAD): Runs in the anterior interventricular groove
- Supplies: anterior wall of LV, anterior 2/3 of interventricular septum, apex
- Branches: septal perforators (supply septum), diagonal branches (supply anterolateral wall)
- LAD occlusion → anterior STEMI (the most dangerous territory — large area of myocardium at risk)
- Left Circumflex (LCx): Runs in the left atrioventricular groove
- Supplies: lateral wall of LV, posterior wall of LV (in left-dominant systems)
- Branches: obtuse marginal branches
- LCx occlusion → lateral STEMI
- Left Anterior Descending (LAD): Runs in the anterior interventricular groove
- Arises from the right coronary sinus
- Runs in the right atrioventricular groove
- Supplies: RV, inferior wall of LV, posterior 1/3 of interventricular septum, SA node (in ~60%), AV node (in ~80% — right dominant circulation)
- Branches: posterior descending artery (PDA) in right-dominant systems (85% of population), marginal branches
- RCA occlusion → inferior STEMI (often with RV involvement)
- Right dominant (~85%): PDA arises from the RCA — so the RCA supplies the inferior wall and AV node
- Left dominant (~8%): PDA arises from the LCx
- Co-dominant (~7%): Both contribute to the PDA
| Culprit Artery | ECG Leads with ST-Elevation | Myocardial Wall | Key Complications |
|---|---|---|---|
| LAD | V1–V4 (± V5–V6) | Anterior, anteroseptal, apex | LV failure, cardiogenic shock (large territory), VSD, LV aneurysm, free wall rupture |
| LCx | I, aVL, V5–V6 (± high lateral leads) | Lateral, posterolateral | Papillary muscle rupture (posteromedial) causing acute MR |
| RCA | II, III, aVF (± V3R–V4R for RV) | Inferior, RV (proximal RCA), posterior (if dominant) | Bradycardia/AV block (AV node ischaemia), RV infarction, papillary muscle rupture |
| Left Main | aVR elevation + widespread ST depression | Global LV ischaemia | Cardiogenic shock, cardiac arrest |
Clinical Pearl — RV Infarction
Always check right-sided ECG leads (V3R, V4R) in any inferior STEMI. RV infarction occurs in ~30–50% of inferior STEMIs (proximal RCA occlusion). Management differs — these patients are preload-dependent, so avoid nitrates and diuretics (which reduce preload and can cause catastrophic hypotension). Instead, give IV fluids.
The heart is uniquely vulnerable to ischaemia because:
- Highest O₂ extraction rate of any organ at rest (~70–80% of delivered O₂ is extracted) → very little reserve to increase extraction
- Therefore, the only way to increase O₂ supply is to increase coronary blood flow
- Coronary perfusion occurs predominantly in diastole (unlike other organs) because systolic contraction compresses intramural vessels
| O₂ Supply Factors | O₂ Demand Factors |
|---|---|
| Coronary blood flow (diastolic BP, coronary vessel calibre) | Heart rate (most important determinant) |
| O₂ content of blood (Hb, SaO₂) | Myocardial contractility |
| Coronary perfusion pressure | Wall stress (= pressure × radius / 2 × wall thickness → Laplace's law) |
| Duration of diastole | Afterload (systolic BP) |
Etiology
The etiology of STEMI can be understood through the lens of why a coronary artery suddenly becomes completely occluded.
Primary Etiology: Atherosclerotic Plaque Rupture / Erosion (> 90%)
The vast majority of STEMI is caused by acute thrombotic occlusion of a coronary artery, triggered by rupture or erosion of a vulnerable atherosclerotic plaque [1][2].
- Endothelial injury (from HTN, smoking, dyslipidaemia, DM) → ↑permeability
- LDL infiltration into the intima → oxidised LDL (oxLDL)
- Inflammatory response: Monocytes migrate into intima → differentiate into macrophages → engulf oxLDL → become foam cells → fatty streak
- Smooth muscle cell (SMC) migration from media to intima → proliferate and produce extracellular matrix → forms a fibrous cap over the lipid-rich necrotic core
- Progressive growth → atherosclerotic plaque with a fibrous cap and a lipid/necrotic core
Not all plaques are equal. The plaque most likely to rupture is the "vulnerable" or "unstable" plaque, which has:
- Thin fibrous cap (< 65 μm) — due to ↓SMC content and ↑matrix metalloproteinase (MMP) activity from activated macrophages
- Large lipid-rich necrotic core (occupying > 40% of plaque volume)
- ↑Inflammatory infiltrate (macrophages, T-cells) at the "shoulder" regions of the plaque
- ↑Neovascularization within the plaque (→ more fragile, prone to intraplaque haemorrhage)
Why Do Mild Stenoses Cause Most STEMIs?
Counterintuitively, most STEMIs arise from plaques causing only mild-to-moderate stenosis ( < 50% luminal narrowing) rather than severe stenoses. Why?
- Severe stenoses tend to have thick, stable fibrous caps (remodelled over time) and well-developed collaterals
- Mild/moderate plaques with thin caps and large lipid cores are the ones prone to sudden rupture
- This is why stress tests and even angiography may fail to predict which plaque will cause a STEMI — the "culprit" plaque often looks innocent on prior imaging
The pathophysiological sequence of STEMI [1]:
Step-by-step:
- Plaque rupture/erosion: Physical disruption of the fibrous cap exposes the thrombogenic lipid core and subendothelial collagen to flowing blood
- Platelet adhesion: vWF mediates platelet adhesion to exposed collagen via GP Ib receptors → platelet activation → release of ADP and TXA₂ → recruits more platelets
- Platelet aggregation: Activated platelets express GP IIb/IIIa receptors which bind fibrinogen, cross-linking platelets together → platelet plug ("white thrombus")
- Coagulation cascade: Exposed tissue factor activates the extrinsic pathway → thrombin generation → converts fibrinogen to fibrin → stabilises the platelet plug → "red thrombus" (fibrin-rich)
- Complete occlusion: The thrombus completely occludes the coronary lumen → no blood flow → ischaemia of the entire downstream territory
This is why STEMI treatment targets every step of this cascade: antiplatelets (aspirin blocks TXA₂; P2Y₁₂ inhibitors block ADP receptors; GP IIb/IIIa inhibitors block the final common pathway of aggregation), anticoagulants (heparin inhibits thrombin and factor Xa), and reperfusion (primary PCI mechanically reopens the vessel, or fibrinolytics dissolve the clot) [1][2].
While > 90% of STEMI is due to atherothrombosis, the following can also cause ST-elevation MI:
| Cause | Mechanism | Clinical Scenario |
|---|---|---|
| Coronary artery spasm (Prinzmetal/variant angina) | Intense vasospasm → transient complete occlusion | Young patients, often smokers, may have normal coronaries; ST-elevation during spasm, resolves with nitrates |
| Spontaneous coronary artery dissection (SCAD) | Intimal tear or vasa vasorum haemorrhage → intramural haematoma → luminal compression | Young women, peripartum, fibromuscular dysplasia |
| Coronary embolism | Embolic material lodges in coronary artery | AF, IE (vegetations), prosthetic valves, paradoxical embolism (PFO) |
| Coronary arteritis/vasculitis | Inflammation → coronary stenosis/occlusion | Kawasaki disease (children — coronary aneurysms), Takayasu arteritis, SLE |
| Supply-demand mismatch (Type 2 MI) | Severe ↑demand or ↓supply without plaque rupture | Severe anaemia, hypotension, tachyarrhythmia, aortic stenosis, thyrotoxicosis — though these more commonly cause NSTEMI/demand ischaemia |
| Cocaine/amphetamines | Coronary vasospasm + ↑demand (↑HR, ↑BP) + prothrombotic | Young patients presenting with chest pain after drug use |
| Aortic dissection | Dissection flap extends into coronary ostium (usually RCA → inferior STEMI) | Tearing chest pain radiating to back, pulse deficits, wide mediastinum on CXR |
| Takotsubo cardiomyopathy | Catecholamine surge → apical ballooning; can mimic anterior STEMI on ECG | Post-menopausal women after intense emotional/physical stress; ST-elevation with apical akinesis but no culprit lesion on angiography |
Don't Miss Aortic Dissection Mimicking STEMI!
If a patient presents with STEMI features but also has tearing back pain, pulse deficits, or a widened mediastinum on CXR, consider aortic dissection [4]. Type A dissection can occlude the RCA ostium → inferior STEMI. Giving antiplatelet/anticoagulant therapy or performing PCI on an undiagnosed dissection is catastrophic. Always consider this differential — a quick CXR and bedside echo can be life-saving.
Pathophysiology of STEMI
Once a coronary artery is completely occluded, a predictable sequence of events unfolds in the myocardium downstream — the ischaemic cascade:
Key points:
- Diastolic dysfunction precedes systolic dysfunction — the myocyte cannot relax properly due to ATP depletion (ATP is needed for calcium reuptake into the sarcoplasmic reticulum via SERCA)
- ECG changes appear before pain — this is why silent ischaemia exists
- Necrosis begins in the subendocardium and progresses outward toward the epicardium as a "wavefront" (Reimer and Jennings, 1979) — this is why early reperfusion salvages myocardium [1]
- Subendocardium is most vulnerable to ischaemia because:
- It is furthest from the epicardial coronary arteries
- It has the highest wall stress (highest intramural pressure during systole → greatest extravascular compression)
- It has the highest metabolic demand (greatest sarcomere shortening)
- Timeline of necrosis (approximate):
- < 20 minutes: Reversible injury — reperfusion at this point results in full recovery ("stunned myocardium")
- 20–60 minutes: Subendocardial necrosis begins
- 3–6 hours: Necrosis extends through most of the wall thickness
- > 6 hours: Transmural necrosis is largely complete; reperfusion benefit diminishes significantly
- 12–24 hours: Essentially complete transmural infarction
This is the basis for the "golden hour" and "door-to-balloon time" targets: every minute of occlusion = more myocardial death. The ESC and ACC/AHA guidelines target a door-to-balloon time of ≤ 90 minutes for primary PCI, and a door-to-needle time of ≤ 30 minutes for fibrinolysis [1].
At the cellular level:
- ATP depletion → failure of Na⁺/K⁺-ATPase → cell swelling → failure of Ca²⁺ homeostasis → calcium overload → hypercontracture, mitochondrial damage
- Anaerobic glycolysis → lactic acid accumulation → intracellular acidosis → further enzyme dysfunction
- Free radical generation (especially upon reperfusion) → lipid peroxidation of cell membranes → cell death
- Irreversible injury markers: mitochondrial swelling, amorphous matrix densities, sarcolemmal disruption → release of intracellular contents (troponin, CK-MB, myoglobin) into the bloodstream → this is what we measure as cardiac biomarkers
Paradoxically, restoring blood flow can itself cause additional injury ("reperfusion injury"):
- Mechanism: Sudden re-introduction of oxygenated blood to ischaemic tissue → massive reactive oxygen species (ROS) generation → oxidative damage, calcium overload, inflammatory cell infiltration, microvascular obstruction ("no-reflow phenomenon")
- Clinical significance: May account for up to 50% of final infarct size
- This is an active area of research; currently no clinically proven therapy specifically prevents reperfusion injury, though ischaemic conditioning protocols are being studied
Classification
STEMI can be classified in several clinically relevant ways:
| Type | Culprit Artery | ECG Leads | Notes |
|---|---|---|---|
| Anterior STEMI | LAD | V1–V4 (± V5–V6, I, aVL) | Largest territory; worst prognosis |
| Anteroseptal STEMI | LAD (septal perforators) | V1–V3 | Risk of septal rupture (VSD) |
| Lateral STEMI | LCx or diagonal branch | I, aVL, V5–V6 | May be electrically "silent" (fewer leads) |
| Inferior STEMI | RCA (or LCx if left-dominant) | II, III, aVF | Check for RV involvement (V4R) |
| Posterior STEMI | RCA or LCx (posterior descending) | V7–V9 (+ reciprocal changes: tall R, ST depression in V1–V3) | Often missed — must actively look |
| Right Ventricular STEMI | Proximal RCA | V3R–V4R (+ inferior leads) | Preload-dependent; avoid nitrates/diuretics |
| Phase | Timing | Pathological Features |
|---|---|---|
| Acute/Evolving STEMI | 0–7 days | Active ischaemia/necrosis; hyperacute T waves → ST elevation → Q wave development |
| Recent STEMI | 7–28 days | Organisation of necrosis; ST segment resolving; T-wave inversion developing |
| Old/Healed MI | > 28 days | Fibrotic scar; persistent Q waves; T-wave changes may normalise or persist |
As described above (Types 1–5). STEMI is overwhelmingly Type 1 MI.
This is a bedside clinical classification that predicts mortality:
| Killip Class | Clinical Features | 30-day Mortality |
|---|---|---|
| I | No evidence of heart failure | ~6% |
| II | Mild HF: S3 gallop, lung crackles in lower half of lung fields, ↑JVP | ~17% |
| III | Overt pulmonary oedema | ~38% |
| IV | Cardiogenic shock (SBP < 90, signs of end-organ hypoperfusion) | ~80% (without intervention) |
Used during angiography to assess flow in the culprit artery:
| TIMI Grade | Description |
|---|---|
| 0 | Complete occlusion — no flow |
| 1 | Penetration without perfusion — contrast passes but doesn't fill the distal vessel |
| 2 | Partial perfusion — distal vessel fills but slowly |
| 3 | Normal flow — complete filling at normal rate |
The goal of primary PCI is to achieve TIMI 3 flow.
Clinical Features
A. Symptoms
This is the defining symptom of STEMI and its characteristics are crucial for recognition:
| OPQRST | Description | Pathophysiological Basis |
|---|---|---|
| Onset | Acute onset, typically takes minutes to develop [2]; may occur at rest or with exertion; often in the early morning (↑catecholamines, ↑platelet aggregability, ↑cortisol on waking) | Sudden complete coronary occlusion → immediate onset of ischaemia |
| Provocation | At rest (unlike stable angina which occurs with exertion) [2]; NOT relieved by rest or sublingual GTN (differentiates from stable angina where GTN works in ≤ 5 min) | Complete occlusion means there is no residual flow — reducing demand alone (rest) or vasodilation (GTN) cannot overcome complete obstruction |
| Quality | Dull, constricting, crushing, choking, squeezing, "heavy" [2]; patients often describe it as a "pressure" or "tightness" rather than a "sharp pain"; Levine's sign: clenched fist on chest | Visceral pain from ischaemic myocardium is poorly localised (transmitted via cardiac sympathetic afferents C7–T4 → referred pain pattern); unlike somatic pain which is sharp and well-localised |
| Radiation | Arms (especially left), shoulder, neck, jaw, epigastrium, interscapular region | Referred pain: cardiac afferents share spinal cord segments (C7–T4) with somatic afferents from these dermatomes → brain misinterprets the origin |
| Severity | Usually described as the "worst pain ever"; typically rated 8–10/10 | Transmural ischaemia stimulates a massive afferent nerve discharge |
| Time | Prolonged > 20 minutes (often 30 min to hours); does not wax and wane like stable angina | Unlike transient ischaemia (stable angina), complete occlusion produces sustained ischaemia until reperfusion occurs |
Atypical Presentations — Don't Miss These!
