ST-elevation myocardial infarction (STEMI) is an acute complete occlusion of a coronary artery resulting in transmural myocardial ischemia, characterized by persistent ST-segment elevation on electrocardiogram and requiring emergent reperfusion therapy.

Exam domain	One-glance essentials
Definition / diagnosis	STEMI = acute coronary occlusion causing transmural ischaemia with persistent ST elevation and myocardial necrosis ^[1]^[2] New J-point ST elevation in ≥ 2 contiguous leads uses sex/lead-specific thresholds ^[1]
Epidemiology / risks	Major risks: smoking, hypertension, diabetes, dyslipidaemia, age and premature family history ^[2] Diabetes, older age and female sex increase the chance of an atypical or painless presentation ^[1]
Core mechanism	Vulnerable plaque rupture/erosion → platelet/fibrin thrombus → complete epicardial artery occlusion ^[2] Ischaemic necrosis progresses subendocardium → epicardium: time is muscle ^[1]
Clinical picture	*Crushing central pain > 20 minutes, unrelieved by rest/GTN, with diaphoresis, nausea or dyspnoea* ^[1] Inferior MI may cause bradycardia, hypotension and nausea; RV infarction gives raised JVP + hypotension + clear lungs ^[2]
Investigations	*ECG within 10 minutes; do not wait for troponin before reperfusion in clear STEMI* ^[1] Inferior STEMI → obtain right-sided V4R; posterior suspicion → V7–V9 ^[1] Echo assesses territory, LVEF and mechanical complications ^[2]
Management	*Primary PCI is preferred; target door-to-balloon ≤ 90 minutes and transfer-to-PCI ≤ 120 minutes* ^[3] If timely PCI is unavailable and onset < 12 hours, use eligible fibrinolysis with *door-to-needle < 30 minutes* ^[3] Give DAPT, procedural anticoagulation, high-intensity statin and indicated beta-blocker/ACEI ^[3]
Complications	First hours: VF/VT, AV block, acute HF and cardiogenic shock ^[2] Days 2–7: papillary muscle rupture, VSR or free-wall rupture → new murmur/collapse ^[2] Weeks: LV aneurysm, mural thrombus, Dressler syndrome and chronic HF ^[2]
Prevention / follow-up	Continue DAPT after PCI, then lifelong antiplatelet therapy as indicated; add cardiac rehabilitation ^[3] High-intensity statin, smoking cessation and control of BP/diabetes reduce recurrence ^[3]
Exam traps	*Exclude aortic dissection before fibrinolysis: abrupt tearing back pain, pulse/BP differential or AR murmur ^[1] RV infarction: avoid nitrates/diuretics and support preload* ^[2] Failed lysis: < 50% ST resolution at 60–90 minutes or persistent pain → rescue PCI ^[3]

References

^[1] Lecture slides: GC 088. Sudden Severe Chest Pain.pdf ^[2] Senior notes: Ryan Ho Cardiology.pdf ^[3] Lecture slides: Handbook of Internal Medicine 2024.pdf

ST-Elevation Myocardial Infarction (STEMI)

STEMI = ST-Elevation Myocardial Infarction. Let's break that down:

ST-Elevation → refers to the ECG finding of ST-segment elevation, indicating transmural (full-thickness) myocardial ischaemia
Myocardial → "myo" = muscle, "cardial" = heart
Infarction → tissue death (necrosis) due to inadequate blood supply (ischaemia)

STEMI is a clinical syndrome defined by symptoms of myocardial ischaemia (typically acute chest pain) in association with persistent ST-segment elevation on ECG and subsequent rise in cardiac biomarkers (troponin), reflecting acute total occlusion of an epicardial coronary artery. ^[1]^[2]

STEMI sits within the broader spectrum of Acute Coronary Syndromes (ACS):

The critical distinction: Complete blockage will result in STEMI → requires thrombolysis / primary PCI. Incomplete blockage will result in NSTEMI → antithrombotic therapy. ^[3]

Key Conceptual Distinction

Unstable angina: ischaemia without myocyte death → troponin normal
NSTEMI: subendocardial ischaemia with some myocyte death → troponin elevated, but NO persistent ST elevation
STEMI: transmural ischaemia with extensive myocyte death → troponin elevated AND persistent ST elevation (or new LBBB)

The difference is the degree of coronary occlusion: STEMI = total occlusion; NSTEMI = subtotal/intermittent occlusion. This is why STEMI demands emergent reperfusion.

2. Epidemiology

Cardiovascular disease remains the leading cause of death worldwide
Among ACS presentations, STEMI accounts for approximately 25–40% of all ACS cases
STEMI is still the diagnosed subtype of ACS causing the most mortality ^[3]
In-hospital mortality for STEMI: ~5–7% with primary PCI, higher without reperfusion (~15–20%)
30-day mortality: ~8–10% overall

IHD is one of the top 3 causes of death in Hong Kong (behind cancer, pneumonia)
Males more common than females for IHD overall ^[4]
Hong Kong has a well-established primary PCI network → door-to-balloon targets are closely monitored
Key risk factor prevalence in HK: high rates of hypertension, diabetes mellitus, hyperlipidaemia, and smoking among middle-aged males
Ageing population → increasing burden of ACS

With medical treatment nowadays, mortality is reducing ^[3]
Undetermined = missed diagnoses, these undiagnosed cases are actually the even bigger killers ^[3]
Shift towards more NSTEMI presentations partly due to better early detection and widespread use of troponin assays
Despite declining mortality, the absolute burden remains substantial

3. Risk Factors

Risk factors for STEMI are essentially risk factors for atherosclerotic coronary artery disease (since atherosclerotic plaque rupture is the overwhelming cause of STEMI).

Risk Factor	Explanation
Age	↑ age → ↑ atherosclerotic burden. Men > 45y, Women > 55y
Male sex	Oestrogen is cardioprotective (promotes NO, ↓LDL oxidation); risk equalises post-menopause
Family history	Premature CAD in 1st-degree relative: male < 55y, female < 65y ^[5]
Ethnicity	South Asians have higher CAD rates at younger ages

Risk Factor	Mechanism
Hypertension	Endothelial shear stress → endothelial dysfunction → accelerated atherosclerosis; also ↑ afterload → ↑ O₂ demand
Diabetes mellitus	Hyperglycaemia → advanced glycation end-products → endothelial dysfunction + accelerated atherosclerosis; also associated with diffuse small-vessel disease
Hyperlipidaemia	↑ LDL → subendothelial LDL accumulation → foam cell formation → fatty streak → atheromatous plaque
Smoking	CO displaces O₂ on Hb → ↓ O₂ delivery; nicotine → sympathetic activation → ↑ HR, ↑ BP; also promotes endothelial injury and platelet activation
Obesity / Metabolic syndrome	Visceral adiposity → insulin resistance, pro-inflammatory state, dyslipidaemia

Sedentary lifestyle
Chronic kidney disease (accelerated atherosclerosis, uraemic toxins)
Family history of premature CVD
Psychosocial stress
Cocaine use (coronary vasospasm + prothrombotic)
Oral contraceptive pills / HRT (prothrombotic in some contexts)

Risk Factors – Arterial vs. Venous Thrombosis

Hypercholesterolaemia, Diabetes Mellitus, Hypertension, Chronic renal impairment, and Male gender are risk factors for arterial thrombosis only, NOT venous thrombosis. ^[6]

Conversely, inherited thrombophilias (Factor V Leiden, Protein C/S deficiency) are risk factors for venous thrombosis (DVT/PE) but NOT arterial events like STEMI.

The exception: Antiphospholipid syndrome and Hyperhomocysteinaemia can cause BOTH arterial and venous thrombosis. ^[6]

4. Anatomy and Function of the Coronary Arteries

Understanding coronary anatomy is essential for localising the infarct and predicting complications.

Artery	Territory Supplied	ECG Leads	Clinical Significance
LAD	Anterior wall of LV, anterior 2/3 of interventricular septum, LV apex	V1–V4 (anterior), V5–V6 (anterolateral)	"Widow-maker" – largest territory; LAD occlusion → largest infarcts, worst prognosis
LCx	Lateral and posterior wall of LV	I, aVL (high lateral), V5–V6 (lateral)	May be "electrically silent" on standard 12-lead ECG
RCA	Inferior wall of LV, posterior 1/3 of septum, RV (in right-dominant circulation), SA and AV nodes	II, III, aVF (inferior)	RCA occlusion → inferior MI ± RV infarction ± bradycardia (SA/AV node ischaemia)
PDA	Inferior wall (variable)	II, III, aVF	Supplied by RCA in 85% (right dominant), LCx in 15% (left dominant)

Right dominant (85%): PDA arises from RCA
Left dominant (10%): PDA arises from LCx
Co-dominant (5%): PDA from both

High Yield – LAD Territory

LAD supplies the anterior wall and anterior 2/3 of the interventricular septum. ^[7] This is why anterior STEMI (LAD territory) is the most dangerous – it involves the largest myocardial mass and can cause:

Severe LV dysfunction / cardiogenic shock
Ventricular septal rupture (septal perforators)
LV aneurysm formation
Ventricular arrhythmias

The subendocardium (innermost layer of the myocardium) is the region most susceptible to ischaemia because:

It is the furthest from the epicardial coronary arteries (perfusion flows from epicardium inward)
It is subject to the highest intramural pressure during systole (compressed by contracting myocardium)
Coronary perfusion occurs predominantly during diastole → shortened diastole (e.g., tachycardia) disproportionately affects subendocardial perfusion

This explains why:

Partial occlusion → subendocardial ischaemia → NSTEMI (ST depression, not elevation)
Complete occlusion → transmural ischaemia → STEMI (ST elevation)

5. Aetiology

Based on aetiology, there are 5 classifications of AMI: ^[3]

Type	Description	Mechanism
Type 1	Spontaneous MI related to ischaemia due to primary coronary event → plaque erosion or rupture, fissuring or dissection	Atherothrombotic – this is the "classic" STEMI
Type 2	MI secondary to ischaemia due to imbalance between oxygen demand and supply → coronary spasm, anaemia, hypotension	Supply-demand mismatch without primary plaque event
Type 3	MI causing death before blood samples could be obtained → SCD with symptoms of ischaemia accompanied by new ST elevation or LBBB / coronary thrombus confirmed by angiography or autopsy	Sudden cardiac death
Type 4a/4b	MI associated with PCI (4a) / verified stent thrombosis (4b)	Procedure-related
Type 5	MI associated with CABG, new Q waves or LBBB, angiography showing new occlusion	Procedure-related

Type 1 is easily the most commonly seen; Type 2 may see sometimes. Type 3 patient is dead and you won't see them. Type 4 and 5 are associated with procedures. ^[3]

Aetiological Categories (Expanded)

The overwhelmingly most common aetiology of IHD is atherosclerosis of the coronary artery. ^[4]

Pathology of atherosclerosis progression: ^[7]

Fatty streaks: slightly raised yellow deposits – earliest lesion, even seen in children
Atheromatous plaque: fibrous cap + necrotic centre – the mature plaque
Unstable plaque: thinner fibrous cap + growing core, causing:
- Plaque rupture: thrombus formation → occlusion
- Aneurysm: pressure atrophy of tunica media
- Atheroembolism

Category	Examples	Mechanism
Coronary spasm	Prinzmetal's variant angina, Cocaine-induced	Intense vasospasm → transient total occlusion → transmural ischaemia. Cocaine blocks norepinephrine reuptake → ↑ sympathetic tone → coronary vasospasm + ↑ O₂ demand
Coronary dissection	Spontaneous coronary artery dissection (SCAD), Aortic dissection Type A with retrograde extension	Intimal tear → intramural haematoma → luminal compression → occlusion
Embolism	AF, Atrial myxoma	Thrombus/tumour fragment embolises to coronary artery
Vasculitis	Takayasu arteritis, PAN, Kawasaki disease, EGPA	Inflammatory vessel wall damage → stenosis/thrombosis
Congenital anomalies	Anomalous coronary artery origin	Compression during exercise, especially if artery courses between aorta and pulmonary artery

Severe anaemia
Hypertension crisis
Aortic stenosis (fixed low output → ↓ coronary perfusion)
Thyrotoxicosis (↑ O₂ demand from ↑ metabolic rate)
Tachyarrhythmias (↑ O₂ demand + ↓ diastolic filling time)
Hypotension/shock (↓ coronary perfusion pressure)

Takotsubo (Stress) cardiomyopathy – catecholamine surge → apical ballooning, ST elevation, but normal coronaries on angiography
Myocarditis – viral inflammation → ST elevation, troponin rise, but no coronary occlusion

6. Pathophysiology

The Core Event: Atherosclerotic Plaque Rupture → Thrombotic Occlusion

This is a step-by-step walkthrough of what happens in a Type 1 STEMI:

Not all plaques are equal. Vulnerable (unstable) plaques have:
- Thin fibrous cap (< 65 μm) – less structural integrity
- Large lipid-rich necrotic core – highly thrombogenic material
- Abundant inflammatory cells (macrophages, T-lymphocytes) – secrete matrix metalloproteinases (MMPs) that degrade the fibrous cap
- Few smooth muscle cells – less collagen synthesis to maintain cap integrity

Think of it like a balloon with a thin wall and a lot of hot liquid inside – it's primed to burst.

Rupture of an atherosclerotic plaque → thrombosis within coronary vessel → blockage of blood supply to the heart ^[3]
Triggers include: haemodynamic stress (↑ BP, ↑ HR), sympathetic surge, morning cortisol spike (explains why MI peaks 6am–12pm), physical exertion, emotional stress
The ruptured cap exposes the subendothelial collagen and tissue factor in the lipid-rich core to flowing blood

Platelet adhesion: Platelets bind to exposed collagen via glycoprotein Ib (GPIb) receptor and von Willebrand factor (vWF)
Platelet activation: Activated platelets release ADP and thromboxane A₂ (TXA₂) → recruit more platelets (positive feedback)
Platelet aggregation: Activated platelets express glycoprotein IIb/IIIa (GPIIb/IIIa) receptors → fibrinogen bridges between platelets → "white thrombus" (platelet plug)
Coagulation cascade activation: Tissue factor exposed by plaque rupture activates the extrinsic pathway → thrombin generation → fibrin mesh → "red thrombus" (fibrin-rich)
In STEMI, this thrombus is occlusive – completely blocks the coronary lumen

Complete occlusion → zero flow distal to the thrombus
Complete necrosis of myocardial cells at risk requires at least 2–4 hours after the onset of ischaemia ^[8]
The ischaemic wavefront progresses from subendocardium → subepicardium (transmural infarction)
This is a time-dependent process → "Time is muscle"

Time from Occlusion	Pathological Change	Clinical Correlate
0–30 min	Reversible injury: ATP depletion, anaerobic glycolysis, lactic acid accumulation, cellular oedema	Chest pain, ECG changes (ST elevation), wall motion abnormalities on echo
30 min – 4 hr	Irreversible injury begins (subendocardium first): coagulative necrosis, contraction band necrosis	Troponin starts to rise (~3–6 hr), CK-MB rises (~4–8 hr)
4–12 hr	Continued expansion of necrosis transmurally	Peak troponin; established infarction
12–24 hr	Coagulative necrosis established, neutrophil infiltration	Risk of arrhythmias (re-entrant circuits around ischaemic border zone)
1–3 days	Ongoing neutrophilic inflammation, early macrophage infiltration	Risk of myocardial rupture (wall is at weakest when necrotic tissue is being removed but before scar forms)
3–7 days	Granulation tissue formation begins at margins	Continued risk of rupture
1–3 weeks	Organized granulation tissue with neovascularisation	Gradual strengthening
> 4 weeks	Dense collagenous scar	Completed healing; may develop ventricular aneurysm if scar is large and thin

This is one of the most commonly asked "why" questions:

In transmural ischaemia, the injured cells cannot maintain normal resting membrane potential – they become partially depolarised
During the ST segment (between QRS and T wave), the normal ventricle is uniformly depolarised (plateau phase) → no voltage difference → isoelectric ST
In STEMI, the ischaemic zone is partially depolarised at rest → during the ST segment, there is a voltage gradient between the normal (fully depolarised) and ischaemic (partially depolarised) myocardium
This creates an "injury current" directed from normal myocardium toward the ischaemic zone
The ECG electrode overlying the ischaemic zone records this current as ST elevation
Reciprocally, electrodes on the opposite side record ST depression (reciprocal changes)

Why Subendocardial Ischaemia Shows ST Depression, Not Elevation

In subendocardial ischaemia (NSTEMI), only the inner layer is ischaemic. The injury current vector points from epicardium toward the endocardium (inward, away from the surface electrode) → the electrode sees a current going away → ST depression. In transmural ischaemia (STEMI), the entire wall is ischaemic, but the epicardial injury dominates (because it's closest to the electrode) → ST elevation.

