• With medical treatment nowadays, mortality is reducing. However, STEMI is still the diagnosed subtype of ACS causing the most mortality ^[1].
• Undetermined cases (missed diagnoses) are actually the even bigger killers ^[1].
• NSTEMI now accounts for roughly 60–70% of all MI presentations globally (and the proportion is rising, as STEMI incidence falls due to better primary prevention and statin use).
• In Hong Kong, coronary heart disease is the 3rd leading cause of death (after cancer and pneumonia). The Hospital Authority reports ~6,000–7,000 ACS admissions per year, with NSTEMI comprising the majority.
• Males more common than females for IHD overall ^[4]. However, women with NSTEMI tend to present later, with more atypical symptoms, and have worse outcomes adjusted for age.

• Incidence of NSTEMI is increasing (ageing population, better troponin assays detecting smaller MIs, increased awareness).
• In-hospital mortality for NSTEMI is lower than STEMI (~3–5% vs ~6–8%), but 6-month and long-term mortality is equivalent or even higher for NSTEMI, because NSTEMI patients tend to be older with more comorbidities (DM, CKD, prior MI).

Hong Kong has some specific epidemiological considerations:

• High prevalence of Type 2 DM (~10% of the adult population) ^[5]
• Rising rates of obesity and metabolic syndrome
• Historically lower smoking rates in women, but increasing in younger demographics
• Relatively lower rates of familial hypercholesterolaemia diagnosis compared to Western populations (likely underdiagnosis rather than true lower prevalence)

LAD = the "widow maker" because LAD territory represents the largest area of myocardium at risk.

This is critical to understanding NSTEMI. The subendocardium is the innermost layer of the myocardium, and it is the most vulnerable to ischaemia for three reasons:

1. Highest wall stress: During systole, intramyocardial pressure is greatest at the subendocardium (it's compressed against the blood in the LV cavity). This compresses the intramural vessels.
2. Last to receive blood: Coronary arteries penetrate from epicardium → endocardium. The subendocardium is at the distal end of the perfusion gradient.
3. Highest oxygen demand: The subendocardium contracts most vigorously.

Therefore, partial occlusion of a coronary artery → the subendocardium is the first zone to become ischaemic and then necrotic → subendocardial infarction → NSTEMI. This is why NSTEMI does not produce ST elevation (ST elevation requires transmural, full-thickness ischaemia reaching the epicardium).

ACS → Unstable angina, NSTEMI, STEMI ^[1][3]

Risk scores (GRACE, TIMI) classify NSTEMI patients into low, intermediate, and high risk to guide the urgency of invasive strategy (discussed in the management section later).

6 non-chest pain symptoms of IHD: Dyspnoea, Non-chest locations of discomfort, Mid-epigastric/abdominal pain, Diaphoresis, Excessive fatigue and weakness, Dizziness and syncope ^[4].

Symptom Pattern in NSTEMI vs Unstable Angina vs STEMI

Unstable angina is defined as any one of: ^[7]

• Resting angina > 20 min
• New-onset angina that markedly limits normal activity
• Increasing angina that is more frequent, lasts longer, or occurs with less exertion than previous angina

The quality of symptoms is identical for UA and NSTEMI — you cannot distinguish them clinically. The distinction requires troponin.

STEMI tends to have more severe, longer-lasting pain (> 30 min), more likely to have haemodynamic compromise, but there is significant overlap.

This classification is quick, bedside, and prognostically powerful. It is used in both STEMI and NSTEMI.

• Subendocardial ischaemia creates an injury current vector pointing from epicardium → endocardium (i.e., away from the surface electrode).
• This causes the ST segment to be depressed in the leads overlying the ischaemic territory.
• ST depression is the ECG hallmark of NSTEMI, along with T-wave inversion ^[3][7].