Up to 30% of MIs present atypically, especially in:
- Elderly (> 75 years): may present with dyspnoea, confusion, syncope, or just "feeling unwell" rather than chest pain
- Women: more likely to present with fatigue, nausea, dyspnoea, or neck/jaw pain without classical chest pain
- Diabetics: autonomic neuropathy → ↓pain perception → "silent MI" (painless); may present with unexplained heart failure, hypotension, or arrhythmia
- Post-operative patients: pain may be attributed to surgical wound
Always maintain a low threshold for ECG in these populations!
| Symptom | Pathophysiological Basis |
|---|---|
| Diaphoresis (profuse sweating) | Massive sympathetic activation in response to pain and haemodynamic compromise → activation of sweat glands (sympathetic cholinergic fibres) |
| Nausea and vomiting | Particularly common in inferior STEMI (vagal afferents from the inferior myocardium → medullary vomiting centre); also due to pain-mediated vagal stimulation (Bezold-Jarisch reflex) |
| Anxiety / "sense of impending doom" (angor animi) | Massive sympathetic discharge + cortical perception of life-threatening event |
| Pallor | Sympathetic vasoconstriction redirecting blood to vital organs (compensatory response to ↓CO) |
The Bezold-Jarisch reflex is important in inferior STEMI: stimulation of vagal afferents in the inferior/posterior LV wall → paradoxical bradycardia and hypotension (vasovagal response). This is why inferior STEMI often presents with sinus bradycardia + hypotension → treat with atropine and IV fluids, not pressors initially.
| Mechanism | Explanation |
|---|---|
| LV systolic dysfunction | Ischaemia/necrosis of myocardium → ↓contractility → ↑LV end-diastolic pressure → pulmonary venous congestion → pulmonary oedema → dyspnoea |
| LV diastolic dysfunction | Ischaemia impairs relaxation (ATP needed for calcium reuptake) → ↑filling pressures even before systolic failure occurs |
| Anxiety and pain | ↑Respiratory rate as part of sympathetic activation |
Dyspnoea may be the predominant or sole symptom in elderly/diabetic patients ("anginal equivalent").
| Mechanism | Explanation |
|---|---|
| Arrhythmia | VT/VF (especially in anterior STEMI) → ↓CO → cerebral hypoperfusion → syncope |
| Bradycardia | AV block (especially inferior STEMI → AV nodal ischaemia from RCA) → ↓HR → ↓CO |
| Cardiogenic shock | Massive LV dysfunction → ↓CO → hypotension → syncope |
| Vasovagal | Bezold-Jarisch reflex in inferior MI |
- Palpitations: Due to arrhythmias (sinus tachycardia, atrial fibrillation, ventricular ectopics, VT)
- Fatigue and weakness: ↓CO → ↓tissue perfusion → generalised weakness
- Epigastric discomfort: Especially in inferior MI — visceral afferents overlap with GI innervation; may be misdiagnosed as "indigestion"
B. Signs
| Sign | Pathophysiological Basis |
|---|---|
| Distressed, anxious, restless | Pain + sympathetic activation + awareness of life-threatening event |
| Pallor, diaphoresis, clammy skin | Sympathetic vasoconstriction (↑peripheral vascular resistance as compensation for ↓CO); cholinergic-mediated sweating |
| Clutching chest / Levine's sign | Characteristic gesture — clenched fist pressed over sternum |
| Sign | Pathophysiological Basis |
|---|---|
| Tachycardia | Sympathetic activation to compensate for ↓stroke volume; pain response; may also be pathological (AF, VT) |
| Bradycardia | Inferior STEMI → AV nodal ischaemia / Bezold-Jarisch vagal reflex; also in high-degree AV block |
| Hypotension (SBP < 90 mmHg) | ↓CO due to extensive LV dysfunction (Killip III–IV), RV infarction, arrhythmia, mechanical complication (papillary muscle rupture, VSD, free wall rupture) |
| Hypertension | Sympathetic activation (pain, catecholamine surge) — especially early in the presentation |
| Low-grade fever (37.5–38.5°C) | Myocardial necrosis → inflammatory response → release of pyrogens (IL-1, IL-6, TNF-α); typically appears at 24–48 hours and lasts several days |
| Tachypnoea | Pulmonary oedema from ↑LV filling pressures; pain; anxiety |
| Sign | Pathophysiological Basis |
|---|---|
| S4 gallop (most common auscultatory finding in STEMI) | Atrial contraction against a stiff, non-compliant LV (diastolic dysfunction from ischaemia) → audible "atrial kick" |
| S3 gallop | Rapid ventricular filling into a dilated, failing LV (systolic dysfunction) → signifies significant LV impairment; if both S3 + S4 → "summation gallop" |
| Soft S1 | ↓dP/dt (rate of pressure rise) in the LV due to ↓contractility → mitral valve closes more slowly |
| Paradoxical splitting of S2 | LBBB or severe LV dysfunction → delayed LV ejection → aortic valve (A2) closes after pulmonic valve (P2) → splitting heard on expiration (opposite of normal) |
| Pansystolic murmur at apex | Acute mitral regurgitation from papillary muscle dysfunction or rupture (especially posteromedial papillary muscle in inferior MI — it has a single blood supply from the PDA, unlike the anterolateral papillary muscle which has dual supply) |
| New pansystolic murmur at LLSB with thrill | Ventricular septal rupture → left-to-right shunt (complication, usually day 3–5 post-MI) |
| Pericardial friction rub | Post-MI pericarditis (Dressler syndrome if late, or early direct irritation from transmural necrosis) → inflamed pericardial surfaces rub together |
| Elevated JVP | RV infarction (preload-dependent → JVP rises) or LV failure with secondary pulmonary hypertension → RV failure |
| Kussmaul's sign (paradoxical ↑JVP on inspiration) | RV infarction → stiff, non-compliant RV cannot accommodate ↑venous return on inspiration → JVP rises |
| Displaced apex beat | Pre-existing LV dilatation (previous MI, DCMP) or acute LV dilatation |
| Sign | Pathophysiological Basis |
|---|---|
| Bilateral basal crepitations (crackles) | LV failure → ↑LV end-diastolic pressure → ↑pulmonary capillary wedge pressure (PCWP) → transudation of fluid into alveoli → pulmonary oedema |
| Wheeze ("cardiac asthma") | Peribronchial oedema from ↑pulmonary venous pressure → airway narrowing → wheeze |
| Pink frothy sputum | Severe pulmonary oedema → transudation of fluid + RBCs into alveoli |
If extensive myocardium is infarcted (typically > 40% of LV mass), cardiogenic shock ensues:
| Sign | Mechanism |
|---|---|
| SBP < 90 mmHg or ≥ 30 mmHg drop from baseline | Massive ↓CO from extensive LV necrosis |
| Cold, clammy, mottled extremities | Peripheral vasoconstriction (sympathetic compensation) |
| Oliguria (< 0.5 mL/kg/hr) | ↓Renal perfusion → ↓GFR |
| Altered mental status | ↓Cerebral perfusion |
| Elevated lactate | Tissue hypoperfusion → anaerobic metabolism |
Cardiogenic shock complicates ~5–8% of STEMI cases and carries a mortality of ~40–50% even with aggressive management (IABP, mechanical circulatory support, primary PCI) [5].
| Sign | Mechanism |
|---|---|
| Elevated JVP with clear lung fields | RV failure → ↑systemic venous pressure → ↑JVP; but LV is not primarily affected → no pulmonary oedema |
| Hypotension | RV cannot pump blood forward to the LV → ↓LV preload → ↓CO |
| Kussmaul's sign | Non-compliant RV cannot handle increased venous return on inspiration |
This combination of ↑JVP + clear lungs + hypotension in the setting of inferior STEMI = RV infarct until proven otherwise.
High Yield Summary
Definition: STEMI = persistent ST-elevation on ECG + symptoms of myocardial ischaemia + troponin rise, caused by acute complete thrombotic occlusion of a coronary artery (almost always Type 1 MI from atherosclerotic plaque rupture).
Epidemiology: Declining STEMI incidence in developed countries due to primary prevention; M > F (3:1); mean age 60–70 years; CAD is the 3rd leading cause of death in HK.
Risk Factors: Same as ASCVD — modifiable: smoking, HTN, dyslipidaemia, DM, obesity, physical inactivity; non-modifiable: age, male sex, family history, prior vascular events.
Key Pathophysiology: Vulnerable plaque (thin cap, large lipid core, inflammation) → rupture → platelet adhesion/aggregation + coagulation cascade → occlusive thrombus → transmural ischaemia → necrosis progressing as a wavefront from subendocardium to epicardium. Time is myocardium — necrosis begins at ~20 min and is largely transmural by 6–12 hours.
Clinical Features:
- Symptoms: Prolonged ( > 20 min) crushing chest pain not relieved by rest/GTN, radiation to arms/jaw/neck, diaphoresis, nausea/vomiting (especially inferior MI), dyspnoea, syncope, "sense of impending doom." Atypical presentations in elderly, women, diabetics.
- Signs: Distressed, diaphoretic; tachycardia/bradycardia; hypotension or hypertension; S4 (most common) ± S3; new murmurs (MR, VSD); pulmonary oedema signs; signs of cardiogenic shock; RV infarct triad (↑JVP + clear lungs + hypotension in inferior STEMI).
Coronary Anatomy — ECG Correlation: LAD → anterior (V1–V4); RCA → inferior (II, III, aVF) ± RV (V4R); LCx → lateral (I, aVL, V5–V6); posterior → V7–V9 / reciprocal V1–V3 changes.
Killip Classification: I (no HF) → II (mild HF) → III (pulmonary oedema) → IV (cardiogenic shock). Predicts mortality.
Always consider aortic dissection as a mimic — tearing pain, pulse deficits, wide mediastinum.
Active Recall - STEMI (Definition, Epidemiology, Anatomy, Etiology, Pathophysiology, Clinical Features)
[1] Lecture slides: GC 088. Sudden Severe Chest Pain.pdf (pp. 2, 9, 14, 22, 36) [2] Senior notes: Ryan Ho Cardiology.pdf (pp. 57, 115, 120) [3] Senior notes: Ryan Ho Endocrine.pdf (pp. 77, 125); Ryan Ho Chemical Path.pdf (p. 46) [4] Senior notes: felixlai.md (Aortic Dissection section, pp. 1327–1361) [5] Senior notes: Ryan Ho Critical Care.pdf (pp. 22, 28) [6] Senior notes: Ryan Ho Fundamentals.pdf (pp. 199, 202–203) [7] Lecture slides: GC 028. Accelerating chest pain_Acute coronary.pdf [8] Lecture slides: GC 032. Chest pain on exertion_ischaemic heart disease; angina pectoris.pdf (p. 76)
Differential Diagnosis of STEMI
When a patient presents with acute chest pain and ST-elevation on ECG, the instinct is to activate the cath lab. But the critical first step is to consider what else can produce this picture — because giving dual antiplatelet therapy and anticoagulation to a patient with aortic dissection, for example, can be fatal. The differential diagnosis operates on two parallel tracks:
- Differential diagnosis of the clinical presentation (acute severe chest pain)
- Differential diagnosis of ST-elevation on ECG (ECG mimics of STEMI)
Both must be considered simultaneously.
The main differential diagnoses of acute chest pain [1][6][7]:
| Category | Differential | Key Distinguishing Features | Why It Mimics STEMI |
|---|---|---|---|
| Cardiac | NSTEMI / Unstable Angina | ST depression or T-wave changes (not ST elevation); troponin may or may not rise | Same underlying pathology (ACS spectrum) but partial, not complete, occlusion |
| Acute pericarditis | Sharp, knife-like, aggravated by respiratory movement; radiates to the trapezius ridge (characteristic site of pericardial pain) [1]; relieved by sitting forward; diffuse concave ST-elevation, PR depression | Pericardial inflammation causes widespread ST-elevation (but the morphology is different — see below) | |
| Myocarditis | Preceding viral illness; chest pain + HF symptoms; diffuse ECG changes, ↑troponin | Myocardial inflammation can cause ST-elevation and troponin rise, mimicking MI | |
| Takotsubo cardiomyopathy | Post-menopausal woman after intense emotional/physical stress; anterior ST-elevation mimicking LAD STEMI; apical ballooning on echo but clean coronaries on angiography | Catecholamine surge → apical stunning → ST-elevation + troponin rise | |
| Tachyarrhythmias | Palpitations, irregular pulse; ECG shows the arrhythmia | Rate-related demand ischaemia can cause ST changes | |
| Acute heart failure | Dyspnoea > chest pain; known cardiomyopathy; BNP markedly elevated | Acute decompensation can cause ST/T changes | |
| Aortic valve stenosis | Exertional angina + syncope + dyspnoea; ejection systolic murmur radiating to carotids; LVH on ECG | LVH strain pattern can cause ST-elevation; also, fixed obstruction causes demand ischaemia | |
| Hypertensive emergency | Markedly elevated BP (often > 180/120); evidence of end-organ damage | Severe afterload → demand ischaemia + LVH strain pattern on ECG | |
| Vascular | Aortic dissection | Radiation to back, ripping or tearing sensation [1]; sudden onset, maximal at onset; BP differential between arms; widened mediastinum on CXR; may have pulse deficits, AR murmur | Type A dissection can extend into RCA ostium → true inferior STEMI; also, aortic dissection itself can cause ST changes via coronary malperfusion |
| Symptomatic aortic aneurysm | Pulsatile abdominal mass (AAA) or back/chest pain; known aneurysm | Leaking aneurysm → shock → demand ischaemia | |
| Pulmonary | Pulmonary embolism | Haemoptysis [1]; pleuritic chest pain; acute dyspnoea; DVT risk factors; sinus tachycardia, S1Q3T3 or RBBB on ECG; D-dimer elevated | Massive PE can cause right heart strain → ST-elevation in V1-V3 and inferior leads (mimics anteroseptal STEMI); also causes troponin rise from RV strain |
| Tension pneumothorax | Sudden onset, maximal at onset; pleuritic; absent breath sounds; tracheal deviation; hypotension | Can cause ST-changes from mediastinal shift and haemodynamic compromise | |
| Pneumonia / pleuritis | Productive cough, fever, pleuritic pain worsening on inspiration; consolidation signs | Usually does not mimic STEMI on ECG but can cause chest pain confusion | |
| Gastrointestinal | Oesophagitis / GERD / oesophageal spasm | Retrosternal burning; relationship with meals, position; relieved by antacids; no ECG changes | Oesophageal spasm can cause severe retrosternal chest pain similar to angina; may even be relieved by GTN (oesophageal smooth muscle relaxation) |
| Peptic ulcer / gastritis | Epigastric pain; relationship to food; history of NSAID/alcohol use | Epigastric pain can be confused with inferior MI presentation | |
| Pancreatitis | Epigastric pain radiating to back; nausea/vomiting; ↑amylase/lipase | Severe epigastric pain can mimic inferior MI | |
| Cholecystitis | RUQ pain; Murphy's sign; fever; ↑WBC | Can cause referred pain and even ECG changes (rarely ST changes in inferior leads) | |
| Musculoskeletal | Costochondritis / chest wall pain | Reproducible on palpation; sharp, localised, positional; no ECG changes | Chest wall tenderness can coexist with ACS (don't be falsely reassured!) |
| Muscle injury / trauma | History of injury; localised tenderness | Usually obvious from history | |
| Other | Herpes zoster | Dermatomal distribution; vesicular rash (may precede pain by days) | Pain precedes rash → can be confusing; no ECG changes |
| Anxiety / panic disorder | Hyperventilation; tingling; young patient; situational trigger; normal ECG and troponin | Diagnosis of exclusion — never assume panic without ruling out serious causes | |
| Anaemia | Pallor; tachycardia; known chronic disease; low Hb | Severe anaemia → demand ischaemia → can precipitate Type 2 MI |
The lecture slide from GC 028 lists the frequency of diagnoses in patients presenting with acute chest pain: Gastrointestinal 42%, Ischaemic heart disease 31%, Chest wall syndrome 28%, Pericarditis 4%, Pleuritis 2%, Pulmonary embolism 2%, Lung cancer 1.5%, Aortic aneurysm 1%, Aortic stenosis 1%, Herpes zoster 1% [7]. This is important — it reminds you that many patients presenting with chest pain do NOT have ACS, and GI causes are actually the most common overall.
The 'Big Five' Life-Threatening Differentials of Acute Chest Pain
When a patient presents with acute severe chest pain, you must systematically exclude five potentially fatal diagnoses before settling on a benign cause:
- Acute coronary syndrome (ACS — STEMI/NSTEMI)
- Aortic dissection
- Pulmonary embolism
- Tension pneumothorax
- Myopericarditis ± cardiac tamponade
These can all present similarly with acute chest pain + haemodynamic compromise. The first 12-lead ECG, CXR, bedside echo, and focused history are your best tools to rapidly triage between them [6].
This is absolutely critical for exams and clinical practice. Not every ST-elevation is a STEMI. Activating the cath lab for a patient with benign early repolarisation wastes resources and exposes the patient to unnecessary risk (arterial access, contrast, anticoagulation). Conversely, missing a true STEMI because you attributed the ST-elevation to pericarditis is deadly.