Over time, chronic ischaemia can stimulate development of collateral vessels from adjacent non-occluded arteries
These collaterals can provide some perfusion to the ischaemic territory, potentially limiting infarct size
Patients with pre-existing collaterals (e.g., from chronic stable angina) may have smaller infarcts for the same degree of occlusion
This is why some patients with chronic stable angina can tolerate acute occlusion better than a previously asymptomatic patient with sudden plaque rupture

7. Classification

ECG Territory	Leads with ST Elevation	Culprit Artery	Reciprocal Changes
Anterior	V1–V4	LAD	ST depression in II, III, aVF
Anteroseptal	V1–V3	LAD (proximal, septal perforators)
Anterolateral	V3–V6, I, aVL	LAD (distal) or LCx
Lateral	I, aVL, V5–V6	LCx or diagonal branch of LAD	ST depression in II, III, aVF
Inferior	II, III, aVF	RCA (85%) or LCx (15%)	ST depression in I, aVL
Posterior	V7–V9 (if recorded); Tall R wave + ST depression in V1–V3 (mirror image)	RCA or LCx
Right ventricular	V3R–V6R (right-sided leads), especially V4R	Proximal RCA

High Yield – Right Ventricular Infarction

Always obtain right-sided leads (V4R) in any patient with inferior STEMI (II, III, aVF). RV infarction complicates ~30–50% of inferior STEMIs and requires specific management (volume loading, avoid nitrates/diuretics which reduce preload and can cause catastrophic hypotension).

Killip Class	Clinical Features	In-Hospital Mortality
I	No heart failure	~6%
II	Mild heart failure: S3 gallop, basal crackles, raised JVP	~17%
III	Acute pulmonary oedema	~38%
IV	Cardiogenic shock	~80% (without intervention)

Grade	Description
0	Complete occlusion – no antegrade flow
1	Minimal penetration – contrast passes but does not opacify distal vessel
2	Partial perfusion – contrast opacifies distal vessel but slowly
3	Normal flow – full opacification of distal vessel

Goal of primary PCI is to restore TIMI 3 flow.

Transmural infarction → full-thickness necrosis; classic STEMI
Subendocardial infarction → partial-thickness; classic NSTEMI (but can rarely present with ST elevation)

8. Clinical Features

Symptom	Pathophysiological Basis
Crushing/squeezing central chest pain	Myocardial ischaemia → release of adenosine, bradykinin, lactate from ischaemic myocardium → stimulation of cardiac afferent nerve fibres (sympathetic C-fibres) → visceral pain; perceived as deep, diffuse, poorly localised (visceral innervation)
Radiation to left arm, jaw, neck, back, epigastrium	Cardiac afferent nerves enter the spinal cord at T1–T5 → convergence with somatic afferents from the arm (T1–T2), jaw (V3 of trigeminal via brainstem), and neck → the brain "misinterprets" the source (referred pain)
Duration > 20 minutes, not relieved by GTN	Unlike stable angina (transient demand ischaemia relieved by rest/GTN), STEMI represents fixed total occlusion → ischaemia persists regardless of demand reduction
Diaphoresis (sweating)	Sympathetic nervous system activation in response to pain and haemodynamic compromise → ↑ catecholamines → activation of sweat glands
Nausea and vomiting	(1) Vagal activation (Bezold–Jarisch reflex), especially in inferior MI (RCA supplies the inferior wall which is richly innervated by vagal afferents); (2) Sympathetic activation → gastroparesis
Dyspnoea	If significant LV dysfunction → ↑ LV end-diastolic pressure → ↑ LA pressure → pulmonary venous congestion → pulmonary oedema → sensation of breathlessness
Palpitations	Ischaemia-induced arrhythmias: premature ventricular complexes, VT, VF (re-entry circuits around the ischaemic border zone)
Syncope / pre-syncope	(1) Arrhythmias (VT/VF → ↓ cardiac output); (2) Vasovagal response (especially inferior MI); (3) Cardiogenic shock
Sense of impending doom (angor animi)	Massive sympathetic discharge + cerebral hypoperfusion; a classic descriptor for MI

Atypical Presentations (High Yield – Easy to Miss!)

Causes of painless MI: ^[7]

Diabetes mellitus – autonomic neuropathy damages cardiac afferent nerves → blunted pain perception
Elderly – altered pain threshold, comorbid conditions mask symptoms
Women – more likely to present with atypical symptoms (fatigue, dyspnoea, nausea) rather than classic crushing chest pain
Post-operative patients – anaesthesia may mask pain
Complete infarct (> 6h) – once all tissue is necrotic, the pain stimulus may diminish ^[7]

Exam Pearl – Atypical STEMI Presentations

Up to 30% of MIs may present atypically. In the elderly, diabetics, and women, STEMI may present as:

Isolated dyspnoea (acute pulmonary oedema)
Syncope
Acute confusional state
Epigastric pain mimicking indigestion
Sudden cardiac arrest

Always have a low threshold for ECG in these patients.

SOCRATES	STEMI Chest Pain
Site	Central/retrosternal
Onset	Sudden; often at rest
Character	Crushing, squeezing, heavy, band-like, pressure (NOT sharp/stabbing/pleuritic)
Radiation	Left arm (most classic), jaw, neck, back, epigastrium
Association	Diaphoresis, nausea/vomiting, dyspnoea, palpitations, syncope
Timing	Prolonged > 20 min; often peaks in early morning (6am–12pm due to circadian ↑ in catecholamines, cortisol, platelet aggregability)
Exacerbating	Not typically exacerbated by movement, breathing, or position (cf. pleuritic, musculoskeletal)
Severity	Often described as the "worst pain ever"; 8–10/10

Sign	Pathophysiological Basis
Distressed, anxious, diaphoretic, pale	Sympathetic activation; catecholamine surge in response to pain and haemodynamic compromise
Tachycardia	Sympathetic activation to compensate for ↓ cardiac output; may also reflect arrhythmia
Bradycardia (especially inferior MI)	Inferior MI → ischaemia of AV node (supplied by RCA in 85%) → AV block; also Bezold–Jarisch reflex (vagal activation from inferior/posterior wall stimulation)
Hypotension	(1) ↓ LV contractility → ↓ cardiac output; (2) Vagal activation (inferior MI); (3) RV infarction → ↓ RV output → ↓ LV preload
Hypertension	Paradoxical; due to intense sympathetic activation and pain → may mask underlying LV dysfunction
S4 gallop	↓ LV compliance from ischaemic/infarcted myocardium → atrial contraction against a stiff ventricle → audible "atrial kick" sound just before S1
S3 gallop	Significant LV systolic dysfunction → ↑ end-diastolic volume → rapid ventricular filling in early diastole → "ventricular gallop" → indicates heart failure (Killip ≥ II)
New systolic murmur	(1) Acute mitral regurgitation → papillary muscle ischaemia/rupture (posteromedial papillary muscle supplied by single artery – PDA – so more vulnerable); (2) Ventricular septal rupture → new VSD
Raised JVP	(1) RV infarction → RV failure → ↑ RA pressure; (2) LV failure → pulmonary congestion → ↑ RV afterload → RV failure
Bilateral basal crackles	LV failure → ↑ pulmonary capillary wedge pressure → transudation of fluid into alveoli → pulmonary oedema
Pericardial friction rub	Transmural infarction → inflammation extends to pericardial surface → fibrinous pericarditis (within 24–72 hours post-MI)
Low-grade fever	Myocardial necrosis → inflammatory response → cytokine release (IL-6, TNF-α) → hypothalamic set-point elevation; typically peaks at 38–38.5°C on day 2–3
Cool, clammy extremities	Peripheral vasoconstriction due to sympathetic activation to maintain BP and redirect blood to vital organs → early sign of cardiogenic shock

High Yield – Bezold–Jarisch Reflex in Inferior MI

The Bezold–Jarisch reflex is a cardio-inhibitory reflex triggered by stimulation of mechanoreceptors and chemoreceptors in the inferoposterior LV wall. The afferent limb travels via the vagus nerve → brainstem → efferent vagal response → bradycardia + hypotension + coronary vasodilation. This is why inferior MI patients can present with bradycardia and hypotension even without significant LV dysfunction. Management is atropine (anti-muscarinic → blocks vagal effect on SA/AV nodes).

The ACS approach: A-C-S ^[5]

A: Abnormal ECG
C: Clinical assessment
S: Stable patient?

If certain STEMI, can immediately send patient to the cath lab. ^[5]

Examination checklist:

General: Level of distress, diaphoresis, pallor, cyanosis
Vitals: HR, BP (both arms – to exclude aortic dissection), RR, SpO₂, temperature
Cardiovascular:
- JVP (↑ in RV infarction, LV failure)
- Apex beat (may be displaced if prior LV remodelling)
- Heart sounds: S3, S4, new murmurs, pericardial rub
- BP in both arms (> 20 mmHg difference → suspect aortic dissection → DO NOT give thrombolytics)
Respiratory: Crackles (pulmonary oedema), wheeze (cardiac asthma)
Peripheral: Peripheral pulses (absent = aortic dissection?), peripheral oedema, signs of peripheral vascular disease
Abdomen: Hepatomegaly (RV failure → hepatic congestion)

Critical Differential – Must Exclude Before Thrombolysis

Before giving thrombolytics for STEMI, you MUST exclude aortic dissection. Aortic dissection can cause ST elevation (if dissection flap occludes coronary ostium) but thrombolysis in dissection is catastrophic (haemorrhage into false lumen → rupture → death).

Red flags for aortic dissection:

Abrupt onset tearing/ripping pain radiating to back
BP difference > 20 mmHg between arms
Pulse deficit
New aortic regurgitation murmur (early diastolic decrescendo)
Wide mediastinum on CXR

If in doubt → CT aortogram BEFORE thrombolysis. If primary PCI is available, this dilemma is less critical because the diagnosis will be clarified on coronary angiography.

STEMI is defined by new ST elevation at the J-point in ≥ 2 contiguous leads: ^[1]^[2]

Lead Type	ST Elevation Threshold
V2–V3 in men ≥ 40 years	≥ 2 mm (0.2 mV)
V2–V3 in men < 40 years	≥ 2.5 mm (0.25 mV)
V2–V3 in women	≥ 1.5 mm (0.15 mV)
All other leads	≥ 1 mm (0.1 mV)
New or presumably new LBBB	Considered STEMI equivalent – treat as STEMI

ECG Evolution of STEMI Over Time

Phase	ECG Finding	Timing
Hyperacute	Tall, peaked, broad-based T waves ("hyperacute T waves")	Minutes
Acute	ST elevation with loss of normal ST concavity (convex upward / "tombstone")	Minutes to hours
Evolving	Q wave development (pathological Q: > 40 ms wide OR > 1/3 height of QRS in that lead)	Hours to days
Resolved	ST normalisation, T wave inversion	Days to weeks
Chronic/Old	Persistent pathological Q waves ± persistent T wave inversion	Weeks to permanent

STEMI Equivalents – Don't Miss These!

Several ECG patterns should be treated as STEMI equivalents even without classic ST elevation:

New LBBB (or presumably new LBBB) in the context of ischaemic symptoms
Wellens' syndrome (Type A: biphasic T waves in V2–V3; Type B: deep symmetric T wave inversions in V2–V3) → signifies critical LAD stenosis
De Winter T waves → upsloping ST depression at the J-point with tall, symmetric T waves in precordial leads → proximal LAD occlusion
Posterior STEMI → ST depression in V1–V3 with tall R waves (mirror image of posterior ST elevation); confirm with V7–V9 leads
Sgarbossa criteria → diagnose STEMI in the presence of LBBB (concordant ST elevation ≥ 1 mm, discordant ST elevation ≥ 5 mm, ST depression ≥ 1 mm in V1–V3)

Pathophysiology	→	Clinical Feature
Total coronary occlusion → transmural ischaemia	→	ST elevation on ECG
Ischaemic myocardium releases adenosine/bradykinin	→	Visceral chest pain
T1–T5 afferent convergence	→	Referred pain to arm/jaw/neck
Sympathetic activation from pain + ↓CO	→	Tachycardia, diaphoresis, pallor
Vagal activation (inferior MI, Bezold–Jarisch)	→	Bradycardia, hypotension, nausea/vomiting
LV systolic dysfunction → ↑ LVEDP	→	S3, pulmonary oedema, dyspnoea
↓ LV compliance (ischaemic stiffening)	→	S4 gallop
Papillary muscle ischaemia/rupture	→	Acute MR (systolic murmur)
Transmural necrosis → pericardial inflammation	→	Pericardial friction rub, low-grade fever
RV infarction → ↓ RV output	→	↑ JVP, hypotension, clear lungs
Myocardial necrosis → cytokine release	→	Low-grade fever (day 2–3)
Re-entrant circuits at ischaemic border	→	Ventricular arrhythmias (VT/VF)

High Yield Summary

STEMI Key Points:

Definition: Acute total coronary occlusion → transmural myocardial ischaemia/necrosis → persistent ST elevation + troponin rise
Most common cause: Type 1 MI – atherosclerotic plaque rupture → thrombotic occlusion
Most dangerous territory: LAD (anterior) → largest infarct, worst prognosis ("widow-maker")
Time is muscle: Complete necrosis requires 2–4 hours; reperfusion within this window salvages myocardium
ECG criteria: ≥ 2 contiguous leads with ST elevation (thresholds vary by lead and demographics); new LBBB = STEMI equivalent
Classic presentation: Crushing central chest pain > 20 min, not relieved by GTN, with diaphoresis, nausea, dyspnoea
Atypical presentations: Elderly, diabetics, women – may present with dyspnoea, syncope, epigastric pain, or confusional state
Always exclude aortic dissection before thrombolysis (BP both arms, pulse deficit, tearing back pain)
RV infarction: Always check V4R in inferior STEMI; manage with volume loading, avoid nitrates/diuretics
Killip classification: I (no HF) → IV (cardiogenic shock) – determines prognosis
Universal classification: Type 1 (plaque rupture) is the classic STEMI; Type 2 (supply-demand mismatch) is also important

Active Recall - STEMI (Definition to Clinical Features)

^[1] Lecture slides: GC 088. Sudden Severe Chest Pain.pdf ^[2] Lecture slides: GC 028. Accelerating chest pain_Acute coronary.pdf ^[3] Senior notes: Block A - Sudden severe chest pain_ acute myocardial infarction; aortic dissection.pdf ^[4] Senior notes: Block A - WCS32 Chest pain on exertion_ ischaemic heart disease; angina pectoris.pdf ^[5] Senior notes: Block A - Chest Pain - Department of Medicine.pdf ^[6] Senior notes: Block A - Leg swelling and chest pain_ deep vein thrombosis; pulmonary embolism; Thrombophilia.pdf ^[7] Senior notes: Maksim Medicine Notes.pdf ^[8] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf

Differential Diagnosis of STEMI

When a patient presents with acute chest pain and ST-segment elevation on ECG, your mind must work in two directions simultaneously:

Confirm that the ST elevation truly represents acute coronary occlusion (STEMI) — because several conditions can mimic ST elevation on ECG
Exclude life-threatening non-ACS causes of acute chest pain — because treating a misdiagnosed aortic dissection as STEMI with thrombolytics is fatal

Have to remember that not all chest pain is AMI, could originate from beyond the heart. ^[3]

Target Hx and PE to rule out other life-threatening emergencies: aortic dissection, pulmonary embolism, tension pneumothorax, perforated peptic ulcer / esophagus. ^[7]

You actually need to think about two overlapping but distinct questions:

Question	Why It Matters
A. "What else causes ST elevation on ECG?"	Prevents you from rushing a patient to the cath lab for a non-coronary cause (e.g., pericarditis, Takotsubo)
B. "What else causes acute severe chest pain?"	Prevents you from missing a life-threatening mimic (e.g., aortic dissection, PE, tension pneumothorax) that requires completely different treatment

Not every ST elevation is STEMI. The following conditions can produce ST elevation and must be considered:

DDx of ST elevation: ^[7]