• Represents repolarisation abnormality.
• Ischaemic but still viable (not yet fully necrotic) myocardium has delayed repolarisation → the epicardium repolarises before the ischaemic subendocardium → inversion of the normal repolarisation vector → T-wave inversion.
• Deep, symmetrical T-wave inversion in the anterior leads (V1–V4) = Wellens' syndrome → critical proximal LAD stenosis. This is a surgical/interventional emergency despite minimal troponin rise — the patient is between events.

• Up to 30–50% of NSTEMI patients may have a normal or non-diagnostic initial ECG.
• This does not exclude the diagnosis — serial ECGs and troponins are essential.

Repeated ECG is important to assess serial changes ^[3]. 12-lead ECG stat and repeat at least daily ×3 days (more frequently in severe cases) ^[8].

Aortic dissection (Type A) with retrograde extension can cause coronary dissection → secondary NSTEMI/STEMI ^[7]. This is a trap: the ST changes are real, but the primary diagnosis is dissection, and PCI is not the answer — the patient needs surgery.

ECG: Differentiate aortic dissection from AMI ^[11]. CXR: Differentiate aortic dissection from pneumothorax ^[11]. Cardiac enzymes (cTnT, cTnI, CK-MB) should be checked ^[11].

Key investigation: D-dimer → very sensitive but not very specific. High negative predictive value → if negative, can rule out. If positive, require more definitive diagnosis ^[13][14]. Age-adjusted cut-off (age × 10 for patients > 50 y) ^[13].

Critically: massive PE can cause troponin elevation (RV strain → subendocardial ischaemia of the RV) and ST depression, mimicking NSTEMI. The clinical context (pleuritic pain, risk factors for VTE, unilateral leg swelling) and CTPA are the keys to differentiation.

This is a clinical (not biochemical) diagnosis. Do not wait for CXR in tension pneumothorax — decompress immediately.

The most important immediate differentiation. The distinction is made by ECG:

STEMI → complete occlusion of artery, require immediate opening up of artery as soon as possible. NSTEMI → lumen is reduced, but blood flow is still possible, so you can get away with giving anti-platelet / anti-thrombotics, with or without revascularization ^[1].

Why is it important to differentiate between STEMI and non-STEMI? Treatment is different ^[1].

NEW LBBB — have to be careful for patients with chest pain → should be managed the same as patients with ST elevation ^[13].

Check ST elevation (> 1mm) in aVR which suggests left main / severe triple vessel disease → directly go for CABG ^[10].

Clinically indistinguishable from NSTEMI — same symptoms, same ECG changes. The only difference:

When is ACS considered NSTEMI? Clinical features of unstable angina, AND elevation of cardiac markers, AND no ST-segment elevation on 12-lead ECG ^[1].

With modern high-sensitivity troponin assays, many patients previously labelled as "UA" are now reclassified as NSTEMI because even tiny amounts of necrosis are detected. The practical importance: NSTEMI warrants more aggressive antithrombotic and often invasive strategy compared to confirmed UA.

Diagnosis of myocarditis: cardiac MRI going to forefront. Endomyocardial biopsy is gold standard ^[16].

Aggravated by respiratory movement, sharp, knife-like (pleuritic pain). Radiates to the trapezius ridge (characteristic site of pericardial pain). Sitting up or leaning forward may ease pain (MI pain not positional) ^[2].

The key pathophysiological difference: pericarditis = inflammation of the pericardial sac (friction between inflamed visceral and parietal pericardium → rub); NSTEMI = intracoronary thrombus → myocyte death.

• "Takotsubo" = Japanese for "octopus trap," named for the apical ballooning shape of the LV on ventriculography.
• Triggered by intense emotional or physical stress → catecholamine surge → direct myocyte toxicity + microvascular spasm.
• Mimics anterior STEMI (ST elevation in precordial leads, troponin elevation, apical wall motion abnormality) but coronary angiography shows no obstructive coronary disease.
• Predominantly affects post-menopausal women.
• Important differential because the treatment is supportive (not antithrombotic/PCI).

GERD: Unrelated to exertion. Worsened when lying down. Relieved by swallowing (warm water) ^[7].