Note that STEMI is NOT the only cause of ST elevation [2][9]:
| Cause of ST-Elevation | ECG Characteristics | How to Distinguish from STEMI |
|---|---|---|
| Acute STEMI | Localised, convex ↑ST ("tombstone"), usually III > II in inferior MI, associated with reciprocal ST depression, evolving Q waves [2][9] | Clinical context (acute chest pain, risk factors); reciprocal changes are virtually pathognomonic; troponin rise |
| Acute pericarditis | Transient PR depression ( > 0.5–0.8 mm), diffuse concave ↑ST (maximum in V5–6, II > I/III/aVF, never in aVR), J/T ratio > 25% in V6, shorter QTc [2][9] | Diffuse (not territorial), concave-up ("smiley face" morphology), PR depression, no reciprocal ST depression, no Q waves |
| LVH with strain pattern | Usually concave up, especially in V1–3, associated with other LVH features (Sokolow-Lyon criteria, Cornell voltage) [2][9] | LVH voltage criteria present; ST changes are "discordant" (opposite direction to QRS); no troponin rise; chronic finding |
| Early repolarisation ("high takeoff") | J-point elevation immediately follows S wave, concave ↑ST (highest at V2–3 up to 3 mm, rarely > 0.5 mm at V5–6, rarely > 2 mm in age > 45y, drops with tachycardia), no reciprocal ↓ST [2][9] | Young, healthy patient; concave ST morphology; "fish-hook" J-point notch; no reciprocal changes; no evolution over time; drops with exercise |
| LBBB | Can be distinguished based on Sgarbossa criteria: (1) Concordant ↑ST ≥ 1 mm in any lead → most specific for MI; (2) Concordant ↓ST ≥ 1 mm in V1–3 → specific for MI; (3) Discordant ↑ST ≥ 5 mm → less specific for MI [2][9] | New LBBB in setting of chest pain is treated as STEMI-equivalent (ESC/ACC guidelines); use Sgarbossa or Modified Sgarbossa (Smith) criteria to identify MI superimposed on LBBB |
| Ventricular aneurysm | Usually ≤ 3 mm at V1–3, may have QS pattern V1–3 if anterior, QR pattern in II/III/aVF if inferior, T wave flat or inverted → confirm by cTn negative and echo positive [2][9] | Persistent ST-elevation that does not evolve; troponin normal (unless new event); old Q waves; echo shows dyskinetic segment with thinned wall |
| Brugada syndrome | Coved ST-elevation in V1–V3 with RBBB morphology | No troponin rise; characteristically in young men of Southeast Asian descent; may have FHx of sudden cardiac death; provocable with ajmaline/flecainide |
| Pre-excitation (WPW) | Delta wave + short PR; can cause ST changes | Delta wave visible; history of palpitations (SVT) |
| Subarachnoid haemorrhage | ST-elevation due to cardiac stunting from adrenaline surge [2][9]; may also show widespread deep T-wave inversion, prolonged QT | Thunderclap headache; ↓consciousness; CT brain positive for SAH |
| Pulmonary embolism | Right heart strain pattern: ST-elevation in V1 (± V2–V3), inferior leads; S1Q3T3; new RBBB; sinus tachycardia | Pleuritic pain; dyspnoea > chest pain; risk factors for VTE; D-dimer elevated; CT-PA confirmatory |
| Hyperkalaemia | Peaked (tented) T waves can be confused with hyperacute T waves; severe hyperK → widened QRS → sine wave | T waves are narrow-based and peaked (vs. hyperacute T waves which are bulky and wide); QT shortened (vs. prolonged in MI); check serum K⁺ |
| Metabolic disturbances | Various ST/T changes | Clinical context; biochemistry |
| Cholecystitis | Rarely causes inferior ST changes | RUQ tenderness; ↑WBC; liver function derangement; abdominal ultrasound |
The lecture slide explicitly lists both false positives and false negatives for ECG diagnosis of MI [1]:
ECG False Positives for STEMI: Benign early repolarisation, LBBB, pre-excitation, Brugada syndrome, peri-/myocarditis, pulmonary embolism, subarachnoid haemorrhage, metabolic disturbances such as hyperkalaemia, failure to recognise normal limits for J-point displacement, lead transposition or use of modified lead configuration, cholecystitis [1]
ECG False Negatives for STEMI: Prior Q waves and/or persistent ST-elevation, paced rhythm, LBBB [1]
LBBB — Both a False Positive AND a False Negative!
LBBB appears on BOTH lists [1]. Here's why:
- False positive: LBBB inherently causes "discordant" ST-elevation (ST segment goes in the opposite direction to the main QRS deflection), which can be mistaken for STEMI
- False negative: LBBB's baseline ST-elevation can mask the concordant ST changes of a true MI — you can't see the STEMI pattern through the LBBB
This is why new LBBB in the setting of ischaemic symptoms is treated as a STEMI-equivalent and warrants emergent reperfusion. Use Sgarbossa criteria to help distinguish true MI from baseline LBBB changes [2].
Distinguishing STEMI from Key Mimics — Quick Visual Guide
The morphology of ST-elevation is your most important clue:
| Morphology | Shape | Think... |
|---|---|---|
| Convex upward ("tombstone" / "frowny face" ⌒) | Dome-shaped, ST merges with T wave | STEMI |
| Concave upward ("smiley face" ⌣) | Saddle-shaped | Pericarditis, early repolarisation, LVH strain |
| Coved (descending slope after J-point elevation) | Downsloping ST into inverted T | Brugada syndrome (V1–V3) |
Quick trick: If you can imagine a "smiley face" on the ST segment (concave up) → less likely to be STEMI. If it looks like a "frown" or a "tombstone" (convex up) → think STEMI until proven otherwise.
C. Distinguishing STEMI from the Three Most Important Mimics in Detail
| Feature | STEMI | Acute Pericarditis |
|---|---|---|
| Pain character | Crushing, heavy, constricting | Sharp, knife-like, aggravated by respiratory movement [1] |
| Pain radiation | Arms, jaw, neck | Trapezius ridge (characteristic) [1]; also back |
| Positional relief | None | Relieved by sitting forward (pericardium moves away from heart) |
| ST morphology | Convex up, localised to territory | Diffuse concave up; max V5–6, II > I/III/aVF, never in aVR [2] |
| PR segment | Normal | PR depression > 0.5–0.8 mm [2] (very specific!) |
| Reciprocal changes | Present (almost pathognomonic for STEMI) | Absent |
| Q waves | Develop in STEMI | Absent |
| Troponin | Always elevated in MI | May be mildly elevated if myocarditis component ("myopericarditis"), but much less |
Why pericarditis causes diffuse ST-elevation: The pericardium envelops the entire heart → inflammation is generalised → diffuse epicardial injury current → widespread ST-elevation (not confined to a single coronary territory). In contrast, STEMI occludes a single artery → ST-elevation is localised to leads overlying that territory.
Why PR depression occurs in pericarditis: The atrium is thin-walled and particularly susceptible to pericardial inflammation → atrial injury current → PR depression (the PR segment is generated during atrial repolarisation).
| Feature | STEMI | Aortic Dissection |
|---|---|---|
| Pain onset | Minutes to develop | Sudden onset, maximal at onset [4][6] |
| Pain character | Crushing, heavy | Tearing, ripping [1][4] |
| Pain radiation | Arms, jaw | Back, interscapular, abdomen [4] |
| BP | ↑ or ↓ | Often hypertension (Type B 70%); may be hypotensive if tamponade/rupture [4] |
| Pulse deficits | Absent | Present — weak/absent carotid, brachial, or femoral [4] |
| New murmur | MR from papillary muscle dysfunction | Early diastolic decrescendo murmur (AR) [4] |
| CXR | Usually non-diagnostic | Widened mediastinum, irregular aortic outline [4] |
| ECG | Territorial ST-elevation | May be normal, non-specific, or show inferior STEMI (if RCA involved) |
| D-dimer | Usually normal or mildly elevated | Markedly elevated (sensitive but not specific) |
| Definitive Ix | Coronary angiography | CT angiography (CTA) in haemodynamically stable patients [4] |
Why this distinction is life-or-death: Aortic dissection + standard STEMI treatment (antiplatelet, anticoagulant, fibrinolytic) = catastrophic haemorrhage. Always have a high index of suspicion when pain is "maximal at onset" or "tearing" in quality, especially with a background of uncontrolled hypertension or connective tissue disease [1][4].
| Feature | STEMI | Massive PE |
|---|---|---|
| Pain character | Crushing, central | Pleuritic (worse on inspiration) ± central if massive; haemoptysis [1] |
| Dyspnoea | Secondary to LV failure | Primary symptom (often severe, disproportionate to pain) |
| Risk factors | ASCVD risk factors | VTE risk factors (immobilisation, surgery, malignancy, OCP, DVT) |
| Examination | LV failure signs | RV failure signs (↑JVP, parasternal heave); DVT signs; hypoxia |
| ECG | Territorial ST-elevation | Sinus tachycardia (most common), S1Q3T3, RBBB, right axis, ST-elevation in V1 ± V2–V3 |
| Troponin | Always elevated | May be mildly elevated (RV strain) |
| D-dimer | Low sensitivity for ruling in | Highly sensitive (normal D-dimer effectively rules out PE) |
| Definitive Ix | Coronary angiography | CT pulmonary angiography |
Why massive PE can mimic anterior STEMI on ECG: Acute RV pressure overload → RV dilatation → the RV pushes against the anterior chest wall → ST-elevation in right-sided leads (V1–V3). The S1Q3T3 pattern (S wave in lead I, Q wave and T-wave inversion in lead III) reflects the acute rightward axis shift from RV strain.
The practical bedside approach when you see ST-elevation:
- Is the patient dying right now? → ABC, resuscitate, treat tension pneumothorax/tamponade immediately
- Does the clinical history fit STEMI? → Crushing chest pain > 20 min, not relieved by GTN, risk factors, sweaty/distressed
- Does the ECG pattern fit STEMI? → Localised, convex ST-elevation with reciprocal depression → strongly favours STEMI
- Are there red flags for an alternative diagnosis? → Tearing pain/pulse deficits (dissection); pleuritic pain/haemoptysis (PE); positional/sharp (pericarditis); young, well, no risk factors (early repolarisation)
- Resolve uncertainty quickly — serial ECGs, point-of-care troponin, bedside echo, CXR can all be done within minutes
When in Doubt — Treat as STEMI
In an ambiguous clinical scenario with ST-elevation and ischaemic symptoms, it is safer to treat as STEMI and proceed to emergent angiography [1][2]. The risk of missed STEMI (ongoing myocardial necrosis, arrhythmia, death) far exceeds the risk of an unnecessary cath lab activation. The only exception is when aortic dissection is strongly suspected — in that case, obtain imaging first [4].
Once you are confident the presentation is ACS (not a mimic), you must differentiate between STEMI, NSTEMI, and unstable angina, because management pathways differ:
Important to differentiate between types of ACS to guide treatment based on: (1) Clinical presentation: severity of pain; (2) ECG: no ST changes < ↓ST < ↑ST; (3) Troponin: ↑cTn → ↑likelihood of STEMI. All features should be integrated to give a diagnosis [2].
| Feature | STEMI | NSTEMI | Unstable Angina |
|---|---|---|---|
| ECG | ST-segment elevation ± reciprocal depression → evolving Q waves [1][2] | ST depression, T-wave inversion, ± loss of R waves [2] | May be normal, or show ST depression / T-wave changes |
| Troponin | Always elevated (rise at 4–6h) | Elevated | Normal (by definition) |
| Pathology | Complete occlusion → transmural MI | Partial occlusion → subendocardial MI | Partial occlusion → ischaemia without necrosis |
| Reperfusion | Emergent (primary PCI or fibrinolysis) | Invasive strategy within 24–72h based on risk | Medical therapy ± elective angiography |
The lecture slide shows the hs-troponin-based diagnostic algorithm for suspected NSTE-ACS: blood sampling at 0h → rule-out if 0h hs-cTn very low with low clinical risk → if not ruled out, repeat at 1h (or 3h depending on assay) → rule-in if significant rise or high absolute value → observe if indeterminate [7]. This algorithm does NOT apply to STEMI — if ST-elevation is present with ischaemic symptoms, you proceed directly to reperfusion without waiting for troponin.
The ECG slide from GC 088 summarises: ST-segment elevation indicates full-thickness cardiac muscle injury; pathological Q-wave indicates muscle necrosis; T-wave inversion indicates muscle ischaemia [1].
High Yield Summary — Differential Diagnosis of STEMI
Three-level differential thinking:
- Differential of acute chest pain — The "Big Five" life-threatening causes: ACS, aortic dissection, PE, tension pneumothorax, myopericarditis/tamponade. Also consider GI causes (most common overall at 42%), musculoskeletal, and anxiety.
- Differential of ST-elevation on ECG — Not every ST-elevation is STEMI. Key mimics: pericarditis (diffuse concave, PR depression), early repolarisation (J-point elevation, young patient), LVH strain, LBBB (use Sgarbossa), Brugada, ventricular aneurysm, PE, SAH, hyperkalaemia. LBBB is both a false positive and false negative for STEMI.
- Differentiating within ACS — STEMI (ST-elevation + troponin rise → emergent reperfusion) vs NSTEMI (no ST-elevation + troponin rise → early invasive strategy) vs UA (no ST-elevation + no troponin rise → medical therapy).
Key distinguishing clues:
- Convex ST + reciprocal changes + evolving Q waves = STEMI
- Tearing pain, maximal at onset, pulse deficits = aortic dissection (get CTA before cath lab!)
- Diffuse concave ST + PR depression + trapezius ridge pain = pericarditis
- Pleuritic pain + haemoptysis + S1Q3T3 = PE
- New LBBB + ischaemic symptoms = STEMI-equivalent → treat as STEMI
Active Recall - Differential Diagnosis of STEMI
References
[1] Lecture slides: GC 088. Sudden Severe Chest Pain.pdf (pp. 2, 13, 26, 30) [2] Senior notes: Ryan Ho Cardiology.pdf (pp. 36, 54, 128, 129, 131) [4] Senior notes: felixlai.md (Aortic Dissection section, p. 1328) [6] Senior notes: Ryan Ho Fundamentals.pdf (pp. 199, 203, 457) [7] Lecture slides: GC 028. Accelerating chest pain_Acute coronary (1).pdf (pp. 16, 17, 27) [9] Senior notes: Ryan Ho Fundamentals.pdf (p. 457)
Diagnostic Criteria for STEMI
The diagnosis of MI rests on demonstrating myocardial necrosis (biomarker rise) in a clinical context consistent with ischaemia. For STEMI specifically, the ECG is the gatekeeper — you act on the ECG pattern before troponin results return.
The formal diagnostic criteria for acute MI (Type 1 and 2) [1][2]:
Detection of rise and/or fall of cardiac biomarkers (preferably troponin) with at least one value above the 99th percentile of the upper reference limit together with evidence of ischaemia with at least one of the following:
Let's unpack why each criterion matters from first principles:
| Criterion | Why It's Included | Pathophysiological Basis |
|---|---|---|
| Rise and/or fall of cardiac biomarker above 99th percentile URL | Proves myocardial necrosis has occurred | Myocyte membrane disruption → release of intracellular structural proteins (troponin) into the bloodstream; the "rise and/or fall" pattern distinguishes acute injury from chronic elevation (e.g., CKD) |
| Symptoms of ischaemia | Places the biomarker rise in clinical context | Chest pain/dyspnoea from ischaemia; without symptoms, a troponin rise alone could be from myocarditis, PE, sepsis, etc. |
| New ST-T changes or new LBBB | Electrochemical evidence of acute ischaemia/injury | Transmural ischaemia → injury current flows from ischaemic zone to normal zone → ST vector points toward injured territory → ST-elevation in overlying leads |
| Pathological Q waves | Evidence of completed transmural necrosis | Dead myocardium is electrically silent → the recording electrode "sees through" the dead tissue to the opposite wall → negative deflection (Q wave) |
| New wall motion abnormality on imaging | Structural proof that myocardium has stopped contracting | Necrotic/stunned muscle cannot contract → akinesis or dyskinesis on echo/MRI |
| Intracoronary thrombus | Direct visualisation of the culprit lesion | Angiographic confirmation of the thrombotic occlusion — the "smoking gun" |
Critical Nuance — STEMI Diagnosis Does NOT Wait for Troponin
In STEMI, the diagnosis is made clinically + ECG and reperfusion is initiated before troponin results are available. Why? Because troponin takes 3–6 hours to rise above the 99th percentile (even with high-sensitivity assays, the earliest detectable rise is ~1–3 hours), but myocardium is dying from the moment of occlusion. The purpose of troponin in STEMI is to confirm the diagnosis retrospectively, NOT to gate the decision for reperfusion [1][6].
The ESC 2017/2023 guidelines define STEMI as new ST-elevation at the J-point in ≥ 2 contiguous leads meeting the following voltage thresholds:
| Lead Group | ST-Elevation Threshold |
|---|---|
| V2–V3 in men ≥ 40 years | ≥ 0.2 mV (2 mm) |
| V2–V3 in men < 40 years | ≥ 0.25 mV (2.5 mm) |
| V2–V3 in women | ≥ 0.15 mV (1.5 mm) |
| All other leads (I, aVL, V4–V6, II, III, aVF) | ≥ 0.1 mV (1 mm) |
| V3R–V4R (right ventricular) | ≥ 0.05 mV (0.5 mm); ≥ 0.1 mV in men < 30 yrs |
| V7–V9 (posterior) | ≥ 0.05 mV (0.5 mm) |
Why are V2–V3 thresholds higher? These leads sit directly over the thin RV free wall and septum, which are closest to the chest surface. The proximity means even normal repolarisation generates larger voltage — hence a higher threshold is needed to avoid false positives (especially early repolarisation in young men).
Why are female thresholds lower? Women generally have smaller hearts with less myocardial mass → smaller amplitude ECG signals → a lower voltage threshold captures the same degree of injury.
STEMI Equivalents (Treated as STEMI for Reperfusion Purposes)
Not all acute complete coronary occlusions produce classic ST-elevation. The following patterns warrant emergent reperfusion as STEMI-equivalents:
| Pattern | Significance |
|---|---|
| New LBBB with ischaemic symptoms | LBBB alters the entire depolarisation/repolarisation sequence → standard ST criteria cannot be applied; new LBBB in the setting of chest pain = presumed acute occlusion. Use Sgarbossa criteria to increase specificity [2][6] |
| Posterior MI (ST depression V1–V3 with tall R waves and upright T waves as reciprocal changes, or ST-elevation ≥ 0.5 mm in V7–V9) [2] | Standard 12-lead ECG does not have leads directly over the posterior wall → posterior STEMI manifests as "mirror-image" changes in V1–V3 |
| De Winter T waves | Upsloping ST depression > 1 mm at the J-point in V1–V6 with tall, symmetric T waves — represents hyperacute LAD occlusion; no ST-elevation is present, but this is a STEMI-equivalent |
| ST-elevation in aVR with diffuse ST depression | Suggests left main stem or proximal LAD occlusion [2] — catastrophic territory |
| Hyperacute T waves alone with ongoing ischaemic symptoms | May represent the earliest phase of STEMI (before frank ST-elevation develops); serial ECGs ± emergent angio |
Criteria for prior MI [1]:
Development of new pathological Q waves with or without symptoms Imaging evidence of a region of loss of viable myocardium that is thinned and fails to contract, in the absence of a non-ischaemic cause Pathological findings post-mortem of a healed or healing myocardial infarction [1]
Pathological Q waves are defined as:
- Any Q wave in V2–V3 ≥ 0.02 s duration or QS complex
- Q wave ≥ 0.03 s duration and ≥ 0.1 mV deep (or QS complex) in any 2 contiguous leads of a lead group
- R wave ≥ 0.04 s in V1–V2 with R/S ≥ 1 (posterior MI equivalent)
Why do Q waves form? Once transmural necrosis is complete, the dead tissue is electrically inert — it neither depolarises nor repolarises. The recording electrode overlying the infarct zone effectively "looks through" the dead wall and records the electrical activity of the opposite, healthy wall moving away from it → inscribes a negative deflection (Q wave).