Condition	ECG Pattern	Key Distinguishing Features
STEMI	Convex ST elevation ("tombstone"), associated with Q waves, localised to a coronary territory with reciprocal ST depression	Acute ischaemic chest pain > 20 min, troponin rise, regional wall motion abnormality, culprit lesion on angiography
Acute pericarditis	Diffuse concave ("saddle-shaped") ST elevation and PR depression	Pleuritic chest pain (worse on inspiration, relieved by leaning forward), radiates to the trapezius ridge ^[3], friction rub, diffuse (not territorial) changes, NO reciprocal depression (except aVR, V1)
LVH with strain pattern	Concave ST elevation in V1–V3, associated with LVH features (tall R in lateral leads, deep S in V1–V2)	Chronic finding in hypertensive patients; no acute symptoms; no troponin rise
LBBB	Discordant ST changes (ST elevation in leads with predominantly negative QRS)	Pre-existing LBBB can mimic STEMI; use Sgarbossa criteria to diagnose true STEMI in the setting of LBBB
Benign early repolarisation (BER)	Concave ST elevation with a "fishhook" or notch at the J-point, typically V2–V5	Young healthy males; no symptoms; no dynamic changes; normal troponin
Brugada syndrome	Coved ("Type 1") or saddleback ("Type 2") ST elevation in V1–V3	Brugada permitting diagnosis with even one lead ^[9]; history of syncope or cardiac arrest; may be unmasked by fever, Na⁺ channel blockers
Takotsubo cardiomyopathy	ST elevation (often anterior leads), diffuse T-wave inversion	Triggered by emotional/physical stress; apical ballooning on echo with basal hyperkinesis; normal coronaries on angiography; predominantly post-menopausal women
Ventricular aneurysm	Persistent ST elevation after old MI ^[10]	History of prior large MI; fixed wall motion abnormality on echo; no dynamic ECG changes; troponin not acutely rising
Myocarditis	ST elevation (can be diffuse or regional), may mimic STEMI exactly	Viral prodrome (fever, myalgia); younger patient; troponin elevated but often disproportionate to ECG changes; cardiac MRI shows late gadolinium enhancement in non-coronary distribution
Hyperkalaemia	Peaked T waves → widened QRS → "sine wave" pattern (can sometimes mimic ST elevation)	Check K⁺; history of CKD, medications (ACEi, K⁺-sparing diuretics)

High Yield – GC Lecture: ST Elevation DDx

DDx of ST elevation (from GC 088): ^[1]

STEMI: convex ST elevation, associated with Q waves
Acute pericarditis: diffuse concave ST elevation and PR depression
LVH with strain pattern: concave ST elevation in V1–V3, associated with LVH features
LBBB

These four are the core exam DDx for ST elevation. Know the morphology of each.

ST-segment elevation indicates full thickness cardiac muscle injury, pathological Q-wave indicates muscle necrosis and T-wave inversion indicates muscle ischaemia. ^[1]

How to Differentiate: A Quick Thinking Framework

Pericardial Disease → widespread upward concave ST elevation. Usually only one coronary territory is blocked for MI. So diffuse blockage is extremely unlikely — the patient would not be surviving and talking to you → so think pericarditis. ^[9]

This is the broader clinical DDx when a patient walks in with "sudden severe chest pain." The DDx of acute chest pain ^[2] is best organised anatomically:

Organ-System-Based DDx Table

Category	Condition	Key Distinguishing Features	Why You Cannot Miss It
Cardiac	Acute Myocardial Infarction (STEMI)	Crushing central pain > 20 min, not relieved by GTN; ST elevation; troponin ↑	Complete coronary occlusion → myocardial necrosis
Cardiac	Unstable Angina / NSTEMI	Similar pain but may be shorter; ST depression / T-wave inversion or normal ECG; troponin ↑ (NSTEMI) or normal (UA)	ACS spectrum – risk of progression to STEMI
Cardiac	Acute pericarditis / myocarditis	Pleuritic pain, radiates to trapezius ridge, sitting up or leaning forward may ease pain (MI pain not positional) ^[3]; friction rub; diffuse ST elevation	Can cause tamponade if effusion develops
Vascular	Aortic dissection (CANNOT miss!!!) ^[8]	Very sudden onset, radiates to back ^[8]; ripping or tearing sensation ^[3]; BP difference between arms; pulse deficit; new AR murmur; widened mediastinum on CXR	Thrombolysis in dissection = death; Type A dissection can cause coronary ostial occlusion mimicking STEMI
Pulmonary	Pulmonary embolism (CANNOT miss!!!) ^[8]	Pleuritic pain, haemoptysis, SOB ^[8]; unilateral leg swelling (DVT); tachycardia; S1Q3T3 on ECG; hypoxia	Massive PE → RV failure → cardiovascular collapse
Pulmonary	Tension pneumothorax (CANNOT miss!!!)	Sudden onset, SOB ^[8]; unilateral absent breath sounds; tracheal deviation; hyperresonance on percussion; hypotension	Mediastinal shift → ↓ venous return → obstructive shock; requires immediate needle decompression
Pulmonary	Pneumonia	Pleuritic pain, fever and SOB ^[8]; productive cough; consolidation on CXR	Can mimic PE or pericarditis
GI	GERD / oesophageal spasm	Unrelated to exertion, worsen when lies down, relieved by swallowing warm water ^[8]; burning character	Can closely mimic angina; "gastro-cardiac reflex" can even trigger ST changes
GI	Perforated peptic ulcer / oesophagus	Acute epigastric/chest pain; rigid abdomen; free air under diaphragm on CXR	Mediastinitis (oesophageal perforation) → sepsis → death
GI	Acute pancreatitis	Epigastric pain boring through to back; ↑ amylase/lipase	Can be part of DDx for aortic dissection
Chest wall	Musculoskeletal pain	Worsen with movement ^[8]; reproducible on palpation; localised tenderness	Benign but must not be diagnosed until serious causes excluded
Chest wall	Thoracic zoster	Thoracic nerve root distribution, precedes typical vesicular rash ^[8]	Dermatomal; pain may precede rash by days → easily misdiagnosed
Mediastinal	Mediastinitis / lymphoma	Central pain ^[8]; widened mediastinum; systemic symptoms	Mediastinitis is surgical emergency
Psychiatric	Panic attack	Young patient; hyperventilation; perioral tingling; no ECG changes; diagnosis of exclusion	Never diagnose without excluding organic causes first

The 'Big Five' Life-Threatening Causes of Acute Chest Pain

These are the diagnoses you must exclude immediately in every acute chest pain presentation:

Acute coronary syndrome (STEMI / NSTEMI)
Aortic dissection
Pulmonary embolism
Tension pneumothorax
Perforated oesophagus / peptic ulcer

As the senior notes emphasise for epigastric pain presentations: the most sinister non-GI causes that you must exclude immediately are MI, PE, DKA, and ruptured AAA. ^[11]

C. Detailed Comparison: STEMI vs. Its Three Most Critical Mimics

These three conditions are the ones most commonly compared with STEMI in exams because they share features and misdiagnosis has catastrophic consequences.

Feature	STEMI	Aortic Dissection
Onset	Minutes to build up	Abrupt, maximal at onset ("worst pain of my life, instantaneously")
Character	Crushing, squeezing, heavy	Sharp, tearing, ripping ^[3]
Radiation	Left arm, jaw, neck	Back (interscapular) ^[3]
Position	Not positional	Not positional (but patients often restless, cannot find comfortable position)
BP	Normal, ↑, or ↓	Hypertension (especially Type B); differential BP between arms (> 20 mmHg)
Pulses	Normal (unless cardiogenic shock)	Pulse deficit (weak or absent peripheral pulses)
Murmur	New murmur if papillary muscle rupture or VSD	New early diastolic decrescendo murmur (aortic regurgitation)
CXR	Usually normal or pulmonary oedema	Widened mediastinum, irregular aortic silhouette
ECG	ST elevation in coronary territory	Usually normal; but Type A dissection can cause STEMI if dissection flap occludes coronary ostium (usually RCA → inferior STEMI pattern)

Key danger: A Type A aortic dissection that occludes the right coronary artery ostium will present with inferior ST elevation + tearing back pain + pulse deficit. If you give thrombolytics, the patient will exsanguinate. This is why aortic dissection CANNOT miss!!! ^[8]

Feature	STEMI	Acute Pericarditis
Pain character	Crushing, heavy	Sharp, pleuritic, knife-like ^[3]
Radiation	Arm, jaw	Trapezius ridge (pathognomonic for pericardial pain) ^[3]
Positional	MI pain not positional ^[3]	Sitting up or leaning forward eases pain ^[3]
Respiratory	Not pleuritic	Aggravated by respiratory movement ^[3]
ECG	Localised ST elevation with reciprocal changes	Diffuse concave ST elevation with PR depression; no reciprocal changes (except aVR)
Troponin	Elevated (always in STEMI)	May be mildly elevated if myopericarditis
Friction rub	Late finding (day 2–3 if transmural)	Early finding; classic triphasic rub
CXR	Normal or pulmonary oedema	May show enlarged cardiac silhouette if effusion

Feature	STEMI	Pulmonary Embolism
Pain character	Crushing, substernal	Pleuritic (sharp, worse on inspiration)
Associated	Diaphoresis, nausea	Haemoptysis ^[3], SOB (disproportionate to pain)
Risk factors	Atherosclerotic risk factors (HT, DM, smoking, dyslipidaemia)	VTE risk factors (immobility, surgery, malignancy, OCP, thrombophilia)
Leg signs	None	Unilateral leg swelling ± tenderness (DVT) ^[5]
ECG	ST elevation in coronary territory	Sinus tachycardia (most common); S1Q3T3 (right heart strain); RBBB; right axis deviation; rarely ST elevation in V1 or III
CXR	Normal or pulmonary oedema	Hampton's hump, Westermark's sign, pleural effusion
ABG	Usually normal unless cardiogenic shock	Hypoxia + hypocapnia (hyperventilation) + respiratory alkalosis

D. ECG Pitfalls: False Positives and False Negatives for STEMI

ECG pitfalls in diagnosis of MI — there are many potential causes of ST elevation and false negatives. ^[1]^[3]

Acute pericarditis
LVH with strain
LBBB
Benign early repolarisation
Brugada syndrome
Takotsubo cardiomyopathy
Hyperkalaemia
Ventricular aneurysm (post-MI)
Myocarditis
Normal variant (high take-off)

New LBBB (masks ST elevation → use Sgarbossa criteria)
Posterior STEMI (ST depression in V1–V3 = "mirror image"; need V7–V9 posterior leads)
RV infarction (need right-sided leads V3R–V6R)
Very early presentation (only hyperacute T waves, ST elevation not yet developed)
De Winter T waves (upsloping ST depression + tall T waves → proximal LAD occlusion → treat as anterior STEMI) ^[7]
Prior CABG with multiple grafts → non-standard territories
Pacemaker rhythm → masks ST changes

Q waves are not specific for MI — HOCM can cause Q waves (V1–V3, massive septal hypertrophy), and dilated cardiomyopathy 10–13%. ^[9]

GC High Yield – STEMI Equivalents That Require Emergent Reperfusion

From GC 088 and GC Introduction to CVS Investigations: ^[1]^[12]

The following must be treated as STEMI equivalents:

New LBBB in context of ischaemic symptoms — NEW LBBB have to be careful for patients with chest pain → should be managed as the same as patients with ST elevation ^[9]
De Winter T waves: depressed ST take-off with hyperacute T wave in precordial leads → proximal LAD occlusion, Tx as anterior STEMI ^[7]
Posterior STEMI: ST depression in V1–V3 with tall R waves
Wellens' syndrome: critical proximal LAD stenosis (not STEMI per se but high risk of imminent anterior STEMI) ^[7]
ST elevation > 1 mm in aVR with diffuse ST depression → suggests left main or severe triple vessel disease → directly go for CABG ^[7]

The approach to ACS: A-C-S ^[5]

A: Abnormal ECG
C: Clinical features
S: Stable patient?

If certain STEMI, can immediately send patient to the cath lab. ^[5]

The clinical approach should be:

Investigations should be based on initial differential diagnoses after Hx and PE. Do not wait for investigations during emergency! ^[12]

Clinical Clue	Points Toward	Points Away From
Pain builds over minutes, crushing, at rest > 20 min	STEMI	Aortic dissection (maximal at onset), musculoskeletal (exercise-related)
Maximal at onset, tearing	Aortic dissection	STEMI (builds up)
Pleuritic, positional, trapezius radiation	Pericarditis	STEMI (not pleuritic, not positional)
Pleuritic + haemoptysis + unilateral leg swelling	PE	STEMI (no haemoptysis, no leg swelling)
Sudden onset + absent breath sounds on one side	Pneumothorax	STEMI (breath sounds normal unless pulmonary oedema)
Burning, postprandial, relieved by antacids	GERD	STEMI (not relieved by antacids)
Reproducible on palpation	Musculoskeletal	STEMI (not reproducible)
Young female, emotional trigger, apical ballooning	Takotsubo	STEMI (though indistinguishable until angiography)
Viral prodrome, young patient, disproportionate troponin	Myocarditis	STEMI (no viral prodrome typically)

Exam Pearl – The 'Non-Cardiac' Chest Pain Red Flags

Never diagnose "non-cardiac chest pain" or "musculoskeletal pain" without first actively excluding the Big Five life-threatening causes. Physical examination should be used to exclude other diagnoses: PE → unilateral lower limb swelling; peptic ulcers → epigastric tenderness; pneumothorax → hyperresonance. ^[5]

Specifically, ask about and examine for:

PE: Unilateral leg swelling, recent immobility, malignancy, haemoptysis
Dissection: Back pain, BP difference, pulse deficit, AR murmur
Pneumothorax: Sudden SOB, absent breath sounds, hyperresonance
Perforated viscus: Rigid abdomen, peritonism

High Yield Summary – Differential Diagnosis of STEMI

Two DDx lists needed: (A) DDx of ST elevation on ECG; (B) DDx of acute severe chest pain
Core DDx of ST elevation: STEMI (convex, territorial, reciprocal changes) vs. pericarditis (diffuse concave, PR depression) vs. LVH strain (V1–V3, chronic) vs. LBBB vs. BER vs. Brugada vs. Takotsubo vs. myocarditis
Big Five life-threatening chest pain DDx: ACS, aortic dissection, PE, tension pneumothorax, perforated oesophagus/peptic ulcer
Aortic dissection is the #1 critical mimic – tearing pain, maximal at onset, radiates to back, BP/pulse difference, AR murmur; thrombolysis is contraindicated
STEMI equivalents: New LBBB, De Winter T waves, posterior MI (ST depression V1–V3), Wellens' syndrome, aVR elevation with diffuse ST depression
ECG pitfalls: Multiple false positives (pericarditis, BER, LVH, Brugada) and false negatives (LBBB, posterior MI, RV infarction, De Winter)
Clinical approach: A (Abnormal ECG) – C (Clinical) – S (Stable) → if certain STEMI, activate cath lab immediately

Active Recall - Differential Diagnosis of STEMI

References

^[1] Lecture slides: GC 088. Sudden Severe Chest Pain.pdf ^[2] Lecture slides: GC 028. Accelerating chest pain_Acute coronary.pdf ^[3] Senior notes: Block A - Sudden severe chest pain_ acute myocardial infarction; aortic dissection.pdf ^[5] Senior notes: Block A - Chest Pain - Department of Medicine.pdf ^[7] Senior notes: Maksim Medicine Notes.pdf ^[8] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf ^[9] Senior notes: Block A - Introduction to CVS investigations (including ECG).pdf ^[10] Senior notes: Ryan Ho Cardiology.pdf ^[11] Senior notes: Block A - Upper abdominal pain_ peptic ulcer; pancreatitis and gallstone.pdf ^[12] Lecture slides: General Clerkship_Introduction to CVS Investigations_2026 Yiu (2 Feb 2026).pdf

Diagnostic Criteria, Diagnostic Algorithm, and Investigations for STEMI

A. Diagnostic Criteria for Myocardial Infarction

The diagnosis of MI is codified by the 4th Universal Definition of Myocardial Infarction (2018). Understanding the logic behind each criterion is key:

Detection of a rise and/or fall of cardiac biomarker values, preferably cardiac troponin (cTn), with at least one value above the 99th percentile upper reference limit (URL) ^[7]^[8]^[10]

PLUS at least one of the following:

Criterion	What It Proves
Clinical: Symptoms of ischaemia	The patient had chest pain or equivalent consistent with myocardial ischaemia
ECG: New or presumed new significant ST-segment–T wave changes, or new LBBB, or development of pathological Q waves	Electrical evidence that myocardium is injured or necrotic
Imaging: New loss of viable myocardium or new regional wall motion abnormality (e.g. lateral wall hypokinesia on echo)	Structural evidence that a region of myocardium has stopped contracting
Identification of an intracoronary thrombus by angiography or autopsy	Direct visualisation of the culprit lesion

High Yield – Why the Two-Part Rule Exists

Troponin alone is necessary but not sufficient. Many conditions raise troponin without an acute coronary event (heart failure, CKD, myocarditis, PE, sepsis, tachyarrhythmias). The additional criterion ensures the troponin rise is due to ischaemic myocardial injury rather than non-ischaemic causes.