Angina pectoris is a differential diagnosis of GERD ^[18]. PPI empirical trial can be considered as initial diagnostic step in patients with non-cardiac chest pain (NCCP) ^[18].

• Peptic ulcer: epigastric tenderness, relationship to food (worse/better), NSAID/aspirin use ^[17].
• Perforation: sudden-onset severe epigastric pain → board-like rigidity → erect CXR shows free air under diaphragm.
• Acute pancreatitis: epigastric pain radiating to the back, elevated amylase/lipase.

PE findings to look for: PE → unilateral lower limb swelling; Peptic ulcers → epigastric tenderness; Pneumothorax → hyperresonance ^[3].

• Worsen with movement ^[7] and reproducible on palpation (point tenderness over a rib or costochondral junction).
• NSTEMI pain is never reproducible on chest wall palpation.
• Costochondritis (Tietze syndrome): localised tenderness at costochondral junctions.
• Pathophysiology: somatic pain from musculoskeletal structures travels via intercostal nerves (well-localised, sharp, positional) — completely different from the visceral, poorly-localised cardiac pain of NSTEMI.

• Thoracic nerve root distribution. Precedes typical vesicular rash of herpes zoster ^[7].
• Reactivation of VZV in dorsal root ganglia → dermatomal pain (burning, lancinating) that can precede the rash by days → may initially mimic NSTEMI.
• Key: unilateral, dermatomal distribution; rash appears later.

• Diagnosis of exclusion.
• Hyperventilation → respiratory alkalosis → ↓ionised calcium → paraesthesias, carpopedal spasm.
• Associated with anxiety, sense of impending doom, palpitations — but ECG normal and troponin normal.

For the diagnosis to be NSTEMI (rather than STEMI or UA):

• Troponin: Elevated (above 99th percentile URL with rise/fall pattern) — this separates NSTEMI from UA
• ECG: No persistent ST elevation — this separates NSTEMI from STEMI. Instead: ST depression and/or prominent T-wave inversion (> 1mm) in 2 contiguous leads, or even a normal ECG ^[10]

Cardiac troponins: gold standard for myocardial ischaemia ^[10].

What is troponin? Troponin is a regulatory protein complex in the cardiac sarcomere (troponin I, T, and C). When myocytes die, troponin leaks into the blood through the disrupted cell membrane.

High-sensitivity assays (hs-cTnT, hs-cTnI) can detect much smaller amounts of troponin, enabling:

• Earlier detection of MI (within 1–3 hours of symptom onset)
• Detection of very small MIs that older assays would miss
• But also detection of non-MI causes of myocardial injury (lower specificity)

Diagnostic cut-off of hsTnT: positive if baseline > 14 ng/L and > 100% rise 3–6h later ^[10].

Troponin: rises early and stays long ^[1]. AMI: peak at 24–48h, return to baseline over 5–14 days ^[10].

CK-MB is cardiac-specific (cf. CK-MM for skeletal muscles, CK-BB for brain / GI tract smooth muscles) ^[10].

Even though troponin is high-sensitivity, CK-MB has value in having shorter half-life. Since in acute phase, you would expect both to elevate. Yet if the patient is presenting late, 48 hours after onset of the AMI, then you would only see +ve troponin, with −ve CKMB → helps with the timeline ^[1].

This is important:

• Early presentation (< 24h): Both troponin and CK-MB elevated → acute MI
• Late presentation (48–72h): Troponin still elevated, CK-MB normalised → MI happened days ago
• Re-infarction: CK-MB re-rises (shorter half-life allows detection of a second peak), while troponin may still be elevated from the first event → > 20% increase in cTnI/TnT value (a 2nd plateau) indicates reinfarction ^[7]

Roles of biochemical markers of ACS ^[7]:

• Risk prediction and prognosis: Categorize patients into high and low risk groups
• Selection of site of care: CCU vs. outpatient
• Selection of therapeutic intervention: Aggressive vs. conservative
• ACS evaluation: Any troponin level > URL = myocardial damage
• Detection of reinfarction
• Assessment of reperfusion: When coronary arteries are reperfused, cardiac markers in blood will gradually wash out and decrease
• Estimation of infarct size: Magnitude and temporal course of markers

CXR: usually non-diagnostic in ACS; look for other causes (e.g. aortic dissection, PE, pneumonia or pneumothorax) ^[8].