The key principle: in STEMI, the clock starts ticking the moment the patient develops symptoms. The diagnostic pathway must be fast enough to achieve reperfusion within target times — door-to-balloon ≤ 90 minutes for primary PCI, or door-to-needle ≤ 30 minutes for fibrinolysis.
Master Algorithm: From Presentation to Reperfusion Decision
The lecture slide from GC 088 explicitly outlines the revascularisation algorithm for STEMI [1]:
Symptom onset < 12h → PCI feasible? → Yes → Primary PCI. No → Fibrinolysis. Symptom onset ≥ 12h → Consider PCI if cardiogenic shock/heart failure, ongoing ischaemia, electrical instability, large myocardium at risk. PCI feasible within 12–24h of symptom onset if symptoms or severe ischaemia persist. Totally occluded infarct artery > 24h and asymptomatic → no routine PCI of the occluded artery [1].
Time Targets in STEMI — Memorise These
| Metric | Target |
|---|---|
| ECG acquisition | ≤ 10 minutes from first medical contact |
| Door-to-needle (fibrinolysis) | ≤ 30 minutes |
| Door-to-balloon (primary PCI) | ≤ 90 minutes (≤ 60 if presenting directly to PCI centre) |
| Total ischaemic time (symptom onset → wire crossing) | ≤ 120 minutes (ideally) |
| Transfer for angiography after successful fibrinolysis | 2–24 hours |
| Rescue PCI after failed fibrinolysis | Immediately |
Every minute of delay = more myocardial death. The ESC considers primary PCI the preferred strategy if it can be performed within 120 minutes of STEMI diagnosis.
Investigation Modalities — Key Findings and Interpretations
Initial investigations for suspected ACS [6]:
Admit CCU if high-risk (ongoing chest pain, ↓BP, APO, ventricular arrhythmia…). Bed rest with continuous ECG monitoring. 12-lead ECG stat and repeat at least daily × 3d (more frequently in severe cases). Cardiac enzymes daily × 3d (repeat troponin 6–12h later if 1st Tn is normal). Basic bloods: CBC, L/RFT, lipid profile (≤ 24h), aPTT/INR (as baseline for heparin). CXR: usually non-diagnostic in ACS, look for other causes (e.g., aortic dissection, PE, pneumonia or pneumothorax) [6].
1. Electrocardiography (ECG)
The single most important investigation in STEMI — and the fastest.
Perform 12-lead ECG as soon as possible [2] — within 10 minutes of first medical contact.
Sequential ECG evolution in STEMI [2]:
| Phase | Timing | ECG Finding | Pathophysiological Basis |
|---|---|---|---|
| Hyperacute | Minutes | Hyperacute T waves: bulky and wide, J point may be depressed, QT usually prolonged [2][6] | Earliest sign of transmural ischaemia; ↑extracellular K⁺ from ischaemic myocytes → altered repolarisation → tall, broad T waves |
| Acute injury | Minutes–hours | ST-elevation + reciprocal ST depression [2] | Injury current: ischaemic zone has a more negative resting potential → current of injury flows from ischaemic to normal zone during the ST segment (TQ depression = baseline shift → apparent ST-elevation) |
| Necrosis | Hours–days | Pathological Q waves (85% persist indefinitely) [2] | Dead myocardium is electrically silent → electrode "sees through" necrotic tissue to opposite wall → records negative deflection |
| Resolution | Days–weeks | Inverted T waves (usually ↓amplitude after acute phase) [2]; ST-elevation resolves | Repolarisation abnormality in recovering/scarred tissue; persistent ST-elevation after STEMI should raise suspicion for ventricular aneurysm [2] |
How to distinguish hyperacute T waves from hyperkalaemia:
| Territory | ECG Leads with ST-Elevation | Culprit Artery | Special Considerations |
|---|---|---|---|
| Anterior / Anteroseptal | V1–V4 (± V5–V6, I, aVL) | LAD | Largest territory at risk; worst prognosis |
| Lateral | I, aVL, V5–V6 | LCx or diagonal | May be "electrically quiet" — fewer leads involved |
| Inferior | II, III, aVF | RCA (85%) or LCx (15%) | Always check V4R for RV involvement |
| Posterior | Reciprocal changes in V1–3 including ↓ST, R:S ≥ 1, tall upright T; ↑ST in V7–9 (typically modest) [2] | LCx or RCA | Easily missed → vigilant in inferior/lateral MI; when present, indicates extensive infarct and suggests ↑risk of death. If suspected, should place V7–9 on posterior chest wall → should show typical STEMI changes [2] |
| RV | ↑ST in V1 > V2 (or ↓ST in V2); ↑ST in III > II; ↑ST in V3–6R [2] | RCA (proximal) | Easily missed → vigilant in inferior MI (complicates 40% of inferior STEMI). Very preload sensitive → C/I to nitrates and other ↓preload agents due to severe hypotension [2] |
| Left Main / Proximal LAD | ST-elevation in aVR with widespread ST depression [2] | Left main stem | Catastrophic — consider emergent CABG |
Don't Miss Posterior and RV MI!
These are the two most commonly missed STEMI patterns because they are not well-seen on the standard 12-lead ECG. Clinical rule: In any inferior STEMI (ST-elevation in II, III, aVF), always obtain:
- Right-sided leads (V3R–V6R) → to detect RV infarction
- Posterior leads (V7–V9) → to detect posterior extension
Missing RV infarction is dangerous because these patients need IV fluids (preload-dependent) and must avoid nitrates and diuretics which can cause catastrophic hypotension [2].
| Pattern | ECG Appearance | Clinical Significance |
|---|---|---|
| Wellens syndrome | Deeply inverted or biphasic T waves in V2–3 [6] | Highly specific for critical LAD stenosis. Extremely high risk for extensive anterior wall MI in the subsequent days/weeks [6] — needs urgent angiography even if troponin is normal and patient is pain-free |
| Pseudonormalisation of T waves | Transient normalisation of T wave from an inverted form [6] | Indicates transient recanalisation of coronary artery → prone to restenosis [6] |
| De Winter T waves | Upsloping ST depression at J-point in V1–V6 with tall symmetric T waves | Hyperacute LAD occlusion — STEMI equivalent despite absence of ST-elevation |
- Repeat at least every 15–30 minutes if initial ECG is non-diagnostic but clinical suspicion remains high
- Repeat at least daily × 3 days [6] to track evolution (development of Q waves, resolution of ST-elevation, T-wave inversion)
- More frequent monitoring if ongoing symptoms, haemodynamic instability, or arrhythmias
2. Serum Cardiac Biomarkers
Primary basis of diagnosing MI [2]:
| Feature | Detail | Why |
|---|---|---|
| What it is | Structural protein of the troponin complex (troponin C, I, T) within the cardiac sarcomere; cardiac isoforms (cTnT, cTnI) are specific to cardiac muscle | Skeletal muscle has different isoforms → cardiac troponin is highly specific for myocardial injury |
| Time course | Rise (4–6h) → elevated for up to 2 weeks [2] | Initial rise reflects release from cytoplasmic pool; prolonged elevation reflects ongoing degradation of myofibrillar-bound troponin from necrotic tissue |
| High-sensitivity assays (hs-cTn) | Can detect troponin at 10–100× lower concentrations than conventional assays; detectable as early as 1–3 hours | Allows earlier rule-in/rule-out; but also detects troponin in non-ACS conditions → must interpret in clinical context |
| Advantages | Not normally present → ↑sensitivity, ↑specificity [2] | Troponin is an intracellular structural protein not found in blood under normal conditions → any elevation implies myocardial injury |
| Use | Detection of first infarct event [2] | Gold standard biomarker for diagnosing MI |
| Rise-and-fall pattern | The "delta" (change over serial measurements) is what distinguishes acute MI from chronic troponin elevation | Acute MI → sharp rise then fall; chronic conditions (CKD, HF) → chronically elevated without significant delta |
Troponin can be elevated (troponin leak) in conditions other than MI [2]:
| Category | Examples |
|---|---|
| Other ischaemia | Tachycardia, coronary spasm, PCI or cardiothoracic surgery, hypoxia or hypotension [2] |
| Other myocardial injury | Myocarditis, heart failure, Takotsubo cardiomyopathy, pulmonary embolism, aortic dissection, other cardiomyopathy (e.g., infiltrative), cardiotoxins [2] |
| Systemic diseases | Renal failure, sepsis, critical illness, stroke, SAH [2] |
The key to interpreting troponin: always correlate with the clinical picture and ECG. A troponin rise in a patient with ST-elevation and crushing chest pain = STEMI. A troponin rise in a patient with sepsis and no chest pain = troponin leak from demand ischaemia or direct toxic injury.
| Feature | Detail | Why |
|---|---|---|
| Time course | Rise (4–6h) → peak (12h) → normalise (48–72h) [2] | Shorter window of elevation than troponin |
| Caveat | Not sensitive or specific (especially consider skeletal muscle damage, e.g., IM injection) [2] | CK-MB is also present in skeletal muscle (1–3% of total CK) → can be elevated from muscle trauma, rhabdomyolysis |
| Use | Mainly to detect early re-stenosis (cTn stays high for up to 10 days) [2] | Because CK-MB normalises within 48–72h, a new rise after initial normalisation clearly indicates a new ischaemic event (reinfarction). Troponin stays elevated too long to detect this reliably |
| Marker | Features | Clinical Role |
|---|---|---|
| Myoglobin | First marker to rise [2] (1–2 hours); but very non-specific (also in skeletal muscle) | Historically used for very early detection; largely superseded by hs-troponin |
| LDH | Rises late (24–48h), peaks at 3–6 days, elevated for 8–14 days | Historical marker; no longer routinely used for MI diagnosis |
| AST | Rises at 12h, peaks at 24–48h | Non-specific (liver, muscle); no longer used for MI |
| BNP / NT-proBNP | Rises with myocardial wall stress (ventricular stretch) | Not diagnostic for MI per se, but prognostically useful — ↑BNP in STEMI reflects degree of LV dysfunction and predicts worse outcomes |
Basic bloods: CBC, L/RFT, lipid profile (≤ 24h), aPTT/INR (as baseline for heparin) [6].
| Test | Rationale | Key Findings to Look For |
|---|---|---|
| CBC | Anaemia can cause Type 2 MI (↓O₂ delivery); WBC may be elevated from stress response/inflammation; platelets as baseline before antiplatelet therapy | ↓Hb → consider demand ischaemia; ↑WBC (leukocytosis) → stress response or infection |
| Renal function (U&E/Cr) | Baseline before contrast (PCI) and nephrotoxic drugs; hyperkalaemia → arrhythmia risk; AKI from cardiogenic shock | ↑Cr → CKD (risk factor + affects drug dosing); ↑K⁺ → arrhythmia risk |
| Liver function | "Shock liver" from cardiogenic shock; baseline before statins | ↑ALT/AST → hepatic congestion from RHF or shock liver |
| Lipid profile | Must be taken ≤ 24h [6] of admission (acute-phase response can lower LDL after 24h, giving falsely reassuring values) | Guides long-term statin therapy targets (LDL < 1.4 mmol/L in very high risk) |
| HbA1c / Glucose | DM is a major risk factor; stress hyperglycaemia is common in STEMI | ↑HbA1c → undiagnosed or poorly controlled DM; hyperglycaemia in STEMI → worse prognosis |
| aPTT / INR | Baseline before heparin therapy [6] | Needed to guide anticoagulant dosing and monitor for over-anticoagulation |
| ABG ± lactate | Assess oxygenation, ventilation, acid-base status; lactate reflects tissue perfusion | Metabolic acidosis + ↑lactate → cardiogenic shock / poor perfusion |
| Magnesium | Hypomagnesaemia → ↑arrhythmia risk (predisposes to Torsades de Pointes) | Correct if low |
CXR: usually non-diagnostic in ACS, but look for other causes (e.g., aortic dissection, PE, pneumonia or pneumothorax) [6].
| Finding | Significance |
|---|---|
| Normal | Common in STEMI — a normal CXR does not exclude MI |
| Pulmonary oedema (upper lobe diversion, Kerley B lines, bat-wing opacities, pleural effusions) | LV failure from extensive MI → ↑pulmonary venous pressure → Killip class II–III |
| Cardiomegaly | Pre-existing LV dysfunction or dilated cardiomyopathy; may also develop acutely with large infarcts |
| Widened mediastinum / irregular aortic outline | Raises suspicion for aortic dissection [4] — must exclude before giving anticoagulation/antiplatelet |
| Pneumothorax | Alternative diagnosis for chest pain |
| Pneumonia/consolidation | Alternative/concurrent diagnosis |
| Normal cardiac silhouette with clear lung fields | Reassuring but does not exclude MI |
Echocardiography is the most important bedside imaging modality in STEMI. It can be done rapidly at the bedside and provides critical information:
| What It Assesses | Finding | Clinical Significance |
|---|---|---|
| Regional wall motion abnormalities (RWMA) | Hypokinesis/akinesis/dyskinesis in territory corresponding to culprit artery | Confirms ischaemia/infarction; correlates with ECG territory |
| LV ejection fraction (LVEF) | ↓LVEF | Strongest predictor of long-term survival [2]; LVEF < 40% → high risk; guides need for ACEI/ARB, BB, aldosterone antagonist, ICD consideration |
| Mechanical complications | New MR jet (papillary muscle rupture), VSD (septal rupture), pericardial effusion (free wall rupture/Dressler's), LV thrombus | Life-threatening — requires urgent surgical/interventional management |
| RV function | RV dilatation, ↓RV contractility (TAPSE < 16 mm) | Confirms RV infarction in inferior STEMI |
| Alternative diagnoses | Aortic dissection flap, pericardial effusion (tamponade), acute severe AR | Helps differentiate from mimics |
The definitive diagnostic and therapeutic investigation for STEMI.
| Aspect | Detail |
|---|---|
| Indication | All STEMI patients undergoing primary PCI (diagnostic + therapeutic in the same session) |
| Access | Radial artery preferred (lower bleeding risk, earlier ambulation) vs. femoral artery |
| Findings | Complete thrombotic occlusion of culprit artery (TIMI 0 or 1 flow); may also identify non-culprit stenoses |
| TIMI flow grade | 0 = complete occlusion; 1 = penetration without perfusion; 2 = partial perfusion; 3 = normal flow (goal of PCI) |
| Intervention | Primary PCI = balloon angioplasty ± drug-eluting stent (DES) to the culprit lesion |
| Additional techniques | Thrombus aspiration (no longer routine — TOTAL trial showed no benefit); optical coherence tomography (OCT) or intravascular ultrasound (IVUS) for lesion characterisation |
| Investigation | Indication | Key Findings |
|---|---|---|
| Cardiac MRI | Post-STEMI for viability assessment, myocarditis vs MI differentiation, assessment of infarct size and microvascular obstruction | Late gadolinium enhancement (LGE) pattern: subendocardial/transmural in MI (follows coronary territory) vs. mid-wall/epicardial in myocarditis |
| CT coronary angiography | Not used acutely in STEMI (patient goes straight to cath lab); useful for stable CAD screening in low-to-intermediate pre-test probability [10][11] | Evaluates coronary anatomy non-invasively; excellent NPV (99–100%) for ruling out significant CAD |
| Myocardial perfusion imaging (MPI / SPECT) | Screening and diagnosis of CAD; determines adequacy of blood flow ± stress; determines viability of myocardium [11] | Normal → homogeneous perfusion; Ischaemia → cold spots under stress only; Infarct → cold spots at rest AND under stress [11] |
| CT aortogram | When aortic dissection is suspected (and patient is haemodynamically stable enough) | Identification of true and false lumens; compressed true lumen is the key radiological finding [4] |
High Yield Summary — Diagnosis of STEMI
Diagnostic Criteria (4th/5th Universal Definition):
- Rise and/or fall of cardiac troponin above 99th percentile URL PLUS ≥ 1 of: ischaemic symptoms, new ST-T/LBBB, pathological Q waves, new RWMA on imaging, intracoronary thrombus on angiography/autopsy.
- In practice, STEMI is diagnosed on ECG + clinical presentation — do NOT wait for troponin before reperfusion.
ECG Criteria for STEMI:
- New ST-elevation at J-point in ≥ 2 contiguous leads: ≥ 2 mm in V2–V3 (men ≥ 40); ≥ 2.5 mm (men < 40); ≥ 1.5 mm (women); ≥ 1 mm all other leads.