Conversely, clinical features + ECG changes alone without troponin elevation = unstable angina, not MI. The troponin is what separates UA from NSTEMI/STEMI.

STEMI is diagnosed when the following ECG criteria are met in a patient with ischaemic symptoms: ^[1]^[7]^[13]

Lead	Threshold for ST Elevation
V2–V3 in men ≥ 40 years	≥ 2 mm (0.2 mV)
V2–V3 in men < 40 years	≥ 2.5 mm (0.25 mV)
V2–V3 in women	≥ 1.5 mm (0.15 mV)
All other leads	≥ 1 mm (0.1 mV)
New or presumably new LBBB	Treated as STEMI equivalent

ST elevation in ≥ 2 contiguous leads is required. At least 2 leads in the same wall → MI. If you have ST elevation in two separate walls, doesn't make sense → potential artefacts. ^[9]

STEMI diagnostic criteria requiring ST elevation in two contiguous leads, with specific thresholds of 2 mm in V1–V3 for men and 1.5 mm for women. ^[13]

Pathological Q waves indicate established myocardial necrosis (dead tissue no longer generates electrical activity, so the electrode "sees through" to the opposite wall):

Criteria for pathological Q waves: ^[3]

Any Q wave in V2–V3 ≥ 0.02 seconds (half a small square)
QS complex in V2–V3
Q wave ≥ 0.03 seconds and ≥ 0.1 mV deep, or QS complex, in any two contiguous leads of I, aVL, V4–V6, II, III, aVF

Q waves are not specific for MI — HOCM can cause Q waves (V1–V3 for massive septal hypertrophy), dilated cardiomyopathy 10–13%. ^[9]

Type	Biomarker Criterion	Additional Criteria
Type 1	cTn rise/fall with ≥ 1 value > 99th URL	+ ≥ 1 of: symptoms, ECG changes, imaging, thrombus on angio/autopsy
Type 2	Same biomarker criterion	Same, but mechanism is supply–demand mismatch (not plaque rupture)
Type 3	Death before biomarkers obtainable	Symptoms of ischaemia + new ST elevation or LBBB; or thrombus on autopsy
Type 4a (PCI-related)	cTn > 5× 99th URL (if normal baseline)	+ symptoms, ECG changes, angiographic findings, or imaging
Type 4b (Stent thrombosis)	cTn rise/fall with ≥ 1 value > 99th URL	+ verified stent thrombosis
Type 5 (CABG-related)	cTn > 10× 99th URL (if normal baseline)	+ new Q waves/LBBB, or new graft/native artery occlusion, or imaging

B. Cardiac Biomarkers – Detailed Interpretation

Cellular contents of damaged cells (e.g. intracellular enzymes) are leaked into the ECF and plasma directly or via lymphatics in cellular necrosis. ^[8] Think of it like a balloon popping – the contents spill out into the surrounding fluid.

Cardiac troponins are the gold standard for myocardial ischaemia. ^[7]

Troponin = regulatory protein complex on the actin thin filament of cardiac muscle
- "Tropo" = relating to tropomyosin, the protein it regulates
- cTnI (cardiac troponin I) and cTnT (cardiac troponin T) are cardiac-specific isoforms
High-sensitivity troponin (hs-cTn): can detect much lower concentrations → earlier diagnosis

Diagnostic cut-off of hsTnT: positive if baseline > 14 ng/L and > 100% rise 3–6 hours later. ^[7]

Feature	hsTnT / hsTnI	CK-MB
Time to initial rise	3–6 hours (can be as early as 1–3h with hs assays)	4–8 hours
Peak	24–48 hours	12–24 hours
Return to baseline	5–14 days	48–72 hours
Cardiac specificity	Very high (cardiac isoform)	Moderate (also in skeletal muscle injury)
Advantage	Early detection, high sensitivity	Shorter half-life → better for detecting reinfarction

Troponin is good: rises early and stays long. CK-MB has its value in having a shorter half-life. In the acute phase, both elevate. If the patient presents late (48 hours after onset), you would only see positive troponin with negative CK-MB → helps with the timeline. ^[2]

Roles of biochemical markers of ACS: ^[8]

Risk prediction and prognosis – categorise into high/low risk for management decisions
ACS evaluation – any troponin > URL = myocardial damage
Detection of reinfarction – CK-MB is better at detecting reinfarction due to its shorter t½; a > 20% increase in cTnI/TnT value (a 2nd plateau) indicates reinfarction ^[8]
Assessment of reperfusion – after successful reperfusion, biomarkers "wash out" rapidly → early peak then rapid decline
Estimation of infarct size – magnitude and temporal course of markers correlate with infarct size

High Yield – Non-ACS Causes of Elevated Troponin

Other causes of elevated troponins: myocarditis, heart failure, CKD. ^[7] Also:

Pulmonary embolism (RV strain)
Sepsis / critical illness
Tachyarrhythmias
Takotsubo cardiomyopathy
Cardiac contusion
Post-cardiac procedures

An elevated troponin does not automatically mean STEMI. You must integrate it with clinical presentation and ECG. This is why the diagnostic criteria require troponin PLUS at least one additional criterion.

Marker	Notes
Urine myoglobin	First marker to rise ^[7] (within 1–2 hours) but not cardiac-specific (also released from skeletal muscle)
AST	Non-specific; rises in liver disease too
LDH	Non-specific; historically used but replaced by troponin
NT-proBNP / BNP	Not a marker of myocardial necrosis; rather a marker of haemodynamic stress – useful for assessing degree of heart failure complicating MI ^[4]

The diagnostic approach to STEMI operates under the principle that time is muscle – every minute of delay in reperfusion increases infarct size and mortality. The algorithm is therefore designed to be fast and decisive.

The approach to ACS: A-C-S ^[5]

A: Abnormal ECG
C: Clinical features
S: Stable patient?

If certain STEMI, can immediately send patient to the cath lab. ^[5]

Do not wait for investigations during emergency! ^[12]

Practical Timeline in the ED

Time Point	Action	Rationale
0 min (arrival)	Assess ABC, vitals, IV access, attach monitor	Ensure patient is haemodynamically stable
< 10 min	12-lead ECG	The single most important first investigation – determines STEMI vs. NSTE-ACS pathway
Immediately if STEMI	Activate cath lab / prepare thrombolysis	If certain STEMI, can immediately send patient to the lab ^[5]; door-to-balloon < 90 min
Concurrent	Bloods: troponin, CBC, RFT, LFT, lipid profile, coagulation, glucose	Baseline assessment; troponin confirms diagnosis but do NOT wait for result before activating cath lab in clear STEMI
Concurrent	CXR (portable)	CXR: usually non-diagnostic in ACS, look for other causes (aortic dissection, PE, pneumonia, pneumothorax) ^[10]
Within 1 hour	Echocardiogram (bedside)	Regional wall motion abnormalities confirm ischaemic territory; assess LV function, complications

Critical Point – Do NOT Wait for Troponin in Clear STEMI

In a patient with classic ischaemic chest pain and clear ST elevation on ECG, you have enough to activate the cath lab immediately. Waiting for the troponin result wastes precious minutes of myocardial salvage time. The troponin result will come back positive, but by then the patient should already be on the cath lab table.

Troponin is more critical for the NSTE-ACS pathway where it differentiates NSTEMI (troponin positive) from unstable angina (troponin negative).

D. Investigation Modalities – Detailed Interpretation

1. Electrocardiography (ECG)

The ECG is the cornerstone of STEMI diagnosis. It must be performed and interpreted within 10 minutes of first medical contact.

ECG changes in STEMI – sequential evolution: ^[7]^[10]

Phase	ECG Finding	Timing	Pathological Basis
Hyperacute	Hyperacute T waves (tall, broad, peaked)	5–30 minutes	Early transmural ischaemia → K⁺ efflux from ischaemic cells → altered repolarisation
Acute	ST elevation (≥ 2 mm V2/V3, ≥ 1 mm other leads) + reciprocal ST depression	Hours	Injury current from transmural ischaemic zone
Evolving	Pathological Q waves (> 1 mm wide / > 2 mm deep, often V1–V3)	12–24 hours	Necrotic tissue is electrically silent → electrode "sees through" to opposite wall
Late	T-wave inversion	Days to weeks	Altered repolarisation in recovering/scarred myocardium

ST-segment elevation indicates full thickness cardiac muscle injury, pathological Q-wave indicates muscle necrosis and T-wave inversion indicates muscle ischaemia. ^[1]

Localizing the infarct (important!): ^[7]

Territory	Leads with ST Elevation	Culprit Artery	Reciprocal Changes
Anterior	V1–V6	LAD	II, III, aVF depression
Anteroseptal	V1–V3	LAD (septal perforators)
Anterolateral	V4–V6	LAD distal / diagonal
Lateral	I, aVL, V6	LCx	II, III, aVF depression
Inferior	II, III, aVF	Distal RCA (80%) or LCx	I, aVL depression
Right ventricular	V3R, V4R (right-sided ECG)	Proximal RCA
Posterior	V7–V9; mirror image in V1–V3 (tall R, ST depression)	RCA or LCx

Indication would be when you see inferior STEMI in II, III, aVF → order right-sided ECG leads (V3R–V6R) to assess for RV infarction. Would see STEMI in V3R, V4R, V5R and V6R. ^[3]

ECG pitfalls in diagnosis of MI – many potential causes of ST elevation: ^[1]^[3]

False positives for STEMI:

Acute pericarditis, BER, LVH strain, LBBB, Brugada, Takotsubo, myocarditis, hyperkalaemia, ventricular aneurysm

False negatives (true STEMI missed):

New LBBB (use Sgarbossa criteria)
Posterior MI (need V7–V9)
RV infarction (need right-sided leads)
De Winter T waves
Very early presentation (only hyperacute T waves)

Inferior-posterior MI can cause complete AV block. Treatment is different → consider pacing before revascularisation. ^[14]

STEMI equivalents that require emergent reperfusion: ^[7]^[9]

New LBBB in context of ischaemic symptoms → should be managed the same as patients with ST elevation ^[9]
De Winter T waves: depressed ST take-off with hyperacute T wave in precordial leads → proximal LAD occlusion, treat as anterior STEMI ^[7]
Posterior STEMI: ST depression V1–V3 with tall R waves → confirm with posterior leads V7–V9
Wellens' syndrome: critical proximal LAD stenosis → Type A: biphasic T waves V2–V3 (25%); Type B: deeply symmetric T-wave inversions V2–V3 (75%) ^[7]
ST elevation > 1 mm in aVR with diffuse ST depression → suggests left main or severe triple vessel disease → directly go for CABG ^[7]

Already discussed in detail above. Key practical points for STEMI:

Serial troponin: daily × 3 days ^[10]
Repeat ECG: at least daily × 3 days (more frequently in severe cases) ^[10]
Cardiac enzymes daily × 3 days ^[10]
Diagnostic cut-off: hsTnT > 14 ng/L and > 100% rise at 3–6 h ^[7]

CXR: usually non-diagnostic in ACS. ^[10] However, it is essential to:

Finding	Significance
Normal	Does not exclude STEMI (most STEMI patients have normal CXR initially)
Pulmonary oedema (bilateral perihilar haziness, Kerley B lines, upper lobe diversion, pleural effusion)	Indicates LV failure complicating MI (Killip II–III)
Cardiomegaly	Suggests pre-existing cardiac disease or developing pericardial effusion
Widened mediastinum, irregular aortic outline	Must exclude aortic dissection before thrombolysis ^[15]
Pneumothorax	Alternative diagnosis
Consolidation	Pneumonia as alternative cause of chest pain

Bedside echo is invaluable in STEMI – both for diagnosis and for detecting complications:

Assessment	Findings in STEMI	Why It Matters
Regional wall motion abnormalities (RWMA)	Hypokinesis, akinesis, or dyskinesis in the territory of the occluded artery	Confirms ischaemic territory; supports diagnosis even before troponin results
LV ejection fraction (LVEF)	Reduced (often < 40% in large infarcts)	LVEF is the single most important prognostic parameter ^[4]; guides need for ICD
Valvular assessment	New mitral regurgitation (papillary muscle ischaemia/rupture)	Mechanical complication requiring urgent surgery
Ventricular septal rupture	Colour Doppler showing flow across the septum	Mechanical complication – surgical emergency
Free wall rupture / tamponade	Pericardial effusion with diastolic collapse of RA/RV	Catastrophic complication – requires emergent surgery
RV function	RV dilation, ↓ TAPSE	Confirms RV infarction in inferior STEMI
Aortic regurgitation, pericardial effusion, dissection flap	Seen in aortic dissection	Differentiate aortic dissection from AMI ^[15]

Coronary angiography is the gold standard for confirming the diagnosis and identifying the culprit lesion.

In STEMI, this is performed emergently as part of primary PCI (not as a separate diagnostic step)
The angiogram will show:
- TIMI 0 flow (complete occlusion) at the culprit lesion – confirms STEMI
- Location and extent of disease (single vs. multivessel)
- Thrombus burden

Significant CAD is usually defined as stenosis ≥ 50% on invasive coronary angiography. Stenosis < 70% are typically not flow-limiting. ^[8]

CCTA is primarily used for stable chest pain / low-to-intermediate risk patients, NOT for acute STEMI (which goes straight to the cath lab). However, it has a role in the acute setting for diagnostic uncertainty:

Concept of "TRIPLE RULE-OUT": the CCTA can help you rule out the three big cannot-miss diagnoses: ^[2]

Myocardial infarction (coronary stenosis/occlusion)
Pulmonary embolism (filling defects in pulmonary arteries)
Aortic dissection (intimal flap, true/false lumen)

High sensitivity for stenosis detection → a normal CTA can reliably rule out disease. ^[2]

Limitations: ^[2]

Radiation exposure (especially concerning for young patients, though ECG-gated protocols reduce dose)
False positives from calcified plaques ^[6] – heavily calcified arteries appear more stenosed than they truly are ("blooming artefact")
Requires IV contrast (risk in CKD patients)

Initial investigations to be done concurrently (do NOT delay reperfusion): ^[7]^[10]

Investigation	What You're Looking For
CBC	Anaemia (Type 2 MI trigger?), leucocytosis (inflammatory response), thrombocytopenia (contraindication to certain anticoagulants)
RFT (U&E, creatinine)	Baseline renal function before contrast for PCI; electrolytes (K⁺, Mg²⁺ → arrhythmia risk); contrast-induced nephropathy risk
LFT	Baseline; hepatic congestion from RV failure
Lipid profile (≤ 24 hours)	Must be obtained within 24h of admission (lipids drop after acute phase reaction, becoming unreliable after ~48h)
Fasting glucose / HbA1c	Screen for diabetes – major risk factor and prognostic indicator
aPTT / INR	Baseline before initiating heparin anticoagulation
ABG	If hypoxic or in cardiogenic shock – assess acid-base status; lactic acidosis indicates poor tissue perfusion
CXR	Exclude differentials; assess pulmonary oedema, heart size

Stress testing is used for stable angina or post-MI risk stratification (typically ≥ 5 days after STEMI in uncomplicated cases), NOT during the acute phase.