CXR: Differentiate aortic dissection from pneumothorax. Widening of mediastinum (erect PA = 6cm, supine AP = 8cm) ^[11].

Bedside echocardiography is a key investigation in NSTEMI for:

Initial investigations ^[10][8]:

High sensitivity for stenosis detection. A normal CTA can reliably rule out disease ^[1].

Concept of "TRIPLE RULE-OUT" → CCTA can help you rule out: Myocardial infarction, Pulmonary embolism, Aortic dissection ^[1].

Coronary imaging has a very low false negative rate → high sensitivity, can be used to confidently rule out issues. But the problem with high sensitivity is that there is a tradeoff — lower specificity → even if you see some abnormal findings, will require further workup before diagnosis ^[4].

Stress testing is primarily for stable chest pain or for risk stratification after NSTEMI (not in the acute phase when the patient is unstable). It identifies inducible ischaemia.

Objective of stress testing is to help you reach diagnosis → diagnose ischaemia of the myocardium ^[4].

The definitive diagnostic test for coronary artery disease. A catheter is threaded (usually from radial or femoral artery) into the coronary ostia → contrast injected → real-time fluoroscopic imaging of the coronary lumen.

Not the CT coronary angiogram → this is the fluoro where they inject contrast. Just one invasive investigation exists for CAD confirmation ^[4].

Indications for invasive coronary angiography ^[4]:

• Unacceptable angina despite medical therapy (for consideration of revascularisation)
• Non-invasive testing results with high-risk features
• Angina or risk factors for CAD in the setting of depressed LVEF
• Diagnostic purposes when non-invasive testing results are unclear

In NSTEMI, the timing of angiography depends on risk stratification (see next section).

MINOCA: subepicardial LGE ^[21] → suggests myocarditis rather than ischaemic MI.

The most validated tool for NSTEMI risk stratification. It predicts in-hospital and 6-month mortality.

8 variables:

7 binary variables (1 point each):

Score 0–2 = low risk; 3–4 = intermediate; 5–7 = high risk.

The coagulation cascade generates thrombin → converts fibrinogen to fibrin → stabilises the platelet plug. Anticoagulation targets this arm.

Unfractionated heparin given in the cath lab, fondaparinux/enoxaparin given at bedside ^[3].

Side effects of heparin: Heparin-induced thrombocytopenia (HIT), osteoporosis, hyperkalaemia ^[10].

• "Nitro-" = nitrogen; nitrates release nitric oxide (NO) → activates guanylyl cyclase → ↑cGMP → smooth muscle relaxation.
• Predominantly venodilators (at low doses) → ↓preload → ↓LV wall stress → ↓O₂ demand.
• At higher doses: also arteriolar dilation (↓afterload) and coronary artery dilation (↑O₂ supply).

Nitrates (long acting or short acting) → in the presence of angina ^[1] (secondary prevention).

Contraindications of Nitrates

5 contraindications in the use of nitrates ^[2]:

1. RV infarction — nitrates ↓preload → RV is preload-dependent → catastrophic ↓CO
2. Use of phosphodiesterase-5 inhibitors (sildenafil/Viagra) in the previous 24 hours — PDE5 inhibitors also work via cGMP → synergistic vasodilation → severe hypotension
3. Hypotension — further ↓BP → shock
4. Tachycardia — reflex tachycardia from vasodilation worsens ischaemia
5. Bradycardia — may worsen haemodynamic compromise

• "Beta" refers to β-adrenergic receptors. β₁ receptors are predominantly in the heart.
• Mechanism: Block β₁ receptors → ↓heart rate + ↓contractility + ↓BP → ↓myocardial O₂ demand. Also ↑diastolic filling time → ↑coronary perfusion time.