- STEMI equivalents: new LBBB, posterior MI (reciprocal V1–V3 changes), De Winter T waves, ST-elevation in aVR with diffuse depression.
Biomarkers:
- hs-Troponin: gold standard; rises 1–6h, elevated up to 2 weeks; confirms MI but does NOT gate reperfusion decision.
- CK-MB: rises 4–6h, normalises 48–72h; useful for detecting reinfarction.
Key Investigations:
- ECG within 10 min → serial ECGs q15–30 min if non-diagnostic but suspicious
- Troponin at presentation → repeat 3–6h (or 1h with hs-assay)
- CBC, RFT, glucose, lipids ≤ 24h, coag (baseline for heparin)
- CXR: exclude mimics (dissection, PTX)
- Bedside echo: RWMA, LVEF, mechanical complications, RV function
- Coronary angiography: definitive — diagnostic + therapeutic (primary PCI)
Time Targets: ECG ≤ 10 min; door-to-balloon ≤ 90 min; door-to-needle ≤ 30 min.
Active Recall - STEMI Diagnostic Criteria, Algorithm, and Investigations
[1] Lecture slides: GC 088. Sudden Severe Chest Pain.pdf (pp. 21, 26, 30, 35, 48) [2] Senior notes: Ryan Ho Cardiology.pdf (pp. 117, 127, 128, 131, 142) [4] Senior notes: felixlai.md (Aortic Dissection section, p. 1328) [5] Senior notes: Ryan Ho Critical Care.pdf (pp. 17, 22) [6] Senior notes: Ryan Ho Fundamentals.pdf (pp. 203, 448, 457) [10] Senior notes: Ryan Ho Diagnostic Radiology.pdf (p. 43) [11] Senior notes: Ryan Ho Diagnostic Radiology.pdf (p. 57)
The management of STEMI follows a time-critical, systematic framework. Think of it in three phases: immediate/acute management (first hours), reperfusion therapy (the defining intervention), and long-term secondary prevention. Every treatment targets a specific pathophysiological step — nothing is given "just because."
The overall management framework [2]:
| Phase | Components |
|---|---|
| Acute ( < 24h) | Bed rest with close monitoring ± CCU; CBC, L/RFT, PT/aPTT, LP, CXR; serial ECG and cardiac enzymes; ± analgesics if required; nitrates, β-blockers always, ± DHP CCB if persistent discomfort; aspirin at/suspect dx, P2Y₁₂ blocker at dx or at PCI; heparin/LMWH at dx; reperfusion (thrombolysis if < 3h or PCI not available, PCI otherwise); β-blockers, ACEI/ARB always (≤ 24h); MRA if LVEF ≤ 40% + HF/DM; high-intensity statin always (≤ 24h) [2] |
| Long-term | Risk stratification: echo, stress test ± angiogram, ECG monitoring; risk factor modulation; mobilisation and rehabilitation; aspirin indefinitely; DAPT for ≥ 12 months if any stent used; β-blockers, ACEI/ARB always; MRA if LVEF ≤ 40% + HF/DM; high-intensity statin always [2] |
The lecture slide algorithm for revascularisation in STEMI [1]:
Symptom onset < 12h → PCI feasible? → Yes → Primary PCI. If PCI not feasible → fibrinolysis. Symptom onset ≥ 12h → Consider PCI if cardiogenic shock or heart failure, ongoing ischaemia, heart failure, or electrical instability. Large area of myocardium at risk within 12–24h → PCI feasible? → Yes → PCI. Totally occluded infarct artery > 24h and asymptomatic → no routine PCI [1].
Phase 1: Immediate / Acute Management
Inform on-call cardiologist. Admit CCU for high-risk cases or STEMI (under consideration for reperfusion therapy) [2].
| Measure | Rationale (Why?) | Detail |
|---|---|---|
| Bed rest with continuous ECG monitoring | Ischaemic myocardium is electrically unstable → ventricular arrhythmias (VF/VT) can occur at any time; bed rest ↓O₂ demand | Telemetry for ≥ 24–48h minimum |
| Correct precipitating factors | Factors that ↑O₂ demand or ↓supply worsen ischaemia | e.g., anaemia, hypoxia, tachyarrhythmia [2] |
| O₂ supplementation | Only if hypoxic — routine O₂ in non-hypoxic STEMI patients does NOT improve outcomes and may be harmful (vasoconstriction, free radical generation) | Keep SpO₂ > 90% and pO₂ > 60 mmHg [2]. ESC 2023 recommends O₂ only if SpO₂ < 90% |
| Nil by mouth or soft diet + stool softener | Ileus common in patients with acute MI [2]; straining (Valsalva) → vagal stimulation → bradycardia; also ↑intrathoracic pressure → ↓venous return | Lactulose or docusate sodium |
| Explain nature of disease to patient → allay anxiety [2] | Anxiety → sympathetic activation → ↑HR, ↑BP → ↑myocardial O₂ demand | Clear, calm communication |
Analgesia: required if nitrates insufficient for symptom relief [2].
| Drug | Dose | Mechanism | Rationale | Cautions |
|---|---|---|---|---|
| IV morphine | IV morphine + IV Maxolon 5–10 mg ± sedation (e.g., diazepam 2–5 mg PO TDS) [2] | μ-opioid receptor agonist → analgesia + anxiolysis + venodilation | ↓Distress, ↓adrenergic drive → ↓SVR, ↓BP, ↓risk of ventricular arrhythmias [2] | Respiratory depression; hypotension (venodilation); nausea/vomiting (give antiemetic); ↓GI motility (worsens ileus). Recent guidelines de-emphasise routine morphine — it may delay oral P2Y₁₂ inhibitor absorption |
| IV Maxolon (metoclopramide) | 5–10 mg IV | D₂ receptor antagonist → antiemetic + prokinetic | Prevents morphine-induced nausea/vomiting; also counteracts morphine's GI-slowing effect | Extrapyramidal side effects (rare, acute dystonia) |
Morphine — A Double-Edged Sword
Morphine reduces pain and sympathetic drive, which is beneficial. However, it also slows gastric emptying, which delays absorption of oral P2Y₁₂ inhibitors (ticagrelor, clopidogrel, prasugrel). This can result in delayed antiplatelet effect precisely when you need it most. Current ESC guidelines recommend using morphine only when genuinely needed for pain control, and considering IV cangrelor as a bridging antiplatelet in patients who have received morphine and may have delayed oral absorption.
Phase 2: Pharmacological Therapies (Concurrent with Reperfusion Planning)
These are given simultaneously while preparing for reperfusion. They are divided by therapeutic target.
C. Antiplatelet Therapy
The rationale is straightforward: the culprit lesion is an occlusive thrombus built on a platelet scaffold. You need to prevent further platelet aggregation and prevent re-thrombosis after mechanical reperfusion.
"Aspirin" → "a-cetyl-salicylic" → derived from salicylic acid found in willow bark ("salix").
| Aspect | Detail |
|---|---|
| Mechanism | Irreversible COX-1 inhibitor → blocks thromboxane A₂ (TXA₂) synthesis in platelets. TXA₂ is a potent platelet aggregator and vasoconstrictor. Because platelets are anucleate (no new protein synthesis), the inhibition lasts the entire platelet lifespan (~7–10 days) |
| Dose — Acute | 300 mg loading dose (chewed for faster buccal absorption) → then 75–100 mg daily maintenance |
| Dose — Long-term | Aspirin 75–100 mg daily, administered indefinitely [7][12] |
| Indication | Aspirin is recommended for all patients without contraindications [7] |
| Contraindications | Active GI bleeding; documented aspirin allergy/hypersensitivity (consider desensitisation); severe asthma with aspirin-exacerbated respiratory disease |
| Side effects | GI ulceration/bleeding (reduced with PPI cover); aspirin-exacerbated respiratory disease; Reye syndrome (children — irrelevant here) |
"P2Y₁₂" → a purinergic receptor subtype on platelets. When ADP binds P2Y₁₂, it amplifies platelet activation. Blocking this receptor provides a second, independent antiplatelet pathway on top of aspirin.
A P2Y₁₂ receptor inhibitor is recommended in addition to aspirin, and maintained over 12 months unless there are contraindications or an excessive risk of bleeding [7]:
| Drug | Class | Mechanism | Dose | Key Features |
|---|---|---|---|---|
| Ticagrelor | Direct-acting, reversible P2Y₁₂ antagonist | Binds P2Y₁₂ at a site distinct from ADP → allosteric inhibition; does NOT require hepatic activation | 90 mg BD [7]; loading dose 180 mg | Faster onset (~30 min), more potent, more predictable than clopidogrel; preferred in STEMI (PLATO trial — ↓mortality vs clopidogrel); causes dyspnoea (↑adenosine levels due to inhibition of ENT-1 equilibrative nucleoside transporter) and ventricular pauses |
| Clopidogrel | Thienopyridine, irreversible P2Y₁₂ antagonist (prodrug) | Requires CYP2C19 activation → active metabolite irreversibly binds P2Y₁₂ | 75 mg QD [7]; loading 300–600 mg | Slower onset; variable response (~15–30% are CYP2C19 poor metabolisers → ↓efficacy); interacts with PPI (inhibit CYP2C19/3A4 activation of clopidogrel prodrug → treatment failure) [2]; used when ticagrelor is not available or contraindicated [12] |
| Prasugrel | Thienopyridine, irreversible P2Y₁₂ antagonist (prodrug) | Requires single-step hepatic activation → more consistent than clopidogrel | 10 mg QD; loading 60 mg | More potent than clopidogrel; preferred over clopidogrel in PCI-treated STEMI (TRITON-TIMI 38 trial); C/I: prior stroke/TIA (↑ICH risk), age ≥ 75, weight < 60 kg (↓dose to 5 mg) |
| Cangrelor | IV, direct-acting, reversible P2Y₁₂ antagonist | Rapid onset (minutes), rapid offset (60 min half-life) | 30 μg/kg bolus then 4 μg/kg/min infusion | Bridge for patients unable to take oral P2Y₁₂ inhibitors (e.g., after morphine, NPO, intubated); transitions to oral agent after infusion stops |
The lecture slide on antiplatelet therapies for ACS [12]:
STEMI: Ticagrelor is first-line; clopidogrel if ticagrelor not available or contraindicated. If PCI performed: prasugrel or ticagrelor. If CABG needed: withdraw ticagrelor for 5 days and prasugrel for 7 days [12].
"GP IIb/IIIa" → glycoprotein IIb/IIIa is the final common pathway receptor for platelet aggregation (binds fibrinogen to cross-link platelets).
| Drug | Mechanism | Indication |
|---|---|---|
| Abciximab | Monoclonal antibody fragment → irreversible GP IIb/IIIa blockade | Selected patients only [2] — given in cath lab during PCI if high thrombus burden; less commonly used now with potent oral P2Y₁₂ inhibitors |
| Eptifibatide / Tirofiban | Small-molecule, reversible GP IIb/IIIa inhibitors | Similar indications; shorter acting |
The role of GP IIb/IIIa inhibitors has diminished with the availability of potent P2Y₁₂ inhibitors (ticagrelor, prasugrel) and is now largely reserved for bail-out situations during PCI (e.g., large thrombus burden, no-reflow, slow flow).
DAPT = aspirin + P2Y₁₂ inhibitor [2]:
- Aspirin: administered indefinitely [2]
- P2Y₁₂ blocker: administered for ≥ 12 months if any stent used (mandatory), 1–12 months even if no PCI done [2]
- Choice: clopidogrel 75 mg QD, prasugrel 10 mg QD or ticagrelor 90 mg BD [2]
Why 12 months? Drug-eluting stents (DES) take ~6–12 months for the polymer coating to allow complete endothelialisation of the strut surface. Until the stent is fully covered by endothelium, exposed metal is thrombogenic → premature DAPT cessation → stent thrombosis (catastrophic — mortality ~20–40%). After 12 months, consider de-escalation based on bleeding risk.
DAPT Duration — Not One-Size-Fits-All
The 12-month standard can be modified:
- Shortened DAPT (3–6 months) → if high bleeding risk (PRECISE-DAPT score ≥ 25)
- Extended DAPT (> 12 months) → if high ischaemic risk and low bleeding risk (e.g., prior stent thrombosis, complex PCI, DM + multivessel disease)
- Always balance ischaemic risk (stent thrombosis, recurrent MI) vs bleeding risk (major GI bleed, ICH)
The rationale: even with antiplatelet therapy, the coagulation cascade (thrombin generation, fibrin formation) continues. You need both antiplatelet AND anticoagulant to fully suppress thrombus propagation.
Heparin/LMWH at diagnosis [2].
| Drug | Mechanism | Dose | Advantages/Disadvantages |
|---|---|---|---|
| Unfractionated heparin (UFH) | Binds antithrombin III → accelerates its inhibition of thrombin (IIa) and factor Xa by ~1000-fold | 60 U/kg IV bolus (max 4000 U) → 12 U/kg/h infusion; target aPTT 50–70 s | Preferred during primary PCI (short half-life, reversible with protamine, dose can be titrated with ACT in cath lab); requires aPTT monitoring |
| Enoxaparin (LMWH) | Preferentially inhibits factor Xa > thrombin (via antithrombin III); more predictable pharmacokinetics | 0.5 mg/kg IV bolus (if PCI) or 1 mg/kg SC BD | More predictable dose-response; does not require routine monitoring; less HIT risk; preferred if fibrinolysis is chosen |
| Fondaparinux | Selective factor Xa inhibitor via antithrombin III | 2.5 mg SC OD | Lowest bleeding risk; good for conservative management; but NOT used during PCI (associated with catheter thrombosis — must give supplemental UFH) |
| Bivalirudin | Direct thrombin inhibitor (no antithrombin III needed) | 0.75 mg/kg bolus → 1.75 mg/kg/h infusion | Alternative to UFH during PCI; lower bleeding risk; useful in HIT (does not interact with PF4 antibodies) |
E. Anti-Ischaemic Therapy
These drugs reduce myocardial oxygen demand and/or improve supply, limiting infarct extension.
"Nitrate" → donates NO (nitric oxide) → activates guanylyl cyclase → ↑cGMP → smooth muscle relaxation.
| Aspect | Detail |
|---|---|
| Mechanism | Venodilation (↓preload → ↓wall stress → ↓O₂ demand) > arteriodilation (↓afterload); also coronary vasodilation (↑supply); dilates collateral vessels |
| Acute use | Sublingual GTN 0.4 mg q5min × 3 doses initially; then IV GTN infusion (10–200 μg/min, titrate to pain/BP) if pain persists |
| Long-term | Nitrates (long-acting or short-acting as PRN) in the presence of angina [7] |
| Contraindications | RV infarction (preload-dependent → nitrates ↓preload → catastrophic hypotension) [2]; SBP < 90 mmHg; severe aortic stenosis; concurrent PDE-5 inhibitor use (sildenafil, tadalafil — potentiates hypotension via ↑cGMP) |
| Side effects | Headache (meningeal vasodilation); hypotension; reflex tachycardia; tolerance with continuous use (need nitrate-free interval) |
"Beta" → β-adrenergic receptors; "blocker" → antagonist.
| Aspect | Detail |
|---|---|
| Mechanism | Block β₁ receptors in heart → ↓HR (negative chronotropy), ↓contractility (negative inotropy), ↓conduction velocity (negative dromotropy) → ↓myocardial O₂ demand; also ↓renin secretion. Anti-arrhythmic: ↑VF threshold → ↓sudden death |
| Indication | Beta-blockers unless contraindicated [7]; given to all stable patients if no C/I [2] |
| Examples | Usually Betaloc (metoprolol) 25–100 mg BD [2]; also bisoprolol, carvedilol (has additional α₁-blocking vasodilatory properties — useful in HF) |
| Contraindications | Bradycardia, AV block, ↓BP, asthma [2] |
| NOT contraindicated in | Heart failure (actually beneficial!), COPD (use cardioselective β₁ agents like bisoprolol), peripheral vascular disease [2] |
| Timing | Oral within 24h if haemodynamically stable; avoid IV in acute phase unless specific tachyarrhythmia |
Why beta-blockers improve survival in STEMI: By ↓HR, they (1) reduce O₂ demand, (2) prolong diastole → ↑coronary perfusion time, (3) ↑VF threshold → ↓sudden arrhythmic death, and (4) limit infarct extension. Long-term, they attenuate adverse LV remodelling.