Choices of stress testing: ^[16]

Modality	Diagnostic Sensitivity	Diagnostic Specificity	Key Advantage	Key Limitation
Stress ECG (Exercise Treadmill Test)	50–80%	80–95%	Simple, cheap, widely available	Conduction or repolarisation anomalies (LBBB, digoxin, LVH) cause false positives; false positive in young females ^[4]
Myocardial Perfusion Scintigraphy (SPECT)	65–90%	90–95%	Identifies ischaemic territory, hibernating myocardium	Radiation exposure
Stress echocardiogram	65–90%	90–95%	No radiation; identifies wall motion abnormalities and hibernating myocardium	Diagnostic images not possible in all patients (body habitus, lung disease)
Cardiac MRI perfusion	70–90%	90–95%	Best for identifying ischaemic territory and hibernating myocardium; no radiation	Claustrophobia and incompatibility with devices (pacemakers, some metallic implants); expensive

Decision algorithm for choosing stress test:

Exercise treadmill ECG is the first-line IF: ^[16]

Resting ECG is interpretable (no LBBB, no LVH strain, no digoxin effect)
Patient can exercise
No previous revascularisation

If any of these criteria are not met → proceed to stress imaging (stress echo, SPECT, or cardiac MRI).

If patient cannot exercise → use pharmacological stress (dobutamine for echo, adenosine/regadenoson for SPECT/MRI).

After doing pharmacological stress test, you can either do cardiac MRI or SPECT. ^[17]

Used selectively in the STEMI setting, cardiac MRI has several important roles:

Application	Finding	Clinical Significance
Myocardial viability	Late gadolinium enhancement (LGE) – subendocardial or transmural	Transmural LGE = irreversible scar; subendocardial LGE = potential for recovery with revascularisation
Myocarditis vs. MI	Subepicardial LGE in myocarditis vs. subendocardial/transmural LGE in coronary distribution for MI ^[6]	Differentiates MINOCA from true MI
Oedema assessment	T2-weighted sequences show myocardial oedema	A lot of cardiomyopathies have an active oedematous "hot" phase, without elevated troponin ^[18]
Thrombus detection	Intracavitary thrombus (especially LV apical thrombus post-anterior MI)	Guides anticoagulation decision

MINOCA = Myocardial Infarction with Non-Obstructive Coronary Arteries ^[6]

When a patient meets diagnostic criteria for MI (troponin rise + symptoms/ECG changes) but coronary angiography shows no significant obstructive CAD (< 50% stenosis), the differential includes:

Coronary vasospasm (Prinzmetal)
Spontaneous coronary artery dissection (SCAD)
Coronary microvascular dysfunction
Takotsubo cardiomyopathy
Myocarditis
Coronary embolism

Cardiac MRI with LGE is the key investigation for MINOCA – it can identify the underlying cause in up to 75% of cases ^[6].

Investigation	Timing in STEMI	Key Finding	Role
12-lead ECG	< 10 min	ST elevation ≥ 2 contiguous leads	Diagnosis – triggers reperfusion pathway
Troponin (hs-cTn)	STAT + repeat at 3–6h	Rise and/or fall with ≥ 1 value > 99th URL	Confirms MI (but don't wait for result in clear STEMI)
CK-MB	Serial	Rise and fall, shorter t½ than troponin	Reinfarction detection
CXR	Concurrent	Pulmonary oedema, widened mediastinum	Exclude DDx (dissection, PTX)
Echocardiography	Within 1 hour	RWMA, LVEF, complications	Assess severity + complications
Coronary angiography	Emergent (as part of primary PCI)	TIMI 0 flow at culprit, thrombus	Gold standard + therapeutic
Basic bloods	Concurrent	CBC, RFT, LFT, lipids, glucose, coagulation	Baseline + risk factors
CCTA	Not for acute STEMI; for diagnostic uncertainty	Triple rule-out	Exclude dissection/PE if unsure
Cardiac MRI	Subacute / convalescent phase	LGE pattern, oedema, viability	Viability, DDx (myocarditis), MINOCA
Stress testing	Post-MI (≥ 5 days, uncomplicated)	Inducible ischaemia in non-culprit territory	Risk stratification

High Yield Summary – Diagnosis of STEMI

Diagnostic criteria: Troponin rise/fall with ≥ 1 value > 99th URL PLUS ≥ 1 of: ischaemic symptoms, ECG changes, imaging evidence, or thrombus on angiography
ECG criteria: ST elevation ≥ 2 mm in V2–V3 (men ≥ 40), ≥ 2.5 mm (men < 40), ≥ 1.5 mm (women), ≥ 1 mm in all other leads; requires ≥ 2 contiguous leads; new LBBB = STEMI equivalent
Troponin: Gold standard biomarker; hsTnT cut-off > 14 ng/L with > 100% rise at 3–6h; peaks at 24–48h; CK-MB is better for reinfarction detection (shorter t½)
Do NOT wait for troponin in clear STEMI – activate cath lab based on ECG + clinical picture
Always get right-sided leads (V4R) in inferior STEMI to assess for RV infarction
CXR: Usually non-diagnostic for ACS; mainly to exclude dissection (widened mediastinum) and PTX
Echo: RWMA confirms territory; LVEF is the most important prognostic parameter
CCTA: Triple rule-out concept (MI, PE, dissection); high sensitivity but false positives from calcified plaques
Cardiac MRI: Key for MINOCA, myocardial viability, and differentiating myocarditis from MI (subepicardial vs. subendocardial LGE)
ECG pitfalls: Know the false positives (pericarditis, BER, LVH, LBBB, Brugada) and false negatives (posterior MI, RV MI, De Winter, new LBBB)

Active Recall - STEMI Diagnosis and Investigations

References

^[1] Lecture slides: GC 088. Sudden Severe Chest Pain.pdf ^[2] Senior notes: Block A - Accelerating chest pain_ Acute Coronary Syndromes.pdf ^[3] Senior notes: Block A - Sudden severe chest pain_ acute myocardial infarction; aortic dissection.pdf ^[4] Senior notes: Block A - WCS32 Chest pain on exertion_ ischaemic heart disease; angina pectoris.pdf ^[5] Senior notes: Block A - Chest Pain - Department of Medicine.pdf ^[6] Senior notes: Block A - Chest Pain - Department of Radiology.pdf ^[7] Senior notes: Maksim Medicine Notes.pdf ^[8] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf ^[9] Senior notes: Block A - Introduction to CVS investigations (including ECG).pdf ^[10] Senior notes: Ryan Ho Cardiology.pdf ^[12] Lecture slides: General Clerkship_Introduction to CVS Investigations_2026 Yiu (2 Feb 2026).pdf ^[13] Senior notes: Learning_Points_All_Lectures.txt ^[14] Senior notes: Block A - Cardiology Data Interpretation.pdf ^[15] Senior notes: MBBS Final MB (Surgery) (Felix PY Lai).pdf ^[16] Lecture slides: GC 032. Chest pain on exertion_ischaemic heart disease; angina pectoris.pdf ^[17] Senior notes: Block A - Cardiology Interactive Tutorial.pdf ^[18] Senior notes: Block A - Inherited Cardiac conditions.pdf

Management of STEMI

The management of STEMI is driven by one overriding principle: "Time is muscle." Every minute of complete coronary occlusion causes irreversible myocardial necrosis. The entire treatment strategy is built around opening the blocked artery as fast as possible and then preventing re-occlusion and managing complications.

In the management of AMI, there are 4 principles of management: ^[3]

General measures — stabilise the patient
Early presentation (< 12h) → Opening of infarct-related artery — reperfusion therapy (primary PCI or fibrinolysis)
Other measures — pharmacotherapy (antiplatelets, anticoagulants, anti-ischaemic agents)
Complications management and rehabilitation — detect and treat mechanical/electrical complications; secondary prevention

General measures: Bed rest, O₂, Morphine, CCU care ± resuscitation ^[3]

Initial management (SAQ!!): ^[7]

Admit CCU for high risk cases
Complete bed rest + NPO for first 12 hours
Close monitoring: BP/P, I/O Q1h, cardiac monitoring with defibrillator standby

Measure	Drug/Intervention	Dose	Rationale / Mechanism
Oxygen	Supplemental O₂	Only if SpO₂ < 90%	Hypoxaemia worsens ischaemia; BUT routine high-flow O₂ in non-hypoxic patients is harmful (causes coronary vasoconstriction via ROS, ↑ afterload). The 2017 DETO2X-AMI trial showed no benefit of routine O₂ in normoxic STEMI patients
Pain relief	IV Morphine	2–5 mg IV, repeat Q5–15 min PRN	Visceral analgesic; also ↓ preload (venodilation) and ↓ sympathetic drive → ↓ HR, ↓ BP → ↓ myocardial O₂ demand. Side effects: nausea/vomiting (give antiemetic), respiratory depression, hypotension, vagotonic (can worsen bradycardia in inferior MI)
Antiemetic	Metoclopramide	10 mg IV	Prevents morphine-induced nausea; also prokinetic (counteracts gastroparesis from vagal activation)
Nitrates	GTN (sublingual or IV)	SL: 0.5 mg Q5 min × 3; IV TNG: Isoket 2–10 mg/hr	Venodilation → ↓ preload → ↓ LVEDP → ↓ myocardial wall tension → ↓ O₂ demand; also mild coronary vasodilation. IV TNG indicated in the first 48h for persistent ischaemia, heart failure, or hypertension ^[19]

High Yield – Nitrate Contraindications in STEMI

Nitrates have 5 contraindications: ^[3]

RV infarction — RV is preload-dependent; nitrate-induced venodilation → catastrophic ↓ preload → ↓ RV output → hypotension and shock
Use of phosphodiesterase-5 inhibitors (sildenafil/Viagra) in the previous 24 hours — both cause cGMP-mediated vasodilation → profound refractory hypotension
Hypotension (SBP < 90 mmHg) — will worsen shock
Tachycardia (HR > 100) — reflex tachycardia from vasodilation further ↑ O₂ demand
Bradycardia (HR < 50) — nitrates can enhance vagal tone

D. Phase 2: Reperfusion Therapy — The Central Decision

This is the most important treatment decision in STEMI. The goal is to restore blood flow (TIMI 3 flow) to the ischaemic myocardium as rapidly as possible.

Two options exist:

Primary PCI (percutaneous coronary intervention) — mechanical reopening
Fibrinolytic therapy — pharmacological clot dissolution

"PCI" → "percutaneous" (through the skin) "coronary" (heart arteries) "intervention" (treatment). A catheter is advanced through the radial or femoral artery to the coronary arteries, the thrombus is aspirated or crossed, and a balloon is inflated to crush the plaque, followed by stent deployment.

Primary PTCA/PCI → gold standard nowadays, evidence shows this is much more effective than fibrinolytic therapy ^[3]

Indications for primary PCI in STEMI: ^[7]

Indication	Detail
Present < 12 hours after onset of chest pain	The standard window for primary PCI
Clinical and/or ECG evidence of ongoing ischaemia between 12–24 hours of onset	Even beyond 12h, if there's evidence the artery is still occluded and myocardium is still at risk
Cardiogenic shock or severe acute HF	Irrespective of onset time — the only chance of survival is opening the artery
Failed thrombolysis (rescue PCI)	Within 3 hours after failed thrombolysis
Post-thrombolytic PCI	Within 24 hours after successful thrombolysis to reduce reinfarction rate

Time targets:

Door-to-balloon time ≤ 90 minutes ^[7] (from first medical contact to guidewire crossing)
If transfer from a non-PCI centre is needed: first medical contact-to-balloon ≤ 120 minutes

Pre-medication before PCI:

GP IIb/IIIa inhibitor (IV abciximab / eptifibatide) if heavy clot load ^[7] — these block the final common pathway of platelet aggregation (fibrinogen bridging between activated platelets)
DAPT loading (see antiplatelet section below)
Anticoagulation (see below)

Stent types:

Drug-eluting stents (DES) — standard of care; coated with anti-proliferative drug (e.g., everolimus, zotarolimus) to prevent in-stent restenosis
Bare-metal stents (BMS) — rarely used now; considered only when DAPT duration must be minimised (e.g., imminent surgery)

Fibrinolytic Therapy

"Fibrinolytic" → "fibrin" = the mesh of the clot, "lytic" = to dissolve. These drugs activate plasminogen → plasmin, which lyses fibrin into fibrin degradation products (FDPs), dissolving the clot.

Fibrinolytics are ONLY indicated in STEMI but NOT UA/NSTEMI. ^[8] This is a crucial distinction — in NSTEMI, the artery is only partially occluded, and the thrombus is platelet-rich ("white thrombus") rather than fibrin-rich ("red thrombus"). Fibrinolytics work on fibrin, not platelets. Also, in NSTEMI, the risk of bleeding from fibrinolytics outweighs the benefit since the artery is not fully occluded.

Indications: ^[7]

STEMI with symptom onset within 12h + PCI not available within 2h from diagnosis (i.e., fibrinolysis is the fallback when primary PCI cannot be achieved in time)

Fibrinolytics are viable alternative to PCI if chest pain < 3 hours: ^[8]

Outcomes of fibrinolytics and PCI are similar within the first few hours
Fibrinolytics have a higher success rate if chest pain < 3 hours in a hospital WITHOUT PCI such that transferring patient to another hospital may delay therapeutic outcomes

Time target:

Door-to-needle time < 30 minutes (from arrival to fibrinolytic bolus)

Choice of agents:

Agent	Type	Key Features
Tenecteplase (TNK-tPA)	Fibrin-specific	Preferred agent: lower rate of non-cerebral bleeding events, easier to use (single IV bolus) ^[8]
Alteplase (tPA)	Fibrin-specific	Requires bolus + two separate infusions (more complex)
Reteplase (rPA)	Fibrin-specific	Double bolus regimen
Streptokinase (SK)	Fibrin-non-specific	Cheaper; but highly antigenic → repeat use is unfavourable; absolutely contraindicated if previous exposure within 6 months ^[8]; cannot give with IV heparin (long half-life → combined use = bleeding risk) ^[7]

Fibrin-specific agents → more rapid fibrinolysis and less bleeding complications. All three agents have comparable efficacy. ^[8]

Fibrin-specific agents need LMWH cover ^[7] (because after lysis, the exposed plaque is still thrombogenic → need anticoagulation to prevent re-occlusion)

This is extremely high yield for exams. The principle: fibrinolytics cause systemic plasmin activation → dissolve clots everywhere, not just in the coronary artery → any site with recent bleeding, vascular injury, or friable vessels is at risk of catastrophic haemorrhage.

Absolute contraindications: ^[8]^[10]^[19]

Category	Specific Contraindication	Why
Vascular	Suspected aortic dissection	Lysis of thrombus sealing the false lumen → haemorrhage → rupture → death
Vascular	Active bleeding or bleeding diathesis (does not include menses)	Will worsen bleeding
Vascular	Severe uncontrolled HTN unresponsive to emergency therapy	↑ risk of intracerebral haemorrhage
CNS	Haemorrhagic stroke at any time	Risk of recurrent haemorrhage into a vulnerable vascular bed
CNS	Ischaemic stroke within 3 months (EXCEPT acute ischaemic stroke within 4.5 hours)	Risk of haemorrhagic transformation
CNS	Known structural cerebrovascular lesion (e.g., AVM, aneurysm)	Friable vessels → high bleeding risk
CNS	Malignant intracranial neoplasm (primary or metastatic)	Tumour vasculature is fragile
Trauma	Significant closed head or facial trauma within 3 months	Risk of intracranial bleed
Surgery	Intracranial or intraspinal surgery within 2 months	Fresh surgical site → haemorrhage
Drug-specific	For streptokinase: prior treatment within previous 6 months	Antigenicity → serious allergic reaction

Relative contraindications: ^[10]

Contraindication	Comment
Severe uncontrolled HTN on presentation (BP > 180/110)	Could be absolute in low-risk patients
History of chronic, severe, poorly controlled HTN	Chronically damaged cerebral vessels
History of prior ischaemic stroke > 3 months or known intracerebral pathology not in absolute CI	Case-by-case assessment
Traumatic or prolonged (> 10 min) CPR	Chest compressions → rib fractures, internal bleeding
Oral anticoagulant therapy	Pre-existing anticoagulation + fibrinolytic = high bleeding risk
Major surgery < 3 weeks	Fresh surgical site
Noncompressible vascular punctures	Cannot apply pressure to stop bleeding
Recent (within 2–4 weeks) internal bleeding	Risk of rebleeding
Pregnancy	Placental bleeding risk
Active peptic ulcer	GI haemorrhage

Major risk of fibrinolytic = intracerebral haemorrhage (haemorrhagic stroke) ^[8] — approximately 1% risk, which is why primary PCI is preferred when available.