Beta-blocker (cardio-selective): proven survival benefit, ↓HR/BP/contractility and improve coronary perfusion ^[10].

Reduce HR and BP (titrate to HR < 70) ^[22].

Contraindications of Beta-Blockers

Contraindications of beta-blockers ^[10]:

• Poor ventricular function (acute decompensation; though long-term BB is beneficial in chronic HFrEF)
• Acute pulmonary oedema
• Heart block (2nd / 3rd degree) — β-blockers ↓AV conduction → worsen block
• Asthma / COPD — β₂ blockade → bronchospasm (even "selective" β₁ blockers lose selectivity at high doses)

Also: severe bradycardia (HR < 50), cardiogenic shock, severe peripheral vascular disease, phaeochromocytoma without prior α-blockade.

• Mechanism: Block L-type voltage-gated calcium channels → ↓Ca²⁺ entry into smooth muscle and cardiac cells.

Verapamil 5–15mg IV slowly (C/I if BP low or on BB, beware of post-conversion angina) ^[12]. Never combine verapamil/diltiazem with beta-blockers — risk of severe bradycardia, AV block, and negative inotropy → haemodynamic collapse.

• "Statin" = inhibitor of HMG-CoA reductase, the rate-limiting enzyme in hepatic cholesterol synthesis → ↓intracellular cholesterol → ↑LDL receptor expression → ↑LDL clearance from blood.
• Pleiotropic effects (beyond lipid lowering): anti-inflammatory (↓hs-CRP), endothelial stabilisation, plaque stabilisation (↑fibrous cap thickness, ↓lipid core), antithrombotic.

Should be given regardless of baseline LDL-C level in the absence of contraindications ^[22].

Other therapy = ACEI + Statins ^[7].

Start within 24 hours of presentation. High-intensity statin is the standard in ACS — the goal is maximal plaque stabilisation early.

Side effects: Myalgia/myopathy (↑CK), rhabdomyolysis (rare), hepatotoxicity (↑ALT), new-onset diabetes.

Contraindications: Active liver disease, pregnancy, concomitant use of potent CYP3A4 inhibitors with certain statins.

• ACEI ("A-C-E-I" = Angiotensin Converting Enzyme Inhibitor): Blocks conversion of angiotensin I → angiotensin II → ↓vasoconstriction, ↓aldosterone secretion → ↓afterload, ↓preload, ↓myocardial remodelling.
• ARB (Angiotensin Receptor Blocker): Blocks AT₁ receptor directly → same downstream effects.

ACEI should be administered within the first 24 hours if LVEF < 40% and in the absence of hypotension or contraindications ^[22].

ACEI → for patients with congestive heart failure, LV dysfunction (EF < 40%), hypertension, diabetes ^[1].

ARBs are recommended for patients who have indications for, but are intolerant of, ACE inhibitors ^[4][22].

Contraindications of ACEI / ARB

Contraindications ^[4]:

• High-grade bilateral renal artery stenosis
• Azotaemia (severely elevated creatinine)
• Pregnancy
• Hyperkalaemia (K⁺ > 5.5)
• Hypotension (SBP < 90)
• History of angioedema (especially for ACEI)

Side effects of ACEI: Cough (ACEI-specific, due to ↑bradykinin), syncope, hypotension, angioedema, hyperkalaemia ^[4].

Proton pump inhibitors for patients at high risk of GI bleeding ^[22].

Why? Patients on DAPT + anticoagulation have significantly ↑GI bleeding risk. PPIs (e.g. omeprazole, pantoprazole) inhibit the gastric H⁺/K⁺ ATPase → ↓gastric acid → gastroprotection.

Add PPI when using 2 or more antithrombotics ^[24].

Note: Omeprazole inhibits CYP2C19 → can reduce clopidogrel activation. Pantoprazole is preferred when clopidogrel is used (less CYP2C19 interaction).