Calcium antagonists (diltiazem or verapamil) if contraindications to beta-blockers and no heart failure [7].
| Aspect | Detail |
|---|---|
| Mechanism | Non-dihydropyridine CCBs (diltiazem, verapamil) block L-type Ca²⁺ channels in cardiac myocytes → ↓HR, ↓contractility, ↓AV conduction (similar to β-blockers); also coronary vasodilation |
| Indication | Only when beta-blockers are contraindicated AND patient has ongoing angina; C/I in heart failure (negative inotropy worsens LV dysfunction) |
| Dihydropyridine CCBs (amlodipine, nifedipine) | Predominantly vasodilatory (less cardiac effect); can be added to β-blocker for refractory angina, but short-acting nifedipine alone is C/I (reflex tachycardia → ↑O₂ demand) |
| Aspect | Detail |
|---|---|
| Mechanism | HMG-CoA reductase inhibitor → ↓hepatic cholesterol synthesis → ↑LDL receptor expression → ↓circulating LDL. Pleiotropic effects: plaque stabilisation (↑fibrous cap thickness, ↓inflammation), endothelial function improvement, ↓thrombogenicity |
| Indication | High-intensity statin always (≤ 24h) [2]; regardless of baseline LDL level |
| Drug and dose | Atorvastatin 80 mg or rosuvastatin 20–40 mg |
| Target | LDL < 1.4 mmol/L AND ≥ 50% reduction from baseline (ESC 2019/2024 for very high-risk patients) |
| Side effects | Myalgia/myopathy (rare), ↑transaminases (monitor LFT), rhabdomyolysis (very rare, especially with drug interactions) |
"ACEI" → angiotensin-converting enzyme inhibitor; "ARB" → angiotensin II receptor blocker.
| Aspect | Detail |
|---|---|
| Mechanism | ACEI: blocks ACE → ↓angiotensin II → ↓aldosterone → ↓preload/afterload, ↓sodium/water retention, ↓LV remodelling; also ↑bradykinin → vasodilation. ARB: blocks AT₁ receptor → similar effects without ↑bradykinin (fewer side effects like cough) |
| Indication | ACEI for patients with CHF, LV dysfunction (EF < 40%), hypertension, or diabetes [7]; ACEI/ARB always (≤ 24h) [2] — in practice, started within 24h for ALL STEMI patients (especially anterior MI, LVEF < 40%, HF, DM) |
| Examples | Ramipril, perindopril, enalapril; ARB: valsartan, candesartan (if ACEI-intolerant due to cough) |
| Contraindications | Bilateral renal artery stenosis; ↑K⁺ > 5.5; pregnancy; angioedema history (for ACEI); SBP < 90 |
| Side effects | Dry cough (ACEI — from ↑bradykinin), hyperkalaemia, AKI (especially if hypovolaemic), angioedema (rare) |
Why ACEI/ARB post-MI? After STEMI, the necrotic zone is replaced by scar tissue. The remaining viable myocardium undergoes adverse remodelling: compensatory hypertrophy + chamber dilatation (mediated by the RAAS and sympathetic nervous system). ACEI/ARB blocks the RAAS axis → ↓wall stress, ↓fibrosis, ↓apoptosis → slows remodelling → ↓progression to HF → ↓mortality.
| Aspect | Detail |
|---|---|
| Mechanism | Blocks aldosterone receptor → ↓sodium/water retention, ↓cardiac fibrosis, ↓LV remodelling |
| Indication | MRA if LVEF ≤ 40% + HF/DM [2] — specifically, post-MI patients who develop HF symptoms or have LVEF ≤ 40% (EPHESUS trial: eplerenone ↓mortality by 15%) |
| Examples | Eplerenone (selective — fewer side effects) or spironolactone |
| Contraindications | K⁺ > 5.0; significant renal impairment (eGFR < 30) |
| Side effects | Hyperkalaemia (monitor K⁺ closely, especially with ACEI); gynaecomastia (spironolactone — it also blocks androgen receptors) |
Phase 3: Reperfusion Therapy
This is the most critical intervention in STEMI — the entire management pathway is designed to get the patient to reperfusion as quickly as possible.
A. Primary Percutaneous Coronary Intervention (Primary PCI)
"PCI" → "percutaneous" = through the skin; "coronary" = coronary artery; "intervention" = therapeutic procedure.
| Aspect | Detail |
|---|---|
| What it is | Catheter-based approach: guide wire crosses the occlusion → balloon angioplasty opens the lumen → drug-eluting stent (DES) deployed to scaffold the artery open |
| Preferred strategy | Primary PCI is the preferred reperfusion strategy when it can be performed within 120 minutes of STEMI diagnosis [1] |
| Time target | Door-to-balloon ≤ 90 minutes (≤ 60 min if presenting directly to PCI centre); first medical contact to wire-crossing ≤ 120 min |
| Access | Radial artery preferred (↓bleeding, ↓vascular complications, earlier ambulation) over femoral |
| Goal | Restore TIMI 3 flow (complete, normal-speed perfusion) in the culprit artery |
| Stent type | Drug-eluting stent (DES) preferred over bare-metal stent (BMS) — ↓restenosis rate (drug coating — usually everolimus or zotarolimus — inhibits neointimal proliferation) |
| Advantages over fibrinolysis | Higher patency rates (~95% vs ~60–80%); lower mortality; lower re-infarction rate; lower stroke rate; lower bleeding rate; can treat residual stenosis; provides anatomical information |
| Indication | Detail |
|---|---|
| Symptom onset < 12h and PCI feasible within 120 min | Standard indication [1] |
| Symptom onset 12–24h | If ongoing ischaemia, heart failure, cardiogenic shock, or electrical instability [1] |
| Cardiogenic shock or heart failure | Regardless of timing — PCI is life-saving in cardiogenic shock (SHOCK trial) [1] |
| Failed fibrinolysis | Rescue PCI immediately |
| Large area of myocardium at risk | Even if symptom onset 12–24h [1] |
There are virtually no absolute contraindications to primary PCI (it is a life-saving procedure). Relative considerations include:
- Severe contrast allergy (pre-treat with steroids/antihistamines)
- Severe CKD (contrast nephropathy risk — weigh against benefit of reperfusion)
- No suitable vascular access
- Patient/family refusal
B. Fibrinolytic (Thrombolytic) Therapy
"Fibrinolytic" → "fibrin" = the protein mesh of a clot + "lytic" = breaking down. These drugs dissolve the fibrin clot by activating plasminogen → plasmin.
Fibrinolytic therapy indication [1]:
AMI – Pain + ST-elevation in 2 contiguous chest leads; time of onset of pain < 12 hours; absence of contraindications – bleeding tendency [1]
| Drug | Mechanism | Dose | Key Features |
|---|---|---|---|
| Alteplase (rt-PA) | Recombinant tissue plasminogen activator; fibrin-specific (preferentially activates plasminogen bound to fibrin in the clot) | 15 mg IV bolus → 0.75 mg/kg over 30 min (max 50 mg) → 0.5 mg/kg over 60 min (max 35 mg) | Gold standard; fibrin-specific → less systemic lytic state |
| Tenecteplase (TNK-tPA) | Modified rt-PA with longer half-life | Single IV bolus (weight-adjusted: 30–50 mg) | Most practical: single bolus dosing; preferred in pre-hospital setting |
| Reteplase | Deletion mutant of rt-PA | 10 U IV bolus × 2, 30 min apart | Double-bolus regimen |
| Streptokinase | Bacterial protein (from Streptococcus); forms complex with plasminogen → activates other plasminogen molecules; NOT fibrin-specific | 1.5 million units IV over 60 min | Cheapest; antigenic (can cause allergic reaction; prior treatment within previous 6 months is an absolute C/I [2]); less effective than fibrin-specific agents |
These are critical to memorise — getting them wrong can cause fatal haemorrhage.
Absolute and relative contraindications [2]:
| Absolute Contraindications | Relative Contraindications |
|---|---|
| Previous haemorrhagic stroke at any time | Severe uncontrolled HTN on presentation (BP > 180/110 mmHg) |
| Other strokes or CVA within 3 months; except acute ischaemic stroke within 4.5 hours | History of chronic, severe, poorly controlled HTN |
| Known malignant intracranial neoplasm (primary or metastatic) | History of prior ischaemic stroke > 3 months or known intracerebral pathology not covered in absolute contraindications |
| Known structural cerebrovascular lesion (e.g., AVM) | Traumatic or prolonged ( > 10 min) CPR |
| Active bleeding or bleeding diathesis (does not include menses) | Oral anticoagulant therapy |
| Suspected aortic dissection | Major surgery < 3 weeks |
| Significant closed head or facial trauma within 3 months | Non-compressible vascular punctures |
| Intracranial or intraspinal surgery within 2 months | Recent (within 2–4 weeks) internal bleeding |
| Severe uncontrolled HTN (unresponsive to emergency therapy) | Pregnancy |
| For streptokinase, prior treatment within previous 6 months | Active peptic ulcer |
Mnemonic for Absolute C/I to Fibrinolysis — 'STAB HEAD'
- Stroke — haemorrhagic (ever) or ischaemic ( < 3 months)
- Tumour — intracranial neoplasm
- Aortic dissection (suspected)
- Bleeding diathesis or active bleeding
- Head/facial trauma ( < 3 months)
- Elevated BP — severe, unresponsive to therapy
- AVM or structural cerebrovascular lesion
- Dural breach — intracranial/intraspinal surgery ( < 2 months)
Documentation of successful fibrinolysis [1][2]:
| Criterion | Detail | Why |
|---|---|---|
| Clinical: ↓chest pain [1] | Restoration of coronary flow → relief of ischaemia | |
| ECG: early resolution of ST-elevation ≥ 50% in worst lead at 60–90 min [1][2] | Reperfusion → resolution of the injury current | This is the most practical and important marker |
| ECG: accelerated nodal or idioventricular rhythm [2] | "Reperfusion arrhythmias" — transient, usually benign; indicate restoration of flow through previously ischaemic tissue | The washout of ischaemic metabolites and sudden electrolyte shifts cause transient automaticity |
| ECG: preservation of R wave [1] | Myocardial salvage — if the R wave is preserved, transmural necrosis has not been completed | |
| Biochemical: early peaking of CPK (11–12h vs normal 22–24h) [1][2] | "Washout phenomenon" — restored blood flow carries released enzymes from the reperfused zone → earlier and higher biomarker peak | |
| Imaging: radionuclide imaging, angiography [1] | Confirms vessel patency and myocardial perfusion |
If fibrinolysis fails (no ≥ 50% ST resolution at 60–90 min, ongoing pain) → rescue PCI immediately.
After successful fibrinolysis → routine angiography within 2–24 hours [1]. Why? Even with clot dissolution, the underlying atherosclerotic plaque remains → residual stenosis → risk of re-occlusion. Angiography ± PCI within 2–24h addresses this residual stenosis (pharmacoinvasive strategy).
CABG if unsuccessful PCI or mechanical complications [2].
| Indication | Detail |
|---|---|
| Failed PCI | Cannot cross lesion or restore flow; ongoing ischaemia |
| Left main stem disease | LMS disease with complex anatomy not suitable for PCI |
| Multivessel disease | Especially with DM + reduced LVEF (SYNTAX trial, FREEDOM trial: CABG > PCI in diabetics with multivessel disease) |
| Mechanical complications | VSD, papillary muscle rupture, free wall rupture → require surgical repair ± concomitant CABG |
| Timing | Usually delayed (ideally > 3–5 days) to allow myocardial recovery; emergent if mechanical complication or cardiogenic shock not amenable to PCI |
| Feature | Primary PCI | Fibrinolysis |
|---|---|---|
| Patency rate | ~95% TIMI 3 flow | ~60–80% TIMI 3 flow |
| 30-day mortality | ~3–5% | ~6–8% |
| Reinfarction | Lower (~1–3%) | Higher (~5–7%) |
| Stroke | Lower (~0.5%) | Higher (~1–2%, mainly ICH) |
| Bleeding | Lower major bleeding | Higher (systemic lytic state) |
| Time-dependency | Less time-dependent (still effective 12–24h in select cases) | Very time-dependent (greatest benefit < 3h; diminishing benefit after 6h) |
| Anatomical information | Yes (diagnostic + therapeutic) | No |
| Availability | Requires cath lab + interventional cardiologist 24/7 | Available anywhere with trained staff |
Phase 4: Long-Term Management and Secondary Prevention
For all patients with STEMI [2]:
- LVEF by echo → guide further management to ↓LV remodelling + ↓arrhythmia risk [2]
- Residual ischaemia → assess risk of future ischaemic event: stress test pre-discharge or symptom-limited stress 2–3 weeks post-MI; angiogram if positive stress test, post-infarct angina, or other high-risk clinical features [2]
- Arrhythmia during convalescent phase by 24h ECG for VT/frequent ventricular arrhythmia → indicates poor ventricular function and may herald sudden death → may benefit from EPS and cardiac defibrillators [2]
| Drug | Duration | Rationale |
|---|---|---|
| Aspirin 75–100 mg daily | Indefinitely [2] | Continuous antiplatelet protection |
| P2Y₁₂ inhibitor | ≥ 12 months if stented [2]; consider extending if high ischaemic risk | Prevent stent thrombosis and recurrent ACS |
| Beta-blocker | Indefinitely (at least 1 year; reassess thereafter) | ↓Mortality, ↓arrhythmia, ↓remodelling |
| ACEI/ARB | Indefinitely (especially if LVEF < 40%, HF, DM, HTN) | ↓Remodelling, ↓mortality |
| MRA | If LVEF ≤ 40% + HF/DM [2] | ↓Fibrosis, ↓mortality (EPHESUS trial) |
| High-intensity statin | Indefinitely | ↓LDL, plaque stabilisation, ↓recurrent events |
| Anticoagulation (warfarin/NOAC) | If concurrent indication (e.g., AF, LV thrombus, mechanical valve) | Prevent systemic embolism |
| Target | Measure |
|---|---|
| Smoking | Drastic ↓MI risk after just 1 year of smoking cessation, doubles 5-year mortality [2] if continued |
| Hyperlipidaemia | High-dose statins for aggressive ↓lipid (regardless of serum cholesterol level) → ↓mortality [2]; target LDL < 1.4 mmol/L |
| Lifestyle | Regular exercise, maintain ideal body weight, Mediterranean diet [2] |
| Other comorbidities | Good control of HTN and DM [2]; aim HbA1c < 7%; BP < 130/80 |
Takes 4–6 weeks to replace necrotic tissue by fibrotic tissue → restrict physical activities until then, offer cardiovascular rehabilitation [2].
- Usually: mobilise in 2 days, discharge in 3–5 days, resume work in 4–6 weeks [2]
- Cardiac rehabilitation programme: supervised exercise training + education + psychological support → proven to ↓mortality, ↑functional capacity, ↑quality of life
Special Management Scenarios
| Do | Don't (and Why) |
|---|---|
| IV fluid bolus (250–500 mL NS, repeat as needed) — RV is preload-dependent | C/I to nitrates and other ↓preload agents → severe hypotension [2] |
| Maintain AV synchrony (atrial kick critical for filling stiff RV) — pace if AV block | Avoid diuretics (↓preload) |
| Inotropic support (dobutamine) if fluids insufficient | |
| Emergent PCI to restore RCA flow |
Management [5]:
- Primary PCI is the single most important intervention (SHOCK trial)
- Inotropes (e.g., IV dobutamine) if adequate filling pressure; fluid resuscitation ± vasopressors if low filling pressure [5]
- Mechanical circulatory support: Intra-aortic balloon pump (IABP), Impella device, or extracorporeal membrane oxygenation (ECMO) as bridge to recovery/transplant/decision
- ACLS should be activated in cases of arrhythmogenic causes [5]
High Yield Summary — Management of STEMI
Immediate measures: O₂ only if SpO₂ < 90%; IV access; monitor; analgesia (morphine if nitrates fail — but cautious due to delayed oral P2Y₁₂ absorption).
Antiplatelet: Aspirin 300 mg load → 75–100 mg daily (indefinitely). P2Y₁₂ inhibitor: ticagrelor 180 mg load → 90 mg BD (preferred); clopidogrel 600 mg load → 75 mg QD if ticagrelor C/I. DAPT for ≥ 12 months.
Anticoagulation: UFH during PCI; enoxaparin if fibrinolysis chosen.
Anti-ischaemic: Nitrates (C/I in RV MI, PDE5i use, hypotension); beta-blockers (to all if no C/I); diltiazem/verapamil only if BB C/I and no HF.
Prognostic drugs started ≤ 24h: High-intensity statin (atorvastatin 80 mg); ACEI/ARB; MRA if LVEF ≤ 40% + HF/DM.
Reperfusion — the core of STEMI treatment:
- Primary PCI if achievable within 120 min of diagnosis (door-to-balloon ≤ 90 min) — preferred strategy.
- Fibrinolysis if PCI not available within 120 min (door-to-needle ≤ 30 min). Assess success at 60–90 min (≥ 50% ST resolution). If failed → rescue PCI. If successful → angiography within 2–24h.
- CABG for failed PCI, LMS disease, multivessel disease (especially DM), or mechanical complications.
Long-term: DAPT ≥ 12 months; BB, ACEI/ARB, statin indefinitely; MRA if LVEF ≤ 40%; aggressive risk factor modification; cardiac rehabilitation.
Special scenarios: RV MI → fluids, avoid nitrates/diuretics; cardiogenic shock → emergent PCI + inotropes ± mechanical support.