Pre-treatment: full-lead ECG, INR, aPTT, cardiac enzymes ^[7]

Successful fibrinolysis documented by: ^[3]^[10]

Parameter	Sign of Success
Clinical	Decrease in chest pain
ECG	Early resolution of ST elevation ≥ 50% in worst ECG lead at 60–90 min after fibrinolytic; accelerated nodal or idioventricular rhythm (reperfusion arrhythmias)
Biochemical	Early peaking of CK — Normal peak: 22–24h; Successful thrombolysis: 11–12h (washout phenomenon: restored blood flow flushes enzymes out of necrotic tissue earlier)
Imaging	Radionuclide imaging, angiography

After thrombolysis: ^[7]

Successful reperfusion → routine angiography within 2–24 hours (pharmaco-invasive strategy)
Failed reperfusion → rescue PCI stat
In thrombolysis patients, up to 50% have post-infarct angina (because of residual stenosis) ^[10]
Side effects: allergy/anaphylaxis (2%), haemorrhagic stroke (1%) ^[7]

E. Phase 3: Pharmacotherapy (Concurrent with Reperfusion)

These medications are given alongside and after reperfusion therapy. Think of them as the "medical scaffolding" that supports the mechanical fix.

The ruptured plaque is a powerful trigger for platelet adhesion and aggregation. Even after PCI opens the artery and a stent is placed, the stent surface itself is thrombogenic until it endothelialises (gets covered by a layer of endothelial cells).

Dual antiplatelet therapy (DAPT) is recommended: ^[2]

a) Aspirin (acetylsalicylic acid, ASA)

Aspect	Detail
Mechanism	Irreversibly acetylates cyclooxygenase-1 (COX-1) in platelets → blocks synthesis of thromboxane A₂ (TXA₂) → inhibits platelet aggregation and vasoconstriction
Loading dose	300–325 mg (chewed for rapid absorption via buccal mucosa)
Maintenance dose	75–100 mg daily ^[2]
Duration	Lifelong
Side effects	GI upset, GI bleeding, aspirin-exacerbated respiratory disease (aspirin triad)

b) P2Y12 Receptor Inhibitor — "P2Y12" is the receptor on platelets for ADP; blocking it prevents ADP-mediated platelet activation

Recommended in combination with aspirin, maintained over 12 months: ^[2]

Agent	Mechanism	Loading → Maintenance	Key Points
Ticagrelor	Reversible, direct-acting P2Y12 inhibitor (no hepatic activation needed)	180 mg → 90 mg BID	Preferred in STEMI (faster onset, more potent, proven mortality benefit in PLATO trial). Side effects: dyspnoea (adenosine reuptake inhibition), bleeding. Does NOT require CYP2C19 metabolism → no "poor metaboliser" problem
Prasugrel	Irreversible thienopyridine prodrug (requires CYP-mediated activation)	60 mg → 10 mg daily	More potent than clopidogrel. Contraindicated in prior stroke/TIA (↑ intracranial bleeding). Dose reduction to 5 mg if weight < 60 kg or age > 75
Clopidogrel	Irreversible thienopyridine prodrug (requires CYP2C19 activation)	300–600 mg → 75 mg daily	Or 75 mg QD if aspirin is not tolerated due to hypersensitivity or GI intolerance ^[2]. Limitation: ~15–30% of East Asians are CYP2C19 poor metabolisers → reduced clopidogrel activation → ↓ antiplatelet effect ("clopidogrel resistance")

If delayed beyond 24h, can give P2Y12 inhibitors → ticagrelor and clopidogrel over prasugrel ^[5]

Try to maintain DAPT for 12 months → if really cannot due to bleeding risk, maintain at least for 3–6 months. You really want to make sure there is no re-thrombosis in your stent. ^[2]

For patients with stable CAD who underwent PCI → 6 months. For patients with acute MI who underwent PCI → 12 months still required. ^[20]

c) GP IIb/IIIa Inhibitors — "GPIIb/IIIa" = glycoprotein IIb/IIIa, the final common receptor for platelet aggregation (binds fibrinogen between platelets)

Agent	Route	Use
Abciximab	IV	Pre-med for PCI if heavy clot load ^[7]; monoclonal antibody fragment
Eptifibatide	IV	Alternative; synthetic peptide
Tirofiban	IV	Alternative

These are not used for maintenance — only during the acute procedural phase.

East Asian Paradox – Clopidogrel in Hong Kong

In Hong Kong, the high prevalence of CYP2C19 loss-of-function alleles (up to 30% are poor metabolisers) means clopidogrel may be less effective. ^[21] This is why ticagrelor or prasugrel are increasingly preferred for STEMI in HK. Pharmacogenomic testing for CYP2C19 is being considered but is not yet routinely done in HK since more evidence is still required. ^[21]

While antiplatelets prevent the "white clot" (platelet plug), anticoagulants prevent the "red clot" (fibrin mesh).

Agent	Mechanism	Use in STEMI	Key Point
Unfractionated heparin (UFH)	Activates antithrombin → inactivates thrombin (IIa) and Factor Xa	Given in cath lab during PCI ^[5]; bolus 60–70 U/kg IV	Short half-life, easily reversible with protamine → preferred during procedures
Enoxaparin (LMWH)	Activates antithrombin → predominantly inactivates Factor Xa	Given at bedside ^[5]; 1 mg/kg SC Q12h	Longer acting, predictable pharmacokinetics, no routine aPTT monitoring needed
Fondaparinux (ULMWH)	Selective Factor Xa inhibitor via antithrombin	Given at bedside ^[5]; 2.5 mg SC daily	Lowest bleeding risk among anticoagulants; but not suitable for primary PCI (risk of catheter thrombosis → must add UFH bolus)
Bivalirudin	IV direct thrombin inhibitor ^[3]	Alternative to UFH during PCI	Does not require antithrombin as cofactor; useful in HIT

Choice: UFH if primary PCI (faster onset), LMWH if thrombolysis, UFH/LMWH if not for reperfusion ^[7]

Side effects of heparin: heparin-induced thrombocytopenia (HIT), osteoporosis, hyperkalaemia ^[7]

Aspect	Detail
Mechanism	Block β₁-adrenergic receptors on the heart → ↓ heart rate, ↓ contractility, ↓ BP → ↓ myocardial O₂ demand; also improves diastolic filling time → better coronary perfusion
Survival benefit	Proven survival benefit ^[7]; reduces infarct size, ventricular arrhythmias, and reinfarction
Target	Titrate to HR < 70 bpm ^[7]^[19]
Agents	Metoprolol 25 mg BD oral (acute); bisoprolol, carvedilol, or metoprolol succinate if reduced EF ^[7]
Contraindications	Cardiogenic shock, severe bradycardia, 2nd/3rd degree heart block, acute decompensated HF, severe asthma, cocaine-induced MI (unopposed alpha stimulation)

Beta-blockers are the cornerstone of anti-ischaemic therapy post-ACS. ^[2] Alternative: rate-limiting CCB (diltiazem/verapamil) if beta-blockers are contraindicated and there is no heart failure ^[2]

After MI, the infarcted myocardium undergoes ventricular remodelling: the necrotic zone thins and expands, the remaining viable myocardium hypertrophies to compensate, and the ventricle dilates. This remodelling → heart failure. ACEi/ARBs counteract this by blocking the renin-angiotensin-aldosterone system (RAAS).

Aspect	Detail
Mechanism	ACEi: blocks angiotensin-converting enzyme → ↓ angiotensin II → ↓ vasoconstriction, ↓ aldosterone, ↓ myocardial fibrosis, ↓ remodelling. ARB: blocks angiotensin II receptor (AT1)
Indication in STEMI	Should be administered within the first 24 hours if LVEF < 40% and in the absence of hypotension or contraindications ^[19]
Broader indications	ACEI for patients with CHF, LV dysfunction (EF < 40%), hypertension, diabetes ^[2]
Agents	Lisinopril 5–20 mg daily; Ramipril 2.5–10 mg daily; Perindopril 2–8 mg daily ^[19]
ARB	Should be used if patient is intolerant of ACEI ^[19] (e.g., ACEi-induced cough — due to ↑ bradykinin from lack of ACE-mediated degradation)
Contraindications	Bilateral renal artery stenosis, azotemia, pregnancy, hyperkalaemia, hypotension ^[4]
Side effects	Cough (ACEi only), hypotension, syncope, angioedema, hyperkalaemia

Consider switching to ARNI (sacubitril/valsartan) if persistent heart failure symptoms despite ACEI/ARB in patient with reduced LVEF. Stop ACEI 36 hours before initiating ARNI. ^[19]

Aspect	Detail
Mechanism	HMG-CoA reductase inhibitors → ↓ hepatic cholesterol synthesis → ↑ LDL receptor expression → ↓ circulating LDL. Also: pleiotropic effects (↓ inflammation, ↑ endothelial function, plaque stabilisation)
Indication	Should be given regardless of baseline LDL-C level in the absence of contraindications ^[19] — the benefit is not just lipid-lowering but also anti-inflammatory plaque stabilisation
Agents	High-intensity: atorvastatin 40–80 mg, rosuvastatin 20–40 mg
Target	LDL < 1.4 mmol/L AND > 50% reduction from baseline (2019 ESC/EAS guidelines)
Side effects	Myalgia, rhabdomyolysis (rare), hepatotoxicity, ↑ blood glucose

Aspect	Detail
Mechanism	Block aldosterone → ↓ Na⁺/H₂O retention, ↓ K⁺ loss, ↓ myocardial fibrosis
Indication	In patients already on therapeutic doses of ACEI and beta-blocker, with LVEF ≤ 40% + diabetes or heart failure, without significant renal dysfunction or hyperkalaemia ^[19]
Agents	Spironolactone 25–50 mg daily; eplerenone 25–50 mg daily
Contraindications	K⁺ > 5.0 mmol/L, CrCl < 30 mL/min

PPI for patients at high risk of GI bleeding ^[19] — given the combination of DAPT + anticoagulation, GI bleeding risk is significant. Omeprazole 20 mg daily or pantoprazole.

Note: Omeprazole may interact with clopidogrel via CYP2C19 inhibition → consider pantoprazole instead.

Consider SGLT2 inhibitor in heart failure ^[19] — empagliflozin or dapagliflozin; proven benefit in HFrEF regardless of diabetes status (DAPA-HF, EMPEROR-Reduced trials). Mechanism: osmotic diuresis + natriuresis → ↓ preload; also cardioprotective effects (↑ ketone utilisation, ↓ fibrosis).

High Yield – SAQ: Initial Management of STEMI

Initial management (SAQ!!): ^[7]

Admit CCU for high-risk cases
Complete bed rest + NPO for first 12 hours
Close monitoring: BP/P, I/O Q1h, cardiac monitoring with defibrillator standby
Exclude life-threatening DDx: aortic dissection, PE, tension pneumothorax, perforated PU/oesophagus
Initial pharmacotherapy:
- Aspirin 300 mg loading (chewed) → 75–100 mg daily
- P2Y12 inhibitor loading (ticagrelor 180 mg or clopidogrel 300–600 mg)
- Anticoagulation: UFH (if for PCI) or enoxaparin (if for thrombolysis)
- Beta-blocker: metoprolol 25 mg BD (titrate to HR < 70)
- GTN: sublingual then IV if ongoing pain (unless contraindicated)
- Morphine IV for pain relief
- Statin: high-intensity (atorvastatin 80 mg) regardless of baseline LDL
- ACEi: within 24h if LVEF < 40%
- O₂: only if SpO₂ < 90%
Reperfusion: primary PCI (door-to-balloon < 90 min) OR fibrinolysis (door-to-needle < 30 min)

G. Phase 4: Secondary Prevention

After the acute phase of ACS, treatment modalities in secondary prevention: ^[2]

A = Antiplatelet therapy (DAPT) + ACEi/ARB
B = Beta-blocker + BP control
C = Cholesterol (statin) + Cigarette cessation
D = Diet + Diabetes control
E = Exercise (cardiac rehabilitation)

Domain	Agent / Intervention	Detail
Antiplatelet	DAPT: Aspirin + P2Y12 inhibitor	Maintained over 12 months after ACS; if bleeding risk too high, at least 3–6 months ^[2]
Beta-blocker	Metoprolol/bisoprolol/carvedilol	Cornerstone of secondary prevention ^[2]; continue indefinitely
ACEi	Lisinopril/ramipril/perindopril	For patients with CHF, LVEF < 40%, HTN, DM ^[2]
Statin	Atorvastatin 80 mg / rosuvastatin 20–40 mg	Target LDL < 1.4 mmol/L
Aldosterone antagonist	Spironolactone/eplerenone	If LVEF ≤ 40% + HF or DM
SGLT2i	Empagliflozin/dapagliflozin	If HF with reduced EF
ARNI	Sacubitril/valsartan	If persistent HF symptoms despite ACEi/ARB + reduced LVEF ^[19]
Calcium channel blocker	Diltiazem / verapamil	If contraindications to beta-blockers and no heart failure ^[2]
Nitrates	Long-acting or short-acting	In the presence of angina ^[2]
Lifestyle	Smoking cessation, exercise rehabilitation, weight management, Mediterranean diet	Critical for long-term risk reduction
Rivaroxaban (very high risk)	2.5 mg BID	For very high risk angina patients, add on top of low-dose aspirin (COMPASS trial) ^[4]

AF with MI → triple therapy (aspirin, clopidogrel, DOAC): ^[20]

Not recommended for the long term, since bleeding risk is unacceptable
No more than 30 days of triple therapy
Then DOAC + one antiplatelet (usually clopidogrel) for up to 1 year
Then lifelong anticoagulation (DOAC alone)
Add PPI when using 2 or more antithrombotics ^[20]

Device	Indication	Mechanism
Implantable Cardioverter-Defibrillator (ICD)	Primary prevention: NYHA II–III with LVEF < 30% (may be considered if LVEF 31–35%) ^[22]; secondary prevention: survived VT/VF	Detects and terminates lethal ventricular arrhythmias (VT/VF) with defibrillation
Cardiac Resynchronisation Therapy (CRT)	NYHA III despite optimal medical therapy, sinus rhythm, QRS > 120 ms (LBBB), LVEF < 35% ^[22]	Biventricular pacing → synchronises LV and RV contraction → improves cardiac output
LVAD / Heart transplant	Intractable ventricular arrhythmias or refractory heart failure	Mechanical circulatory support; bridge to transplant or destination therapy

Prophylactic ICD placement should be considered following 3 months of optimal medical therapy in patients with PMHx of MI; following 6 months of optimal medical therapy in non-ischaemic patients. ^[22] The waiting period ensures the LVEF does not recover with medical therapy alone (some patients improve enough to not need an ICD).