Very high risk / high risk features (Consult Cardiologists) ^[22]:

• Haemodynamic instability
• Cardiogenic shock, acute heart failure
• Recurrent/refractory chest pain despite medical treatment
• Life-threatening arrhythmias
• Established NSTEMI diagnosis
• Dynamic new or presumably new contiguous ST/T segment changes
• GRACE risk score > 140

Immediate revascularization if haemodynamically unstable / mechanical complications ^[10].

• "Percutaneous" = through the skin; "coronary" = heart arteries; "intervention" = treatment.
• A catheter is threaded into the culprit coronary artery → balloon angioplasty ± stent deployment to restore lumen patency.

Stent types:

• Bare-metal stent (BMS): Metal scaffold only; higher restenosis rate (~20–30%); requires shorter DAPT (1–3 months)
• Drug-eluting stent (DES): Coated with antiproliferative drug (sirolimus, everolimus, paclitaxel) → inhibits neointimal hyperplasia → lower restenosis (~5–10%); requires longer DAPT

You really want to make sure there is no re-thrombosis in your stent ^[1] — hence the extended DAPT duration.

Indications for CABG over PCI in NSTEMI:

ST elevation (> 1mm) in aVR suggests left main / severe triple vessel disease → directly go for CABG ^[10].

• Left main disease (> 50% stenosis)
• Severe triple-vessel disease (especially with diabetes or reduced LVEF)
• Complex anatomy not amenable to PCI
• Failed PCI

Graft types:

• Left internal mammary artery (LIMA) → LAD: Gold standard; > 90% patency at 10 years (arterial graft)
• Saphenous vein graft (SVG): ~50% patency at 10 years (venous grafts degenerate faster)

Maintained over 12 months, unless there are contraindications or excessive bleeding risk ^[1]:

• Ticagrelor 90mg BID
• Clopidogrel 75mg/day

Try to maintain for 12 months → if really cannot due to bleeding risk, maintain at least for 3–6 months ^[1].

For patients with stable CAD who underwent PCI → 6 months. For patients with acute MI who underwent PCI → 12 months still required ^[24].

Left main artery stenting → extended double antiplatelet beyond 12 months has better outcomes ^[24].

AF with MI → triple therapy (aspirin, clopidogrel, DOAC) ^[24]:

• Not recommended for the long term, since bleeding risk is unacceptable
• No more than 30 days
• Then step down to dual therapy (DOAC + single antiplatelet) for up to 12 months
• Then lifelong anticoagulation alone (DOAC)

Beta-blockers unless contraindicated — cornerstone ^[1].

ACEI → for patients with congestive heart failure, LV dysfunction (EF < 40%), hypertension, diabetes ^[1].

Calcium-channel blockers (diltiazem, verapamil) → if there are contraindications to beta-blockers, or if there is no heart failure ^[1].

Statin should be used in all patients unless contraindicated ^[22]. Target LDL-C < 1.4 mmol/L (or > 50% reduction from baseline) per 2019 ESC guidelines.

For patients who develop heart failure post-NSTEMI (LVEF ≤ 40%), the four pillars of HFrEF apply ^[22]:

Consider ARNI: Stop ACEI 36 hours before initiating ARNI ^[22] (to avoid dual RAAS blockade → angioedema risk).

Very high risk angina patients: on top of low-dose aspirin (81–100mg daily), add rivaroxaban/Factor Xa inhibitor 2.5mg twice daily ^[4] — the COMPASS regimen for very high-risk patients with stable CAD post-ACS.

Treat as VT until proven otherwise in the setting of ACS ^[12]. This is a vital principle — any wide-complex tachycardia in a patient with known or suspected MI should be treated as VT.

Cardiac arrest causes: Coronary artery disease (85%): myocardial ischaemia, AMI, prior MI with myocardial scarring ^[26]. This statistic tells you that ischaemic heart disease (and by extension, MI) is the single most common cause of sudden cardiac death.