Active Recall - Management of STEMI
[1] Lecture slides: GC 088. Sudden Severe Chest Pain.pdf (pp. 39, 48) [2] Senior notes: Ryan Ho Cardiology.pdf (pp. 120, 131, 132, 136, 138, 139, 144) [5] Senior notes: Ryan Ho Critical Care.pdf (pp. 22, 36, 39) [6] Senior notes: Ryan Ho Fundamentals.pdf (pp. 203, 217) [7] Lecture slides: GC 028. Accelerating chest pain_Acute coronary (1).pdf (pp. 40, 54, 55) [12] Lecture slides: GC 028. Accelerating chest pain_Acute coronary (1).pdf (p. 40)
Complications of STEMI
Complications are what kill patients after the acute reperfusion window has passed. Understanding them requires knowing what happens to necrotic myocardium over time and how loss of functional muscle mass affects cardiac physiology. I'll organise them chronologically and by category, because the timing of complications maps directly onto the underlying pathology.
| Time Post-MI | Pathological Process | Complication Window |
|---|---|---|
| 0–24h | Coagulative necrosis begins; neutrophil infiltration; electrically unstable tissue | Arrhythmias (VF/VT peak); early pump failure |
| 1–3 days | Neutrophil-mediated enzymatic digestion of necrotic muscle; myocardium at its weakest structurally | Arrhythmias continue; early mechanical complications begin |
| 3–7 days | Macrophage infiltration; granulation tissue formation begins; dead muscle is being removed but not yet replaced → structural nadir | Peak risk of mechanical complications (free wall rupture, VSD, papillary muscle rupture) |
| 1–3 weeks | Granulation tissue matures; fibroblast proliferation; collagen deposition beginning | Pericarditis (early and Dressler's); embolism from mural thrombus |
| 4–6 weeks | Scar formation (fibrotic tissue replaces necrotic tissue) [2] | LV remodelling; ventricular aneurysm formation |
| Months–years | Chronic remodelling; LV dilatation; neurohormonal activation | Chronic heart failure; recurrent ACS; sudden cardiac death |
Arrhythmias are the most common complication of STEMI and the leading cause of pre-hospital death. Most sudden cardiac deaths from MI occur within the first hour, before the patient reaches hospital [5].
Why does STEMI cause arrhythmias? Ischaemic and necrotic myocardium creates an electrically heterogeneous environment:
- Ischaemic cells have depolarised resting membrane potential (↓ATP → failure of Na⁺/K⁺-ATPase → ↑intracellular K⁺ leak → ↑extracellular K⁺ around ischaemic zone) → altered conduction velocity
- Re-entry circuits form at the border between healthy and ischaemic tissue (the "border zone") where conduction velocities differ
- Enhanced automaticity from catecholamine surge and metabolic derangement
- Triggered activity from calcium overload (delayed afterdepolarisations)
Management of specific arrhythmias post-MI [2]:
| Arrhythmia | Mechanism | Timing | Management |
|---|---|---|---|
| Symptomatic sinus bradycardia | Inferior MI → ischaemia of SA node (supplied by RCA in ~60%) or Bezold-Jarisch reflex (vagal) | Early (hours) | Atropine 0.3–0.6 mg IV bolus; pacing if unresponsive to atropine [2] |
| AV block | Inferior MI → AV nodal ischaemia (AV node supplied by RCA in ~80%); anterior MI → infranodal conduction tissue necrosis | Variable | Conservative if 1° or Mobitz type I 2° AVB. Pacing if Mobitz type II 2° AVB or complete HB. Conservative Tx under careful monitoring as alternative if inferior MI with narrow QRS escape rhythm and adequate rate. Other indications for temporary pacing: bifascicular block + 1° AVB, alternating BBB/RBBB + alternating LAFB/LPFB (anterior infarct → ↑risk of sudden asystole) [2] |
| PSVT | Re-entry (AVNRT/AVRT) triggered by catecholamines and electrolyte shifts | Variable | Cardioversion if severe haemodynamic compromise or intractable ischaemia. ATP 10–20 mg IV bolus → verapamil 5–15 mg IV slowly (C/I if BP low or on BB) [2] |
| AF/AFlu | Atrial stretch from ↑LV filling pressures; atrial ischaemia; catecholamine surge; pericarditis | Common and frequently transient, can be a sign of impending or overt LVF [2] | Digoxin 0.25 mg IV/PO stat → loading; diltiazem 10–15 mg IV over 5–10 min; amiodarone 5 mg/kg IV over 60 min as loading [2] |
| Wide complex tachycardia | Re-entry in border zone; enhanced automaticity of Purkinje fibres | Early (highest risk first 24–48h) | Treat as VT until proven otherwise in the setting of ACS. Cardioversion if haemodynamic compromise. Stable sustained monomorphic VT: amiodarone 150 mg over 10 min (repeat if needed) → 600–1200 mg/24h infusion; lignocaine 50–100 mg IV bolus → 1–4 mg/min; procainamide 20–30 mg/min. Sustained polymorphic VT: unsynchronised cardioversion starting at 200 J [2] |
| VF | The most lethal arrhythmia; re-entry circuits in heterogeneous border zone tissue | Peak incidence first 4 hours; 80% of pre-hospital MI deaths | Prompt defibrillation with reference to ACLS algorithm [2][5] |
| Reperfusion arrhythmias | Sudden restoration of flow → washout of ischaemic metabolites (K⁺, lactate, adenosine) → transient automaticity | Immediately after PCI or fibrinolysis | Accelerated idioventricular rhythm (AIVR, "slow VT" at 60–120 bpm) — usually benign and self-limiting; observe. Only treat if haemodynamically compromising |
AV Block in Inferior vs Anterior STEMI — Very Different Prognoses
- Inferior MI → AV nodal block (usually at the level of the AV node itself). The escape rhythm is junctional (narrow QRS, rate 40–60 bpm). Usually transient (resolves as ischaemia resolves), well-tolerated, and responds to atropine. Rarely needs permanent pacing.
- Anterior MI → Infranodal block (below the AV node, within the His-Purkinje system). The escape rhythm is ventricular (wide QRS, rate 20–40 bpm). Indicates massive septal necrosis, carries a very poor prognosis, and typically requires temporary ± permanent pacing.
Pump failure mechanism: downward spiral exacerbating myocardial ischaemia. ↓Systolic function → ↓coronary perfusion → ↓supply → ischaemia. ↓Diastolic function → ↑pulmonary congestion → hypoxaemia → ischaemia. Indicates extensive myocardial damage → poor prognosis (↑likelihood of other complications) [2].
This is classified by the Killip classification (from Part 1):
| Killip Class | Clinical Features | ~30-Day Mortality | Pathophysiology |
|---|---|---|---|
| I | No HF signs | ~6% | Small infarct; adequate residual LV function |
| II | Mild HF: S3 gallop, lung crackles < 50% of fields, ↑JVP | ~17% | Moderate LV dysfunction; ↑LVEDP → early pulmonary congestion |
| III | Frank pulmonary oedema | ~38% | Severe LV dysfunction; PCWP markedly elevated → alveolar flooding |
| IV | Cardiogenic shock: SBP < 90, signs of end-organ hypoperfusion | ~80% (without intervention) | Typically > 40% of LV mass infarcted; cardiac output insufficient to maintain systemic perfusion |
AMI Complications: Heart failure [1].
Management of Pump Failure [2]
Management is based on clinical assessment of whether there is ↓CO or APO (bedside echo is essential) [2]:
a) RV dysfunction (↓CO without APO, ~5%):
- Usually occurs in inferior MI [2]
- Bedside echo should show non-compressible IVC [2] (indicating ↑RA pressure)
- Swan-Ganz catheter to monitor PCWP [2] → volume expansion with colloids/crystalloids if low or normal [2]
- Avoid nitrates and diuretics (↓preload in a preload-dependent ventricle → catastrophic)
- Dobutamine if fluids alone are insufficient
b) LV dysfunction (normal/↓CO with APO, ~95%):
- Vasodilators (especially ACEI) if BP stable (± PCWP monitoring) [2]
- Inotropes: preferably via central vein; start with dopamine 2.5 μg/kg/min if SBP ≤ 90 → ↑by increments of 0.5 μg/kg/min; consider dobutamine 5–15 μg/kg/min when high-dose dopamine needed [2]
- IABP with view for catheterisation ± revascularisation [2]
- Watch out for other causes, e.g., mechanical complications, arrhythmia, excessive use of anti-HTN [2]
Shock: Large area (~40%) myocardium involved [13]. When ~40% or more of the LV is infarcted, the heart simply cannot generate enough forward flow. This is why cardiogenic shock carries such devastating mortality — there is not enough muscle left to pump.
III. Mechanical Complications
Acute mechanical complications from MI: Shock (large area ~40% myocardium involved), VSD (transmural infarct and rupture of muscular septum), MR (rupture of papillary head), Tamponade (free wall rupture, myocarditis, pericarditis, iatrogenic). Anyone of this is high risk for mortality [13].
Mechanical complications occur in 0.3% of all MI patients, majority occurring in STEMI due to ↑myocardial damage. Associated with high in-hospital mortality (accounts for 10–15% of in-hospital deaths from AMI) [2].
These complications share a common pathological basis: necrotic myocardium becomes structurally weak during the first week as neutrophils and macrophages digest dead tissue (day 3–7 is the structural nadir). Before collagen scar has been deposited, the wall is at its most vulnerable to mechanical rupture.
Causes: papillary muscle dysfunction or rupture, chordae rupture, or acute LV dilatation or aneurysm [2].
| Aspect | Detail |
|---|---|
| Anatomy | The mitral valve apparatus requires intact papillary muscles → chordae tendineae → leaflets. Two papillary muscles: posteromedial and anterolateral |
| Why posteromedial is most commonly affected (6–12×) | Posteromedial papillary muscle has a single blood supply by the posterior descending artery (from RCA in right-dominant circulation). Anterolateral has dual supply from LAD and LCx [2]. Therefore, inferior STEMI (RCA occlusion) → isolated posteromedial papillary muscle ischaemia → dysfunction or rupture |
| MR complicating papillary muscle dysfunction (inferior MI) | [1] |
| Timing | Papillary muscle rupture: occurs 2–7 days after infarct [2] — the structural nadir |
| Pathophysiology | Complete rupture → the papillary muscle head detaches → mitral leaflet flails → torrential MR into a non-compliant LA → acute ↑LA pressure → flash pulmonary oedema + ↓forward CO → cardiogenic shock |
| S/S | Often poorly tolerated with APO and shock (but may be silent). PSM with S3 on auscultation. Murmur may be absent if MR too severe [2] — why? If MR is truly massive, there is rapid equalisation of LV and LA pressures → minimal pressure gradient → barely audible murmur despite catastrophic regurgitation |
| Dx | By echo (to confirm papillary muscle disease) [2] — transoesophageal echo (TOE) is more sensitive |
| Mx | Observe if stable (may be transient if only dysfunction). Emergency MVR with papillary muscle repair if severe [2]. Bridge with IABP (↓afterload → ↓regurgitant fraction) and vasodilators while arranging surgery |
AMI Complications: VSD (anterior MI) [1].
IV septal rupture: occurs in ~0.1% of MI, usually occurs in ~24h from MI but may occur in up to 2 weeks [2].
| Aspect | Detail |
|---|---|
| Typical territory | Usually complicates anterior MI (LAD) especially if extensive MI with poor collateral [2] |
| Site of rupture | Rupture occurs at margin of necrotic and non-necrotic myocardium [2] — the junction between dead and living tissue is where mechanical stress is greatest |
| VSD: Transmural infarct and rupture of muscular septum [13] | |
| Pathophysiology | Septal rupture → left-to-right shunt (LV → RV) → acute RV volume overload → RV failure + ↓forward LV output → cardiogenic shock |
| Consequence and presentation | L-to-R shunting → sudden haemodynamic deterioration + new-onset PSM (to RLSB). Usually develops RV failure [2] |
| How to distinguish from acute MR | Both present with new PSM and shock. Key differences: VSD murmur → loudest at LLSB/RLSB with thrill; RV failure predominant (↑JVP, hepatomegaly). MR murmur → loudest at apex radiating to axilla; LV failure predominant (APO) |
| Dx | Echo, right heart catheterisation [2] — echo shows septal defect with colour Doppler flow across septum; right heart cath shows "step-up" in O₂ saturation from RA to RV (oxygenated blood entering RV from LV) |
| Mx | Observe with delayed surgery if stable, emergency cardiac cath followed by repair if unstable. Note that surgical repair of MI-related VSD is associated with relatively high mortality [2] — because the surrounding tissue is necrotic and friable, sutures don't hold well. Percutaneous device closure is an emerging alternative |
Tamponade: Free wall rupture, myocarditis, pericarditis, iatrogenic [13].
LV free wall rupture: occurs in < 1% (uncommon), 50% occurs ≤ 5 days, > 90% occurs ≤ 2 weeks [2].
| Aspect | Detail |
|---|---|
| Risk factors | First MI (no prior fibrosis/scarring to reinforce wall), anterior MI, large transmural infarct, hypertension, elderly, female, delayed or no reperfusion |
| Complete rupture | Blood pumped into pericardial cavity → cardiac tamponade. Usually presents with sudden profound right HF + shock followed by PEA and death [2] |
| Incomplete (contained) rupture | Ventricular defect sealed by pericardial tissue and thrombus. Presents with persistent/recurrent pleuritic chest pain [2] — forms a "pseudoaneurysm" which may expand and rupture later |
| Pathophysiology | Necrotic LV wall cannot withstand systolic pressure → ruptures → blood fills pericardial space → pericardium cannot expand acutely → ↑intrapericardial pressure → compresses cardiac chambers → ↓filling (tamponade) → ↓CO → PEA → death |
| Dx | Should be made clinically supported by ECG/CXR/echo features of cardiac tamponade [2] — bedside echo shows pericardial effusion with diastolic collapse of RA/RV |
| Mx | Emergency percutaneous pericardiocentesis → surgical repair if blood aspirated [2]. This is essentially a surgical emergency — without immediate intervention, mortality approaches 100% |
The Three Mechanical Complications — A Quick Comparison
| Feature | Acute MR | VSD | Free Wall Rupture |
|---|---|---|---|
| Timing | 2–7 days | 24h to 2 weeks | 50% ≤ 5 days |
| Territory | Inferior MI (posteromedial PM) | Anterior MI (LAD) [1] | Any (anterior most common) |
| Murmur | PSM at apex ± absent if severe | PSM at LLSB with thrill | No murmur (tamponade) |
| Predominant failure | LV failure (APO) | RV failure | Tamponade → PEA |
| Dx | Echo (TOE) | Echo ± right heart cath | Bedside echo |
| Mx | MVR ± IABP bridge | Surgical repair ± device | Pericardiocentesis → surgery |
IV. Pericardial Complications
AMI Complications: Pericarditis [1].
Peri-infarction pericarditis (PIP): common on 2nd/3rd day post-MI, occurs in 1.2% of MI patients [2].
| Aspect | Detail |
|---|---|
| Pathophysiology | Transmural infarction → necrotic epicardium directly contacts pericardium → local inflammatory reaction → pericarditis. Only occurs in transmural (STEMI) not subendocardial (NSTEMI) infarcts |
| S/S | Development of a different pain: positional, sharp pleuritic, especially at trapezius ridge. Pericardial rub (diagnostic) [2] — the rub is a high-pitched scratchy sound, best heard with the patient sitting forward at end-expiration |
| ECG | New widespread ↑ST or ↓PR beyond typically anatomic regional boundary [2] — this is the key distinction from the territorial ST-elevation of the MI itself |
| Mx | Paracetamol ± aspirin (650 mg Q6–8h) ± opiate-based analgesia (usually self-limited). Avoid NSAIDs/steroids 7–10 days after acute MI due to ↑risk of aneurysm/rupture [2] — why? NSAIDs impair collagen deposition and scar formation in the healing infarct zone → weakened wall → ↑rupture risk |
Post-MI pericardial effusion: common, occurs in ~1/3 of acute STEMI, often minimal [2].
Post cardiac injury (Dressler) syndrome: in weeks/months post-MI, usually subsides in a few days [2].
"Dressler" syndrome — named after William Dressler who described it in 1956.
| Aspect | Detail |
|---|---|
| Mechanism | Probably autoimmunity due to release of cardiac antigens into pericardial space [2] — myocardial necrosis releases intracellular proteins (myosin, troponin) that are normally sequestered from the immune system → immune system recognises them as foreign → autoimmune pericarditis |
| Timing | 2–10 weeks post-MI (sometimes months); much less common in the reperfusion era (early reperfusion → smaller infarcts → less antigen release) |
| S/S | Persistent fever, pericarditis, pleurisy with compatible history of prior cardiac injury [2] |
| Ix | Often associated with ↑inflammatory markers (↑WCC, CRP/ESR) with pericardial ± pleural effusion [2] |
| Mx | High-dose aspirin/NSAID (e.g., indomethacin 25–50 mg TDS × 1–2 days), colchicine ± steroid [2]. Unlike early pericarditis, NSAIDs are safe here because the acute infarct has healed by this time |
V. Thromboembolic Complications
Most common in (1) anterior STEMI (2) LAD infarct (3) large infarct with EF < 30% [2].
| Aspect | Detail |
|---|---|
| Why anterior MI? | Anterior wall akinesis/dyskinesis → blood stasis in the LV apex → Virchow's triad (endothelial injury from necrosis + stasis + hypercoagulability from acute-phase response) → mural thrombus formation |
| Mechanism | Ventricular thrombus due to wall motion abnormality/aneurysm → risk of embolisation in non-coagulated documented LV thrombus is 10–15% [2]. Atrial thrombus due to AF [2] |
| Consequences | Stroke, ischaemic limb… classically occurring in 1–3 weeks after MI [2] |
| Prevention/Mx | Usually indicated to start anticoagulation to prevent systemic embolisation [2] |
| Lecture slide | Warfarin: for established venous thrombosis or embolisation. Echocardiographic evidence of LV thrombus [1] |
| Heparin | Subcutaneous heparin (5000 U Q8H) for prophylaxis against DVT; IV heparin (aPTT ratio 1.5–2) for preventing embolisation (prevention of mural thrombosis) [1] |
- Immobilisation in CCU + acute inflammatory state → ↑VTE risk
- Prophylaxis: SC LMWH or UFH (usually already receiving anticoagulation as part of STEMI treatment)
- Early mobilisation (day 2) reduces risk
VI. Ventricular Remodelling, Aneurysm, and Chronic Heart Failure
Echocardiogram: Abnormal wall motions, ventricular function (use of ACEI), complications including VSD, PE, ventricular thrombus, RV infarct [1].