Arrhythmia	Management
Symptomatic sinus bradycardia	Atropine 0.3–0.6 mg IV bolus; pacing if unresponsive to atropine ^[10]
1° AV block or Mobitz type I 2° HB	Conservative (these are generally benign, especially in inferior MI due to AV node ischaemia) ^[10]
Mobitz type II 2° HB or complete HB	Pacing ^[10] (high risk of sudden asystole, especially in anterior MI)
AF/AFlu	Digoxin 0.25 mg IV/PO loading; diltiazem 10–15 mg IV; amiodarone 5 mg/kg IV ^[10]
Stable sustained monomorphic VT	Amiodarone 150 mg IV over 10 min; lignocaine 50–100 mg IV bolus; cardioversion if haemodynamically compromised ^[10]
Sustained polymorphic VT	Unsynchronised cardioversion starting with 200 J ^[10]
VF	Prompt defibrillation with ACLS algorithm ^[10]
PSVT	ATP (adenosine) 10–20 mg IV bolus → verapamil 5–15 mg IV; cardioversion if haemodynamic compromise ^[10]

Inferior-posterior MI causing complete AV block → treatment is different → consider pacing before revascularisation ^[14]

High Yield Summary – STEMI Management

Immediate: Bed rest, O₂ only if SpO₂ < 90%, morphine, GTN (check for contraindications – RV infarction, PDE5 inhibitors, hypotension), cardiac monitoring with defibrillator standby
Reperfusion: Primary PCI is gold standard (door-to-balloon < 90 min); fibrinolysis is the fallback if PCI unavailable within 120 min (door-to-needle < 30 min)
DAPT: Aspirin (300 mg load → 75–100 mg daily lifelong) + P2Y12 inhibitor (ticagrelor preferred → 90 mg BID for 12 months)
Anticoagulation: UFH during PCI; LMWH for thrombolysis; fondaparinux at bedside
Beta-blocker: Metoprolol (titrate HR < 70); proven survival benefit; cornerstone of secondary prevention
ACEi/ARB: Within 24h if LVEF < 40%; prevents adverse ventricular remodelling
Statin: High-intensity regardless of LDL; plaque stabilisation + lipid lowering
Fibrinolysis: Only for STEMI, not NSTEMI; know absolute contraindications (suspected dissection, haemorrhagic stroke, active bleeding, structural cerebrovascular lesion, uncontrolled severe HTN, recent head/spinal surgery)
Successful reperfusion signs: ↓ pain, ≥ 50% ST resolution at 60–90 min, early CK peak (11–12h vs normal 22–24h), reperfusion arrhythmias
Secondary prevention: ABCDE — Antiplatelet/ACEi, Beta-blocker/BP, Cholesterol/Cessation, Diet/DM, Exercise
Device therapy: ICD if LVEF < 30% after 3 months optimal medical therapy; CRT if LBBB + LVEF < 35% + NYHA III despite medical therapy

Active Recall - STEMI Management

References

^[2] Senior notes: Block A - Accelerating chest pain_ Acute Coronary Syndromes.pdf ^[3] Senior notes: Block A - Sudden severe chest pain_ acute myocardial infarction; aortic dissection.pdf ^[4] Senior notes: Block A - WCS32 Chest pain on exertion_ ischaemic heart disease; angina pectoris.pdf ^[5] Senior notes: Block A - Chest Pain - Department of Medicine.pdf ^[7] Senior notes: Maksim Medicine Notes.pdf ^[8] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf ^[10] Senior notes: Ryan Ho Cardiology.pdf ^[14] Senior notes: Block A - Cardiology Data Interpretation.pdf ^[19] Lecture slides: Handbook of Internal Medicine 2024.pdf ^[20] Senior notes: Block A - Clinical pharmacology of antiplatelets and anticoagulation.pdf ^[21] Senior notes: Introduction to Clinical pharmacology (I) (Pharmaco- Genomics, Precision Medicine).pdf ^[22] Senior notes: Block A - Shortness of breath on exertion_ heart failure.pdf

Complications of STEMI

The complications of STEMI are among the highest-yield exam topics in cardiology. They are best understood by thinking about what happens to dead or dying myocardium and how that affects the heart's electrical, mechanical, and haemodynamic function.

The simplest organising principle: once myocardium is infarcted, the complications arise from three pathological processes:

Electrical instability → arrhythmias
Mechanical failure → pump failure, structural rupture
Thromboembolism → mural thrombus, systemic emboli
Inflammation → pericarditis

The timing of each complication relative to the MI is also crucial — examiners love asking "when" things happen.

Timing	Complications
Immediate (minutes to hours)	Ventricular arrhythmias (VF, VT), sinus bradycardia, AV block, cardiogenic shock
Early (hours to days)	Acute heart failure / pulmonary oedema, reinfarction, post-infarct angina, early pericarditis
Subacute (days to 2 weeks)	Mechanical complications (free wall rupture, VSD, papillary muscle rupture), mural thrombus, RV infarction complications
Late (weeks to months)	LV aneurysm, Dressler syndrome, chronic heart failure, late arrhythmias, LV remodelling

B. Electrical Complications — Arrhythmias

Arrhythmias are the leading cause of death in the first hour after STEMI and the primary reason patients need CCU monitoring with defibrillator standby.

The ischaemic border zone (the transitional area between healthy and infarcted myocardium) creates an electrically unstable environment:

Ischaemic cells are partially depolarised (due to K⁺ efflux from damaged cells, intracellular acidosis, ATP depletion)
This creates voltage gradients between healthy and ischaemic tissue
These gradients allow re-entrant circuits to form → sustained arrhythmias
Additionally, catecholamine surge → ↑ automaticity of ischaemic cells

Arrhythmia	Mechanism	Timing	Management
VF (ventricular fibrillation)	Re-entry in ischaemic border zone; chaotic electrical activity	Within first hour (peak); ~80% of pre-hospital cardiac deaths	Prompt defibrillation with ACLS algorithm ^[10]; unsynchronised shock; 10% ↓ survival per minute of delay
Sustained monomorphic VT	Re-entrant circuit around scar/ischaemic border	Hours to days; or late (scar-related)	Amiodarone 150 mg IV over 10 min; lignocaine 50–100 mg IV bolus; cardioversion if haemodynamically compromised ^[10]
Sustained polymorphic VT	Ongoing ischaemia with heterogeneous repolarisation	Hours to days	Unsynchronised cardioversion starting with 200 J ^[10]; treat underlying ischaemia; correct electrolytes (K⁺, Mg²⁺)
Accelerated idioventricular rhythm (AIVR)	Reperfusion arrhythmia — enhanced automaticity in Purkinje fibres as blood flow is restored	At time of reperfusion (good sign!)	Usually benign and self-limiting; no treatment needed unless haemodynamically significant; rate typically 60–120 bpm
Symptomatic sinus bradycardia	(1) Inferior MI → AV node ischaemia (RCA supply); (2) Bezold–Jarisch reflex (vagal activation)	Early, especially inferior MI	Atropine 0.3–0.6 mg IV bolus; pacing if unresponsive ^[10]
AF / Atrial flutter	(1) LA stretch from ↑ LVEDP; (2) Atrial ischaemia; (3) Pericarditis; (4) ↑ catecholamines	Common and frequently transient; can be a sign of impending or overt LVF ^[10]	Digoxin 0.25 mg IV/PO loading; diltiazem 10–15 mg IV; amiodarone 5 mg/kg IV over 60 min ^[10]
PSVT (paroxysmal SVT)	Re-entry involving AV node	Variable	ATP (adenosine) 10–20 mg IV bolus → verapamil 5–15 mg IV slowly; cardioversion if severe compromise ^[10]

AV block is particularly important and the management differs based on the location of the MI:

AV Block Type	Inferior MI	Anterior MI
1° AV block or Mobitz I (Wenckebach)	Conservative ^[10] — block is at AV node level (supplied by RCA); usually transient, narrow escape rhythm, adequate rate	Monitor closely — may progress
Mobitz II 2° AV block	Less common in inferior MI	Pacing ^[10] — block is infra-nodal (His-Purkinje); wide QRS escape rhythm; high risk of sudden progression to complete heart block with asystole
Complete (3°) heart block	Conservative Tx under careful monitoring as alternative if narrow QRS escape rhythm and adequate rate ^[10] — usually reversible over days as AV node oedema resolves	Pacing ^[10] — unstable wide complex escape; anterior infarct → ↑ risk of sudden asystole

Other indications for temporary pacing: bifascicular block + 1° AVB, alternating BBB / RBBB + alternating LAFB/LPFB ^[10] — these patterns suggest extensive conducting system damage and impending complete heart block.

Inferior-posterior MI causing complete AV block → treatment is different → consider pacing before revascularisation ^[14]

Why Is AV Block in Anterior MI More Dangerous Than in Inferior MI?

In inferior MI (RCA occlusion), the AV block is at the AV node level — the node is directly ischaemic but has the potential to recover. The escape rhythm originates from the junctional tissue → narrow QRS, adequate rate (~40–60 bpm), relatively stable.

In anterior MI (LAD occlusion), the AV block occurs at the infra-nodal level (His bundle / bundle branches) because the LAD supplies the interventricular septum where the conducting system runs. The escape rhythm originates from ventricular tissue → wide QRS, slow and unreliable rate (~20–40 bpm), high risk of asystole. This extensive septal damage also means a very large infarct with poor prognosis.

C. Mechanical Complications — "Pump Failure and Structural Rupture"

Pump failure mechanism: a downward spiral exacerbating myocardial ischaemia ^[10]:

↓ Systolic function → ↓ coronary perfusion → ↓ supply → further ischaemia
↓ Diastolic function → ↑ pulmonary congestion → hypoxaemia → further ischaemia

This creates a vicious cycle where ischaemia begets more ischaemia.

Indicates extensive myocardial damage → poor prognosis (↑ likelihood of other complications) ^[10]

Watch out for other causes of shock: mechanical complications, arrhythmia, excessive use of anti-hypertensives ^[10]

Killip Classification (already discussed):

Killip Class	Features	Mortality
I	No HF	~6%
II	Mild HF (S3, basal crackles, JVP↑)	~17%
III	Acute pulmonary oedema (frank APO)	~38%
IV	Cardiogenic shock	~80% without intervention

Cardiogenic shock is defined as:

SBP < 90 mmHg for > 30 min (or vasopressor requirement)
CI < 2.2 L/min/m²
PCWP > 18 mmHg
Signs of end-organ hypoperfusion (oliguria, altered consciousness, cold extremities)

Clinical features of cardiogenic shock: ^[23]

Forward failure: pallor, peripheral cyanosis, cold extremities, delayed capillary refill, oliguria, altered consciousness
Backward failure: dyspnoea, wheeze, cough with pink frothy sputum, basal crackles, displaced apex, gallop

Management of cardiogenic shock: ^[23]

Sit patient upright
High-flow O₂ (15 L/min with BVM with reservoir) to keep SpO₂ > 94%
Optimise cardiac workload:
- Inotropes (e.g., IV dobutamine) if adequate filling pressure
- Fluid resuscitation ± vasopressors if low filling pressure
Urgent reperfusion (PCI or emergency CABG)
Consider mechanical circulatory support (IABP, Impella, ECMO)

Complicates 30–50% of inferior STEMIs (since the RCA supplies both the inferior LV wall and the RV).

Why it matters: The RV is a preload-dependent pump. When the RV infarcts:

RV contractility drops → cannot push blood into the pulmonary circulation
↓ Pulmonary flow → ↓ LV preload → ↓ LV output → hypotension
Clinically: hypotension + raised JVP + clear lungs (no pulmonary oedema because blood is not reaching the pulmonary vasculature)
Kussmaul's sign may be present (paradoxical rise in JVP on inspiration)

Management:

Volume loading (IV normal saline) — to maintain RV preload
Avoid nitrates, diuretics, morphine — all reduce preload and can cause cardiovascular collapse
Maintain sinus rhythm (RV is particularly dependent on atrial kick)
Inotropic support if needed (dobutamine)

These are the most feared mechanical complications and typically occur 3–7 days post-MI (when the infarcted wall is at its weakest — necrotic tissue is being removed by macrophages but scar tissue has not yet formed). The risk is highest with:

Large transmural infarcts
First MI (no prior collateral development)
Elderly females
Hypertension during acute phase (↑ wall stress)
Paradoxically, patients who did NOT receive reperfusion therapy (reperfusion limits infarct size)

Complication	Mechanism	Clinical Presentation	Timing	Management
Free wall rupture	Transmural necrosis → weakening and rupture of ventricular free wall → blood enters pericardial space	Sudden haemodynamic collapse → cardiac tamponade → PEA / electromechanical dissociation → death. May be preceded by recurrent chest pain, agitation, transient hypotension	Day 3–7 (peak; but can occur day 1–14)	Emergency pericardiocentesis → emergency surgery (repair). Usually fatal (> 90% mortality)
Ventricular septal rupture (VSR)	Necrosis of interventricular septum → perforation → left-to-right shunt (LV → RV)	New harsh pansystolic murmur at left sternal border + haemodynamic deterioration; ↑ O₂ saturation step-up between RA and RV on catheterisation	Day 3–7	Stabilise with vasodilators ± IABP → emergency surgical repair or percutaneous closure
Papillary muscle rupture	Necrosis/ischaemia of papillary muscle → rupture → flail mitral valve leaflet → severe acute mitral regurgitation	New loud pansystolic murmur at apex radiating to axilla + flash pulmonary oedema + cardiogenic shock; severe haemodynamic collapse	Day 2–7	Stabilise with vasodilators, IABP → emergency mitral valve surgery (repair or replacement)

High Yield – Papillary Muscle Vulnerability

The posteromedial papillary muscle is supplied by a single artery (the PDA, usually from RCA), whereas the anterolateral papillary muscle has dual supply (from LAD and LCx). This is why papillary muscle rupture is much more common in inferior/posterior MI (RCA territory) — the posteromedial muscle has no collateral "backup" and is more vulnerable to ischaemic necrosis.

Exam Pearl – VSR vs. Papillary Muscle Rupture

Both present with a new systolic murmur and haemodynamic deterioration. How to differentiate:

Feature	Ventricular Septal Rupture	Papillary Muscle Rupture (Acute MR)
Murmur location	Left sternal border (parasternal)	Apex, radiating to axilla
Murmur character	Harsh, often with thrill	Blowing pansystolic
Echocardiography	Defect in septum with L→R shunt on colour Doppler	Flail mitral leaflet, severe MR jet
Catheterisation	O₂ step-up between RA and RV	Tall v-wave on PCWP tracing
Territory	Anterior (LAD, septal perforators) or inferior (RCA)	Inferior > anterior (posteromedial PM)

Occurs weeks to months after a large transmural MI (usually anterior/apical — LAD territory)
The infarcted segment is replaced by thin, fibrotic scar tissue that bulges paradoxically during systole (dyskinesia)
Persistent ST elevation on ECG after STEMI should raise suspicion for ventricular aneurysm ^[10]

Consequences:

Heart failure (paradoxical systolic expansion → ↓ effective cardiac output)
Mural thrombus formation (stagnant blood in the aneurysm → Virchow's stasis) → systemic thromboembolism (stroke)
Ventricular arrhythmias (re-entrant circuits around the scar border)
Rupture (uncommon — the fibrotic wall is stronger than acute necrotic tissue)

Management:

Anticoagulation if mural thrombus present (warfarin for ≥ 3 months, or DOAC)
Heart failure management (ACEi, beta-blocker, diuretics)
ICD if significant arrhythmia burden
Surgical aneurysmectomy if refractory HF or recurrent arrhythmias (rarely needed)

LV Mural Thrombus

Forms on the akinetic/dyskinetic endocardial surface of the infarcted wall (especially large anterior/apical MI — LAD territory)
Mechanism: Virchow's triad — (1) endocardial injury (from infarction), (2) stasis (from akinetic wall segment), (3) hypercoagulability (acute phase response)
Risk: embolisation → ischaemic stroke, mesenteric ischaemia, renal infarction, limb ischaemia

Detection: Echocardiography (especially with contrast-enhanced echo or cardiac MRI)

Prevention/Treatment:

Anticoagulation (warfarin with INR target 2–3, for at least 3–6 months; DOACs increasingly used)
Adequate reperfusion (limits infarct size and therefore akinetic area)

E. Inflammatory Complications — Pericarditis

Occurs within 24–72 hours of transmural MI
Mechanism: Transmural necrosis → inflammation extends to the adjacent visceral pericardium → localised fibrinous pericarditis
Clinical features: Sharp pleuritic chest pain (worse on inspiration, relieved by leaning forward), pericardial friction rub
ECG: May show diffuse ST elevation, but in the context of recent MI, the changes are often difficult to distinguish from ongoing ischaemia
Management: Aspirin (high-dose, e.g., 650 mg TDS) is the treatment of choice; avoid NSAIDs and corticosteroids in the acute post-MI period (they impair myocardial healing and may increase risk of myocardial rupture)

Occurs 2–10 weeks after MI
Mechanism: An autoimmune reaction — myocardial necrosis exposes intracellular antigens (myosin, troponin) to the immune system → generation of anti-myocardial antibodies → immune-mediated pericarditis and pleuritis
Named after William Dressler (1890–1969), American cardiologist who described it in 1956
Clinical features: Fever, pleuritic chest pain, pericardial effusion ± pleural effusion, elevated ESR/CRP
ECG: Diffuse ST elevation with PR depression (typical pericarditis pattern)
Now rare due to early reperfusion therapy (smaller infarcts → less antigen exposure)
Management: Aspirin or colchicine; short course of NSAIDs if aspirin insufficient; corticosteroids as last resort (risk of impaired healing)

Complications of PCI (mortality < 0.5%): ^[8]^[10]