Why does AF occur post-MI? Acute ischaemia → ↑left atrial pressure (from LV dysfunction) → atrial stretch → triggers AF. Also, catecholamine surge and inflammatory mediators contribute.

Other indications for temporary pacing: bifascicular block + 1st-degree AV block, alternating BBB / RBBB + alternating LAFB/LPFB (anterior infarct → ↑risk of sudden asystole) ^[12].

Inferior-posterior MI causing a complete AV block — Treatment is different → pacing before revascularization? ^[27].

• Pathophysiology: Loss of contractile myocardium → ↓LVEF → ↑LV end-diastolic pressure → ↑pulmonary capillary pressure → fluid transudation into alveoli → pulmonary oedema → hypoxaemia → further ischaemia.
• Clinical features: Acute dyspnoea, orthopnoea, pink frothy sputum, bilateral crackles, S3 gallop, tachycardia.
• Killip classification (introduced in Part 1) grades the severity: Killip III = frank pulmonary oedema.

• Defined as: SBP < 90 mmHg (or need for vasopressors) + signs of end-organ hypoperfusion (altered consciousness, oliguria, cold clammy extremities, elevated lactate).
• Occurs when > 40% of LV myocardium is lost.
• In-hospital mortality remains ~40–50% despite modern therapy.
• Management: Inotropes (e.g. IV dobutamine) if adequate filling pressure. Fluid resuscitation ± vasopressors if low filling pressure ^[19]. Mechanical circulatory support (IABP, Impella, ECMO) as bridge to revascularisation.

Watch out for other causes: mechanical complications, arrhythmia, excessive use of anti-HTN ^[12]. Not all post-MI hypotension is pure pump failure — always consider mechanical rupture or arrhythmia.

• Pathophysiology: The papillary muscles anchor the mitral valve leaflets via chordae tendineae. They are vulnerable because they are at the most distal end of the coronary perfusion pathway (subendocardial). The posteromedial papillary muscle is supplied by a single artery (PDA, usually from RCA), making it much more vulnerable than the anterolateral papillary muscle (dual supply from LAD + LCx).
• Presentation: Sudden-onset severe dyspnoea, new loud pansystolic murmur at the apex radiating to the axilla, flash pulmonary oedema.
• Diagnosis: Echocardiography (flail mitral leaflet, severe MR jet on Doppler).
• Management: Haemodynamic stabilisation (vasodilators to ↓afterload, IABP) → emergent surgical mitral valve repair/replacement.

Look for complications of IHD: Cardiomegaly, Heart failure, Mitral regurgitation ^[4].

• Pathophysiology: Full-thickness necrosis of the interventricular septum → physical rupture → left-to-right shunt (blood flows from high-pressure LV → low-pressure RV).
• Presentation: New harsh pansystolic murmur at the left sternal border (different location from MR murmur which is at the apex), acute RV volume overload → biventricular failure.
• Diagnosis: Echocardiography with colour Doppler (visualises the shunt); step-up in O₂ saturation from RA to RV on right heart catheterisation.
• Management: Haemodynamic support (IABP) → urgent surgical repair or percutaneous closure.

• Pathophysiology: Full-thickness necrosis of the LV free wall → rupture → blood leaks into pericardial space → acute cardiac tamponade.
• Presentation: Sudden haemodynamic collapse, pulseless electrical activity (PEA), Beck's triad (hypotension, muffled heart sounds, raised JVP).
• This is almost always rapidly fatal unless recognised immediately and treated with emergency pericardiocentesis + surgical repair.
• Subacute "contained" rupture: A pseudoaneurysm forms when the rupture is sealed by adherent pericardium or thrombus → presents more gradually with persistent chest pain and haemodynamic instability.

• Pathophysiology: The necrotic wall segment heals with thin, fibrotic scar tissue → under systemic pressure, the scar bulges outward during systole (paradoxical motion) → true aneurysm (all layers of the wall present, unlike pseudoaneurysm).
• Clinical significance:
  • Reduces effective LVEF (part of the stroke volume goes into the aneurysm)
  • Stasis within the aneurysm → mural thrombus → systemic embolism (stroke)
  • Substrate for re-entrant ventricular tachycardia (scar border zone)
  • Persistent ST elevation on ECG (the scar tissue creates a permanent injury current)
• Management: Anticoagulation if mural thrombus; surgical aneurysmectomy if refractory arrhythmia or severe HF.