Pathophysiology — this is the chronic sequel of STEMI that leads to heart failure over months to years:
- Acute MI → loss of functional myocardium → remaining myocardium must compensate
- Neurohormonal activation: ↓CO → activation of RAAS (↑angiotensin II, ↑aldosterone) + sympathetic nervous system
- Angiotensin II → myocyte hypertrophy + fibrosis; aldosterone → sodium/water retention + fibrosis
- LV dilatation (Frank-Starling compensation initially → maladaptive dilatation later) → ↑wall stress (Laplace's law: wall stress = pressure × radius / 2 × thickness → as radius ↑, wall stress ↑)
- ↑Wall stress → ↑O₂ demand on surviving myocardium → further ischaemia → more cell death → vicious cycle
- End result: progressive LV dilatation + dysfunction → chronic heart failure
Why ACEI/ARB and beta-blockers are critical: They interrupt this neurohormonal cascade at multiple points — ACEI/ARB blocks RAAS, beta-blockers block sympathetic drive. MRA blocks aldosterone-mediated fibrosis. Together they ↓remodelling, ↓HF progression, ↓mortality.
Ventricular aneurysm: occurs in 8–15% with STEMI, especially for those with persistent occlusion [2].
| Aspect | Detail |
|---|---|
| Location | 70–85% located at anterior or apical walls → due to LAD total occlusion without collateral [2] |
| Pathophysiology | Transmural necrosis → scar tissue forms → thin, compliant scar bulges outward during systole (dyskinetic/paradoxical wall motion) → "true aneurysm" (wall composed of all three layers, unlike pseudoaneurysm from contained rupture) |
| Consequences | Acute decompensated HF with angina (wasted mechanical energy to enlarge aneurysm). Ventricular arrhythmia due to myocardial irritation. Systemic embolisation: mural thrombus occurs in > 50% [2] |
| Diagnosis | Paradoxical impulse on chest wall (outward when systole). ECG: persistent ↑ST and Q despite reperfusion. CXR: unusual bulge from cardiac silhouette. Echo: diagnostic [2][6] |
| Management | Oral anticoagulation if documented mural thrombus. Aneurysmectomy + CABG if intractable VAs or heart failure refractory to medical therapy [2] |
Indicated by symptoms/ECG changes + new rise in cTn > 20% or to > 5× ULN (if normal baseline) [2].
| Aspect | Detail |
|---|---|
| Cause of post-PCI MI | Side branch occlusion (60%), stent complications, microembolisation [2] |
| In thrombolysis patients | Up to 50% have post-infarct angina (because of residual stenosis) [2] |
| Mx | Should consider early (6–24h) coronary angiography/PCI in all thrombolysis patients. If can't do PCI ≤ 24h, still do coro/PCI if ischaemia before discharge [2]. High risk → prompt coro/PCI + IV GP IIb/IIIa inhibitor (if dynamic ECG changes) [2] |
Since most STEMI patients undergo primary PCI with stent implantation, stent-specific complications are important [2]:
| Complication | Mechanism | Timing | Prevention/Mx |
|---|---|---|---|
| Stent thrombosis (1–2%) | Formation of thrombus at exposed stent surface before endothelialisation [2] | Occurs intraprocedurally, acutely ( < 24h), subacutely ( < 30d), late ( < 1y), but MAJORITY occurs < 30d [2] | Prevention: DAPT (aspirin + P2Y₁₂ inhibitor) until endothelialisation [2]. Presents as severe STEMI or cardiac death → emergent angiography + thrombectomy ± restenting |
| In-stent restenosis (ISR) | Due to intimal proliferation leading to gradual re-stenosis at stent sites [2] | Usually occur ≥ 6–9 months after stenting [2] | Prevention: drug-eluting stent (DES) to prevent intimal proliferation [2]. Presents as recurrent stable angina → angiography → drug-coated balloon or re-stenting |
Stent Thrombosis vs In-Stent Restenosis — Know the Difference
| Feature | Stent Thrombosis | In-Stent Restenosis |
|---|---|---|
| Mechanism | Thrombus on exposed metal before endothelialisation | Neointimal hyperplasia (smooth muscle proliferation) |
| Presentation | Severe STEMI or cardiac death [2] — acute, catastrophic | Recurrent stable angina — gradual, chronic |
| Timing | Mostly < 30 days | ≥ 6–9 months |
| Prevention | DAPT (aspirin + P2Y₁₂ inhibitor) | Drug-eluting stent (DES) |
| Cause of failure | Premature DAPT cessation | DES failure or under-expansion |
AMI Complications [1]:
- Heart failure — Killip I–IV; manage with vasodilators, inotropes, IABP, revascularisation
- Arrhythmias — VF/VT (defibrillation/amiodarone), bradycardia/AV block (atropine/pacing), AF (rate control)
- VSD (anterior MI) — new PSM at LLSB, RV failure, echo ± right heart cath, surgical/device repair
- Mitral regurgitation complicating papillary muscle dysfunction (inferior MI) — PSM at apex, APO/shock, echo → MVR if severe
- Pericarditis — sharp positional pain, pericardial rub, widespread ST/PR changes; treat with aspirin ± colchicine; avoid NSAIDs/steroids in first 7–10 days
Post-MI management [1]:
- Risk stratification: residual ischaemia (exercise test, angiogram), electrical instability (24h ECG for VT or frequent ventricular arrhythmia) [1]
- Secondary prevention: risk factor modulation (exercise, smoking, aggressive lipid lowering with statin ± ezetimibe ± PCSK9 inhibitor); beta-blocker, aspirin, ACEI/ARB; cardiac rehabilitation and prevention (risk factor control, work, exercise, sex, alcohol, travel) [1]
High Yield Summary — Complications of STEMI
Arrhythmias (most common): VF/VT (peak first 4h → defibrillation); sinus bradycardia and AV block (inferior MI → atropine/pacing); AF (sign of LVF). Treat VT as VT until proven otherwise.
Pump Failure: Killip I–IV. Cardiogenic shock when ≥ 40% LV mass infarcted. RV failure in inferior MI → fluids, avoid nitrates. LV failure → vasodilators, inotropes, IABP.
Mechanical Complications (day 3–7 structural nadir): Acute MR (posteromedial papillary muscle rupture in inferior MI → single blood supply from PDA → emergency MVR); VSD (anterior MI → new PSM at LLSB → surgical repair); Free wall rupture ( < 1% → tamponade → PEA → pericardiocentesis + surgery). All carry high mortality.
Pericardial: Peri-infarction pericarditis (day 2–3, avoid NSAIDs); Dressler syndrome (weeks-months, autoimmune, treat with aspirin + colchicine ± steroids).
Thromboembolic: Mural thrombus (anterior MI, LVEF < 30% → anticoagulation); DVT/PE (immobilisation → prophylaxis).
Remodelling/Aneurysm: RAAS and sympathetic activation → LV dilatation → chronic HF. LV aneurysm (8–15%, anterior wall, persistent ST-elevation + Q waves → anticoagulate if thrombus, aneurysmectomy if refractory).
Stent: Stent thrombosis (acute, < 30d, catastrophic STEMI → prevented by DAPT) vs in-stent restenosis (chronic, ≥ 6–9 months, stable angina → prevented by DES).
Active Recall - Complications of STEMI
References
[1] Lecture slides: GC 088. Sudden Severe Chest Pain.pdf (pp. 31, 38, 48, 51, 54, 56) [2] Senior notes: Ryan Ho Cardiology.pdf (pp. 124, 137, 139, 140, 141, 142, 144) [5] Senior notes: Ryan Ho Critical Care.pdf (p. 28) [6] Senior notes: Ryan Ho Fundamentals.pdf (pp. 203, 457) [13] Lecture slides: Cardiac Surgery Tutorial_Prof. D Chan.pdf (p. 31)
High Yield Summary
Definition: STEMI = persistent ST-elevation on ECG + symptoms of myocardial ischaemia + troponin rise, caused by acute complete thrombotic occlusion of a coronary artery (almost always Type 1 MI from atherosclerotic plaque rupture).
Epidemiology: Declining STEMI incidence in developed countries due to primary prevention; M > F (3:1); mean age 60–70 years; CAD is the 3rd leading cause of death in HK.
Risk Factors: Same as ASCVD — modifiable: smoking, HTN, dyslipidaemia, DM, obesity, physical inactivity; non-modifiable: age, male sex, family history, prior vascular events.
Key Pathophysiology: Vulnerable plaque (thin cap, large lipid core, inflammation) → rupture → platelet adhesion/aggregation + coagulation cascade → occlusive thrombus → transmural ischaemia → necrosis progressing as a wavefront from subendocardium to epicardium. Time is myocardium — necrosis begins at ~20 min and is largely transmural by 6–12 hours.
Clinical Features:
- Symptoms: Prolonged ( > 20 min) crushing chest pain not relieved by rest/GTN, radiation to arms/jaw/neck, diaphoresis, nausea/vomiting (especially inferior MI), dyspnoea, syncope, "sense of impending doom." Atypical presentations in elderly, women, diabetics.
- Signs: Distressed, diaphoretic; tachycardia/bradycardia; hypotension or hypertension; S4 (most common) ± S3; new murmurs (MR, VSD); pulmonary oedema signs; signs of cardiogenic shock; RV infarct triad (↑JVP + clear lungs + hypotension in inferior STEMI).
Coronary Anatomy — ECG Correlation: LAD → anterior (V1–V4); RCA → inferior (II, III, aVF) ± RV (V4R); LCx → lateral (I, aVL, V5–V6); posterior → V7–V9 / reciprocal V1–V3 changes.
Killip Classification: I (no HF) → II (mild HF) → III (pulmonary oedema) → IV (cardiogenic shock). Predicts mortality.
Always consider aortic dissection as a mimic — tearing pain, pulse deficits, wide mediastinum.
High Yield Summary
Three-level differential thinking:
- Differential of acute chest pain — The "Big Five" life-threatening causes: ACS, aortic dissection, PE, tension pneumothorax, myopericarditis/tamponade. Also consider GI causes (most common overall at 42%), musculoskeletal, and anxiety.
- Differential of ST-elevation on ECG — Not every ST-elevation is STEMI. Key mimics: pericarditis (diffuse concave, PR depression), early repolarisation (J-point elevation, young patient), LVH strain, LBBB (use Sgarbossa), Brugada, ventricular aneurysm, PE, SAH, hyperkalaemia. LBBB is both a false positive and false negative for STEMI.
- Differentiating within ACS — STEMI (ST-elevation + troponin rise → emergent reperfusion) vs NSTEMI (no ST-elevation + troponin rise → early invasive strategy) vs UA (no ST-elevation + no troponin rise → medical therapy).
Key distinguishing clues:
- Convex ST + reciprocal changes + evolving Q waves = STEMI
- Tearing pain, maximal at onset, pulse deficits = aortic dissection (get CTA before cath lab!)
- Diffuse concave ST + PR depression + trapezius ridge pain = pericarditis
- Pleuritic pain + haemoptysis + S1Q3T3 = PE
- New LBBB + ischaemic symptoms = STEMI-equivalent → treat as STEMI
High Yield Summary
Diagnostic Criteria (4th/5th Universal Definition):
- Rise and/or fall of cardiac troponin above 99th percentile URL PLUS ≥ 1 of: ischaemic symptoms, new ST-T/LBBB, pathological Q waves, new RWMA on imaging, intracoronary thrombus on angiography/autopsy.
- In practice, STEMI is diagnosed on ECG + clinical presentation — do NOT wait for troponin before reperfusion.
ECG Criteria for STEMI:
- New ST-elevation at J-point in ≥ 2 contiguous leads: ≥ 2 mm in V2–V3 (men ≥ 40); ≥ 2.5 mm (men < 40); ≥ 1.5 mm (women); ≥ 1 mm all other leads.
- STEMI equivalents: new LBBB, posterior MI (reciprocal V1–V3 changes), De Winter T waves, ST-elevation in aVR with diffuse depression.
Biomarkers:
- hs-Troponin: gold standard; rises 1–6h, elevated up to 2 weeks; confirms MI but does NOT gate reperfusion decision.
- CK-MB: rises 4–6h, normalises 48–72h; useful for detecting reinfarction.
Key Investigations:
- ECG within 10 min → serial ECGs q15–30 min if non-diagnostic but suspicious
- Troponin at presentation → repeat 3–6h (or 1h with hs-assay)
- CBC, RFT, glucose, lipids ≤ 24h, coag (baseline for heparin)
- CXR: exclude mimics (dissection, PTX)
- Bedside echo: RWMA, LVEF, mechanical complications, RV function
- Coronary angiography: definitive — diagnostic + therapeutic (primary PCI)
Time Targets: ECG ≤ 10 min; door-to-balloon ≤ 90 min; door-to-needle ≤ 30 min.
High Yield Summary
Immediate measures: O₂ only if SpO₂ < 90%; IV access; monitor; analgesia (morphine if nitrates fail — but cautious due to delayed oral P2Y₁₂ absorption).
Antiplatelet: Aspirin 300 mg load → 75–100 mg daily (indefinitely). P2Y₁₂ inhibitor: ticagrelor 180 mg load → 90 mg BD (preferred); clopidogrel 600 mg load → 75 mg QD if ticagrelor C/I. DAPT for ≥ 12 months.
Anticoagulation: UFH during PCI; enoxaparin if fibrinolysis chosen.
Anti-ischaemic: Nitrates (C/I in RV MI, PDE5i use, hypotension); beta-blockers (to all if no C/I); diltiazem/verapamil only if BB C/I and no HF.
Prognostic drugs started ≤ 24h: High-intensity statin (atorvastatin 80 mg); ACEI/ARB; MRA if LVEF ≤ 40% + HF/DM.
Reperfusion — the core of STEMI treatment:
- Primary PCI if achievable within 120 min of diagnosis (door-to-balloon ≤ 90 min) — preferred strategy.
- Fibrinolysis if PCI not available within 120 min (door-to-needle ≤ 30 min). Assess success at 60–90 min (≥ 50% ST resolution). If failed → rescue PCI. If successful → angiography within 2–24h.
- CABG for failed PCI, LMS disease, multivessel disease (especially DM), or mechanical complications.
Long-term: DAPT ≥ 12 months; BB, ACEI/ARB, statin indefinitely; MRA if LVEF ≤ 40%; aggressive risk factor modification; cardiac rehabilitation.
Special scenarios: RV MI → fluids, avoid nitrates/diuretics; cardiogenic shock → emergent PCI + inotropes ± mechanical support.
High Yield Summary
Arrhythmias (most common): VF/VT (peak first 4h → defibrillation); sinus bradycardia and AV block (inferior MI → atropine/pacing); AF (sign of LVF). Treat VT as VT until proven otherwise.
Pump Failure: Killip I–IV. Cardiogenic shock when ≥ 40% LV mass infarcted. RV failure in inferior MI → fluids, avoid nitrates. LV failure → vasodilators, inotropes, IABP.
Mechanical Complications (day 3–7 structural nadir): Acute MR (posteromedial papillary muscle rupture in inferior MI → single blood supply from PDA → emergency MVR); VSD (anterior MI → new PSM at LLSB → surgical repair); Free wall rupture ( < 1% → tamponade → PEA → pericardiocentesis + surgery). All carry high mortality.
Pericardial: Peri-infarction pericarditis (day 2–3, avoid NSAIDs); Dressler syndrome (weeks-months, autoimmune, treat with aspirin + colchicine ± steroids).
Thromboembolic: Mural thrombus (anterior MI, LVEF < 30% → anticoagulation); DVT/PE (immobilisation → prophylaxis).
Remodelling/Aneurysm: RAAS and sympathetic activation → LV dilatation → chronic HF. LV aneurysm (8–15%, anterior wall, persistent ST-elevation + Q waves → anticoagulate if thrombus, aneurysmectomy if refractory).
Stent: Stent thrombosis (acute, < 30d, catastrophic STEMI → prevented by DAPT) vs in-stent restenosis (chronic, ≥ 6–9 months, stable angina → prevented by DES).
Stable Angina
Stable angina is a predictable pattern of chest pain or discomfort caused by myocardial ischemia that occurs with exertion or emotional stress and is relieved by rest or nitroglycerin.
Unstable Angina
Unstable angina is an acute coronary syndrome characterized by new-onset, worsening, or rest angina due to coronary plaque disruption and thrombosis without myocardial necrosis.