Category	Complication	Details
Vascular / Access site	Access site bleeding	Manual compression for haemostasis; reverse or stop anticoagulation ^[8]
	Retroperitoneal bleeding	Femoral access with artery puncture; diagnosed with haemodynamic compromise (↑ HR, ↓ BP) ^[8]
	Haematoma, AV fistula, pseudoaneurysm	Local complications
Coronary artery	Coronary artery dissection and acute closure	Dissections found in up to 50% immediately after PTCA due to guidewire passage or controlled injury; ↑ risk of acute closure and MI → routine use of stenting ^[8]
	Coronary artery perforation	Requires inflation of perfusion balloon at site to stop blood into pericardium → emergency covered stent ^[8]
Myocardium	Peri-procedural MI	Side branch occlusion (60%), stent complications, microembolisation ^[10]
Stent-related	Stent thrombosis (1–2%)	Acute event, usually presents with severe STEMI or cardiac death; associated with cessation of DAPT; majority occurs < 30 days ^[10] — prevented by DAPT
	In-stent restenosis (ISR)	Chronic event presenting with recurrent stable angina; due to intimal proliferation; usually ≥ 6–9 months; prevented by drug-eluting stent ^[10]
Systemic	Stroke	Ischaemic (dislodgement of thrombus/calcific material during catheter manipulation) or haemorrhagic (antiplatelet-induced) ^[8]
	Contrast-induced AKI	Manifests within 48 hours, peaks at Day 3–5 ^[8]; risk factors: CKD, diabetes, volume depletion; prevention: adequate hydration, minimise contrast volume

Stent Thrombosis vs. In-Stent Restenosis – Key Distinction

Feature	Stent Thrombosis	In-Stent Restenosis
Timing	Acute (< 24h), subacute (< 30d), late (< 1y), very late (> 1y)	Chronic (≥ 6–9 months)
Mechanism	Thrombus on exposed stent surface before endothelialisation	Neointimal hyperplasia (smooth muscle proliferation)
Presentation	Severe STEMI or cardiac death (acute event)	Recurrent stable angina (gradual event)
Prevention	DAPT (aspirin + P2Y12 inhibitor)	Drug-eluting stent (DES)
Treatment	Emergency PCI	Repeat PCI with drug-coated balloon or new DES

Post-ACS ischaemia is indicated by symptoms/ECG changes + new rise in cTn > 20% or to > 5× ULN (if normal baseline) ^[10]

Causes of post-PCI MI: side branch occlusion (60%), stent complications, microembolisation ^[10]

In thrombolysis patients, up to 50% have post-infarct angina (due to residual stenosis) ^[10]:

Should consider early (6–24h) coronary angiography/PCI in all thrombolysis patients
If PCI cannot be done ≤ 24h, still do coronary angiography/PCI if ischaemia occurs before discharge

Complication	Mechanism	Notes
Venous thromboembolism (DVT/PE)	Immobility + hypercoagulable state post-MI	Prophylactic LMWH + compression stockings
Shoulder-hand syndrome (reflex sympathetic dystrophy)	Immobilisation → complex regional pain syndrome	Rare; physiotherapy
Depression	Multifactorial: major life event, disability, biochemical (inflammatory cytokines)	Screen for post-MI depression; significant impact on rehabilitation and adherence; SSRIs are safe post-MI
Recurrent MI	Plaque instability in other coronary segments; stent thrombosis	Secondary prevention is critical (DAPT, statin, lifestyle modification)

Timing	Complication	Key Clinical Clue
Minutes	VF / VT → cardiac arrest	Collapse, loss of consciousness
Minutes–hours	Sinus bradycardia / AV block (inferior MI)	HR < 50, hypotension, Bezold–Jarisch reflex
Hours	Acute heart failure / cardiogenic shock	Killip III–IV: APO, cold extremities, oliguria
Hours	Reperfusion arrhythmias (AIVR)	Benign; sign of successful reperfusion
24–72 hours	Early pericarditis	Pleuritic pain, friction rub; pain changes with position
Day 2–7	Papillary muscle rupture	New loud apical pansystolic murmur + flash APO
Day 3–7	Ventricular septal rupture	New harsh parasternal pansystolic murmur + thrill
Day 3–7	Free wall rupture	Sudden PEA / tamponade → death
Days–weeks	Mural thrombus → systemic embolism	Stroke, limb ischaemia, mesenteric ischaemia
Weeks	LV aneurysm	Persistent ST elevation; dyskinesia on echo
2–10 weeks	Dressler syndrome	Fever, pleuritic pain, pericardial/pleural effusion, ↑ ESR
Months	In-stent restenosis	Recurrent stable angina
Long-term	Chronic heart failure, LV remodelling	Progressive dyspnoea, ↓ LVEF
Long-term	Sudden cardiac death from VT/VF	May warrant ICD

High Yield Summary – Complications of STEMI

Arrhythmias are the #1 cause of early death; VF peaks within the first hour; requires defibrillator standby
AV block: Inferior MI → nodal block (usually benign, conservative); Anterior MI → infra-nodal block (dangerous, needs pacing)
Cardiogenic shock: Vicious cycle of ↓ function → ↓ perfusion → ↓ function; Killip IV; needs urgent reperfusion + inotropes
RV infarction: Hypotension + ↑ JVP + clear lungs; treat with volume, AVOID nitrates/diuretics
Mechanical complications (Day 3–7): Free wall rupture (tamponade → death), VSR (new parasternal murmur + thrill), papillary muscle rupture (new apical murmur + flash APO); all need emergency surgery
Papillary muscle rupture: Posteromedial > anterolateral (single artery supply from PDA)
LV aneurysm: Persistent ST elevation post-MI; risk of mural thrombus → embolism; risk of VT
Pericarditis: Early (24–72h, direct inflammation) vs. Dressler syndrome (2–10 weeks, autoimmune); treat with aspirin, avoid NSAIDs in acute phase
Stent thrombosis vs. ISR: Thrombosis = acute STEMI (prevented by DAPT); Restenosis = chronic angina (prevented by DES)
Mural thrombus: Large anterior MI → akinetic apex → stasis → thrombus → stroke; needs anticoagulation

Active Recall - Complications of STEMI

References

^[3] Senior notes: Block A - Sudden severe chest pain_ acute myocardial infarction; aortic dissection.pdf ^[8] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf ^[10] Senior notes: Ryan Ho Cardiology.pdf ^[14] Senior notes: Block A - Cardiology Data Interpretation.pdf ^[22] Senior notes: Block A - Shortness of breath on exertion_ heart failure.pdf ^[23] Senior notes: Ryan Ho Critical Care.pdf

High Yield Summary

STEMI Key Points:

Definition: Acute total coronary occlusion → transmural myocardial ischaemia/necrosis → persistent ST elevation + troponin rise
Most common cause: Type 1 MI – atherosclerotic plaque rupture → thrombotic occlusion
Most dangerous territory: LAD (anterior) → largest infarct, worst prognosis ("widow-maker")
Time is muscle: Complete necrosis requires 2–4 hours; reperfusion within this window salvages myocardium
ECG criteria: ≥ 2 contiguous leads with ST elevation (thresholds vary by lead and demographics); new LBBB = STEMI equivalent
Classic presentation: Crushing central chest pain > 20 min, not relieved by GTN, with diaphoresis, nausea, dyspnoea
Atypical presentations: Elderly, diabetics, women – may present with dyspnoea, syncope, epigastric pain, or confusional state
Always exclude aortic dissection before thrombolysis (BP both arms, pulse deficit, tearing back pain)
RV infarction: Always check V4R in inferior STEMI; manage with volume loading, avoid nitrates/diuretics
Killip classification: I (no HF) → IV (cardiogenic shock) – determines prognosis
Universal classification: Type 1 (plaque rupture) is the classic STEMI; Type 2 (supply-demand mismatch) is also important

High Yield Summary – Differential Diagnosis of STEMI

Two DDx lists needed: (A) DDx of ST elevation on ECG; (B) DDx of acute severe chest pain
Core DDx of ST elevation: STEMI (convex, territorial, reciprocal changes) vs. pericarditis (diffuse concave, PR depression) vs. LVH strain (V1–V3, chronic) vs. LBBB vs. BER vs. Brugada vs. Takotsubo vs. myocarditis
Big Five life-threatening chest pain DDx: ACS, aortic dissection, PE, tension pneumothorax, perforated oesophagus/peptic ulcer
Aortic dissection is the #1 critical mimic – tearing pain, maximal at onset, radiates to back, BP/pulse difference, AR murmur; thrombolysis is contraindicated
STEMI equivalents: New LBBB, De Winter T waves, posterior MI (ST depression V1–V3), Wellens' syndrome, aVR elevation with diffuse ST depression
ECG pitfalls: Multiple false positives (pericarditis, BER, LVH, Brugada) and false negatives (LBBB, posterior MI, RV infarction, De Winter)
Clinical approach: A (Abnormal ECG) – C (Clinical) – S (Stable) → if certain STEMI, activate cath lab immediately

High Yield Summary – Diagnosis of STEMI

Diagnostic criteria: Troponin rise/fall with ≥ 1 value > 99th URL PLUS ≥ 1 of: ischaemic symptoms, ECG changes, imaging evidence, or thrombus on angiography
ECG criteria: ST elevation ≥ 2 mm in V2–V3 (men ≥ 40), ≥ 2.5 mm (men < 40), ≥ 1.5 mm (women), ≥ 1 mm in all other leads; requires ≥ 2 contiguous leads; new LBBB = STEMI equivalent
Troponin: Gold standard biomarker; hsTnT cut-off > 14 ng/L with > 100% rise at 3–6h; peaks at 24–48h; CK-MB is better for reinfarction detection (shorter t½)
Do NOT wait for troponin in clear STEMI – activate cath lab based on ECG + clinical picture
Always get right-sided leads (V4R) in inferior STEMI to assess for RV infarction
CXR: Usually non-diagnostic for ACS; mainly to exclude dissection (widened mediastinum) and PTX
Echo: RWMA confirms territory; LVEF is the most important prognostic parameter
CCTA: Triple rule-out concept (MI, PE, dissection); high sensitivity but false positives from calcified plaques
Cardiac MRI: Key for MINOCA, myocardial viability, and differentiating myocarditis from MI (subepicardial vs. subendocardial LGE)
ECG pitfalls: Know the false positives (pericarditis, BER, LVH, LBBB, Brugada) and false negatives (posterior MI, RV MI, De Winter, new LBBB)

High Yield Summary – STEMI Management

Immediate: Bed rest, O₂ only if SpO₂ < 90%, morphine, GTN (check for contraindications – RV infarction, PDE5 inhibitors, hypotension), cardiac monitoring with defibrillator standby
Reperfusion: Primary PCI is gold standard (door-to-balloon < 90 min); fibrinolysis is the fallback if PCI unavailable within 120 min (door-to-needle < 30 min)
DAPT: Aspirin (300 mg load → 75–100 mg daily lifelong) + P2Y12 inhibitor (ticagrelor preferred → 90 mg BID for 12 months)
Anticoagulation: UFH during PCI; LMWH for thrombolysis; fondaparinux at bedside
Beta-blocker: Metoprolol (titrate HR < 70); proven survival benefit; cornerstone of secondary prevention
ACEi/ARB: Within 24h if LVEF < 40%; prevents adverse ventricular remodelling
Statin: High-intensity regardless of LDL; plaque stabilisation + lipid lowering
Fibrinolysis: Only for STEMI, not NSTEMI; know absolute contraindications (suspected dissection, haemorrhagic stroke, active bleeding, structural cerebrovascular lesion, uncontrolled severe HTN, recent head/spinal surgery)
Successful reperfusion signs: ↓ pain, ≥ 50% ST resolution at 60–90 min, early CK peak (11–12h vs normal 22–24h), reperfusion arrhythmias
Secondary prevention: ABCDE — Antiplatelet/ACEi, Beta-blocker/BP, Cholesterol/Cessation, Diet/DM, Exercise
Device therapy: ICD if LVEF < 30% after 3 months optimal medical therapy; CRT if LBBB + LVEF < 35% + NYHA III despite medical therapy

High Yield Summary – Complications of STEMI

Arrhythmias are the #1 cause of early death; VF peaks within the first hour; requires defibrillator standby
AV block: Inferior MI → nodal block (usually benign, conservative); Anterior MI → infra-nodal block (dangerous, needs pacing)
Cardiogenic shock: Vicious cycle of ↓ function → ↓ perfusion → ↓ function; Killip IV; needs urgent reperfusion + inotropes
RV infarction: Hypotension + ↑ JVP + clear lungs; treat with volume, AVOID nitrates/diuretics
Mechanical complications (Day 3–7): Free wall rupture (tamponade → death), VSR (new parasternal murmur + thrill), papillary muscle rupture (new apical murmur + flash APO); all need emergency surgery
Papillary muscle rupture: Posteromedial > anterolateral (single artery supply from PDA)
LV aneurysm: Persistent ST elevation post-MI; risk of mural thrombus → embolism; risk of VT
Pericarditis: Early (24–72h, direct inflammation) vs. Dressler syndrome (2–10 weeks, autoimmune); treat with aspirin, avoid NSAIDs in acute phase
Stent thrombosis vs. ISR: Thrombosis = acute STEMI (prevented by DAPT); Restenosis = chronic angina (prevented by DES)
Mural thrombus: Large anterior MI → akinetic apex → stasis → thrombus → stroke; needs anticoagulation

STEMI

1. Definition

2. Epidemiology

Global

Hong Kong Context

Temporal Trends

3. Risk Factors

Non-Modifiable Risk Factors

Modifiable Risk Factors ("The Big Five")

Other Risk Factors

4. Anatomy and Function of the Coronary Arteries

Coronary Arterial Supply

Territory Supplied by Each Artery

Coronary Dominance

The Subendocardium is Most Vulnerable

5. Aetiology

Universal Classification of Myocardial Infarction (4th Universal Definition, 2018)

Aetiological Categories (Expanded)

A. Atherosclerotic CAD (> 95% of STEMI – Type 1 MI)

B. Non-Atherosclerotic Causes of STEMI

C. Ischaemia Without Plaque Rupture (Type 2 MI Causes)

D. Direct Myocardial Injury (Can Mimic STEMI)

6. Pathophysiology

The Core Event: Atherosclerotic Plaque Rupture → Thrombotic Occlusion

Step 1: Vulnerable Plaque

Step 2: Plaque Rupture / Erosion

Step 3: Thrombus Formation

Step 4: Myocardial Ischaemia → Infarction

Myocardial Response to Ischaemia – A Temporal Sequence

Why Does the ECG Show ST Elevation?

Coronary Collateral Circulation

7. Classification

By ECG Localisation

By Killip Classification (Haemodynamic Severity)

By TIMI Flow Grade (Angiographic)

By Infarct Depth

8. Clinical Features

8.1 Symptoms

Typical Pain Characteristics (SOCRATES)

8.2 Signs

Physical Examination – Systematic Approach in Suspected STEMI

9. ECG Criteria for STEMI Diagnosis

10. Summary of Pathophysiology-to-Clinical Feature Connections

Active Recall - STEMI (Definition to Clinical Features)

References

Conceptual Framework: Two Differential Diagnosis Lists

A. Differential Diagnosis of ST Elevation on ECG

B. Differential Diagnosis of Acute Severe Chest Pain (Non-ECG Based)

C. Detailed Comparison: STEMI vs. Its Three Most Critical Mimics

1. STEMI vs. Aortic Dissection

2. STEMI vs. Acute Pericarditis

3. STEMI vs. Pulmonary Embolism

D. ECG Pitfalls: False Positives and False Negatives for STEMI

False Positives (ST Elevation Without True STEMI)

False Negatives (True STEMI Without Classic ST Elevation)

E. Systematic Clinical Approach to Differentiating STEMI from Mimics

F. How History and Examination Features Guide You Toward the Correct Diagnosis

Active Recall - Differential Diagnosis of STEMI

A. Diagnostic Criteria for Myocardial Infarction

The Two-Part Rule

STEMI-Specific ECG Criteria

What Constitutes a Pathological Q Wave?

Criteria for Each MI Type (Summary)

B. Cardiac Biomarkers – Detailed Interpretation

Why Do Biomarkers Rise?

Troponin (Gold Standard)

Other Biomarkers (For Completeness)

C. Diagnostic Algorithm – Step-by-Step Approach

D. Investigation Modalities – Detailed Interpretation

1. Electrocardiography (ECG)

Localising the Infarct

When to Order Right-Sided Leads

ECG Pitfalls

STEMI Equivalents (Must Know)

2. Cardiac Biomarkers

3. Chest X-Ray (CXR)

4. Echocardiography

5. Coronary Angiography (Invasive – Gold Standard for Coronary Anatomy)

6. CT Coronary Angiography (CCTA)

7. Additional Investigations (Baseline Workup in STEMI)