• Pathophysiology: Akinetic or dyskinetic myocardial segments create blood stasis within the LV cavity → thrombus formation (Virchow's triad: stasis + endothelial injury + hypercoagulability from the inflammatory response). The thrombus adheres to the damaged endocardium.
• Risk factors: Large anterior MI (akinetic apex), LVEF < 40%, ventricular aneurysm, AF.
• Consequence: Dislodgement → systemic embolism → ischaemic stroke (most feared), mesenteric ischaemia, limb ischaemia.
• Detection: Echocardiography (TTE or TEE).
• Management: Therapeutic anticoagulation (warfarin or DOAC) for ≥ 3–6 months if mural thrombus detected.

Post-ACS ischaemia indicated by symptoms/ECG changes + new rise in cTn > 20% or to > 5× ULN (if normal baseline) ^[12].

Cause of post-PCI MI: side branch occlusion (60%), stent complications, microembolization ^[12].

High risk → prompt coronary angiography/PCI + IV GPIIb/IIIa inhibitor (if dynamic ECG changes) ^[12].

In thrombolysis patients, up to 50% have post-infarct angina (because of residual stenosis) ^[12].

• Timing: Days 1–3 post-MI.
• Pathophysiology: Transmural (or near-transmural) necrosis → inflammation extends to the adjacent visceral pericardium → acute pericarditis.
• Clinical features: Pleuritic chest pain (sharp, worse lying flat, better leaning forward), pericardial friction rub, diffuse ST elevation on ECG (different from the localised ST changes of MI).
• Management: Aspirin (high-dose, 650mg Q4–6H); avoid NSAIDs (may impair scar formation and increase risk of myocardial rupture in the acute post-MI period); avoid corticosteroids (same concern).
• Important: Must differentiate from recurrent MI (recurrent ischaemic pain) — ECG and troponin serial measurements help.

• Timing: 2–10 weeks post-MI (late complication).
• Pathophysiology: Autoimmune-mediated pericarditis. Myocardial necrosis exposes intracellular antigens (e.g. cardiac myosin) to the immune system → autoantibody formation → immune complex deposition in the pericardium → inflammation.
• Clinical features: Fever, pleuritic chest pain, pericardial effusion ± pleural effusion, elevated ESR/CRP.
• Management: NSAIDs (safer at this stage — scar has formed), colchicine, short course corticosteroids if refractory.
• Now rare in the modern era (incidence < 1%) because early reperfusion therapy limits the extent of myocardial necrosis → less antigen exposure.

• Pathophysiology: Extensive myocardial necrosis → replacement fibrosis (scar) → loss of contractile mass → progressive LV dilatation (remodelling) → HFrEF.
• This is the most common long-term consequence of MI and the reason why secondary prevention (ACEI/ARB, BB, statin, SGLT2i, MRA) is so critical.
• The final common path of all cardiac diseases is: Heart failure ^[20].

Prophylactic ICD placement should be considered in patients with NYHA II–III (LVEF < 30%), may be considered in LVEF 31–35%. Following 3 months of optimal medical therapy in patients with PMHx of MI ^[20]. The chance of lethal ventricular arrhythmias increases with reducing LVEF ^[20].

• Late VT/VF from scar-related re-entry circuits.
• This is why prophylactic ICD is indicated in patients with severely depressed LVEF post-MI (see management section).

ICD: Primary prevention in patients with low LVEF, CAD ± inducible VT on electrophysiology study. Secondary prevention of VT/VF in patients who have already had an episode ^[20].

• Residual atherosclerotic disease → risk of recurrent plaque rupture at the same or a different site.
• This is why lifelong secondary prevention is essential.