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50 High-Yield MCQs: Ischemic Heart Disease

HK-MLE Preparation

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SECTION A: STABLE ANGINA (Questions 1–6)

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• A) CCS Class I
• B) CCS Class II
• C) CCS Class III
• D) CCS Class IV
• E) Unstable angina

• A) CCS Class I: Angina only with strenuous or prolonged exertion, not ordinary activity — this patient's symptoms occur with ordinary daily tasks.
• C) CCS Class III: Marked limitation, angina with walking one to two blocks or one flight of stairs — more severe than described.
• D) CCS Class IV: Inability to carry out any physical activity without angina, or angina at rest — not applicable here.
• E) Unstable angina: New-onset or rest angina, or rapidly worsening pattern — this patient has a stable exertional pattern.

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• A) Echocardiogram at rest
• B) Coronary CT angiography (CCTA)
• C) Coronary angiography
• D) 24-hour Holter monitor
• E) Cardiac MRI perfusion imaging

• A) Echocardiogram at rest: Adds little information when exercise testing has already defined functional ischaemia; does not assess coronary anatomy.
• B) CCTA: Appropriate for intermediate pre-test probability, but this patient's high-risk stress test demands definitive anatomical assessment and potential intervention.
• D) Holter monitor: Evaluates arrhythmias, not ischaemia localisation or coronary anatomy.
• E) Cardiac MRI perfusion: A reasonable non-invasive option when coronary anatomy is uncertain, but not the priority after a high-risk stress test in this setting.

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• A) Digoxin
• B) Long-acting nitrate (isosorbide mononitrate)
• C) Warfarin
• D) Amiodarone
• E) Ivabradine as monotherapy replacement

• A) Digoxin: Indicated for heart failure and rate control in AF; has no role in angina management.
• C) Warfarin: Anticoagulation is not used for stable angina unless there are co-existing indications (e.g., AF, prosthetic valve).
• D) Amiodarone: An antiarrhythmic without anti-anginal indication in stable coronary disease.
• E) Ivabradine: A useful add-on if the patient is in sinus rhythm and cannot tolerate beta-blockers; replacing (not adding to) a beta-blocker is inappropriate if the beta-blocker is tolerated.

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• A) PCI with bare-metal stent
• B) PCI with drug-eluting stent (DES)
• C) CABG with left internal mammary artery (LIMA) to LAD
• D) Medical therapy escalation alone
• E) Rotational atherectomy

• A) Bare-metal stent: Higher in-stent restenosis rates than DES; rarely preferred in modern practice.
• B) PCI with DES: Appropriate alternative if surgical risk is high, but DES patency is inferior to the LIMA graft at 10 years.
• D) Medical therapy alone: Does not improve survival in single-vessel LAD disease and fails to relieve symptoms when maximal therapy is insufficient.
• E) Rotational atherectomy: Used for heavily calcified lesions to facilitate PCI, not as a standalone revascularisation strategy.

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• A) PCI with DES to all vessels
• B) CABG
• C) Medical therapy only
• D) PCI to the LAD only (culprit-only)
• E) Transcatheter aortic valve implantation (TAVI)

• A) PCI with DES: Inferior to CABG in diabetic multivessel disease due to higher rates of incomplete revascularisation and restenosis.
• C) Medical therapy only: Inadequate for triple-vessel disease with diabetes, which represents a high-risk state where revascularisation improves survival.
• D) Culprit-only PCI: Incomplete revascularisation in multivessel disease; not the standard of care in stable triple-vessel disease.
• E) TAVI: For severe aortic stenosis, not coronary artery disease.

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• A) Stable angina from atherosclerosis
• B) Coronary vasospasm (Prinzmetal's/variant angina)
• C) Takotsubo cardiomyopathy
• D) Pericarditis
• E) Pulmonary embolism

• A) Stable angina from atherosclerosis: Requires obstructive coronary lesions; this patient has smooth arteries.
• C) Takotsubo: Stress-induced transient LV apical ballooning, not precipitated by exertion or acetylcholine provocation.
• D) Pericarditis: Pleuritic chest pain, positional, with diffuse saddle-shaped ST elevation — not exertional or provoked by vasomotion.
• E) Pulmonary embolism: Pleuritic pain with dyspnoea; does not produce reproducible exertional symptoms or respond to vasodilators.

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SECTION B: UNSTABLE ANGINA / NSTEMI (Questions 7–13)

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• A) Stable angina
• B) Unstable angina
• C) NSTEMI
• D) STEMI
• E) Acute pericarditis

• A) Stable angina: Exertional, predictable, self-limiting symptoms with no biomarker rise.
• B) Unstable angina: Identical presentation but troponin remains negative — the elevated troponin here confirms myocardial necrosis.
• D) STEMI: Requires ST elevation ≥1 mm in ≥2 contiguous limb leads or ≥2 mm in ≥2 contiguous precordial leads; this patient has ST depression.
• E) Acute pericarditis: Diffuse saddle-shaped ST elevation with PR depression; not focal ST depression with troponin rise.

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• A) Immediately on arrival (within 2 hours)
• B) Within 24 hours
• C) Within 72 hours
• D) After 2 weeks of medical stabilisation
• E) Only if the patient fails to respond to thrombolysis

• A) Immediate angiography (within 2 hours): Reserved for very high-risk features such as refractory chest pain, haemodynamic instability, life-threatening arrhythmias, or acute heart failure.
• C) Within 72 hours: Appropriate for intermediate-risk patients; insufficient urgency for high-risk GRACE score.
• D) Two weeks of stabilisation: Delayed invasive strategy is associated with worse outcomes in high-risk NSTEMI.
• E) Post-thrombolysis: Thrombolysis has no role in NSTEMI/UA management.

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• A) Unfractionated heparin (UFH)
• B) Fondaparinux
• C) Enoxaparin (LMWH)
• D) Bivalirudin
• E) No anticoagulation needed in NSTEMI

• A) UFH: Cleared hepatically; safe in renal impairment with appropriate dose titration via aPTT monitoring.
• B) Fondaparinux: Associated with reduced bleeding compared to enoxaparin in NSTEMI (OASIS-5 trial); preferred in moderate-to-severe renal impairment (but contraindicated if eGFR <20).
• D) Bivalirudin: A direct thrombin inhibitor with minimal renal clearance; considered safe with dose adjustment.
• E) Anticoagulation is indicated in NSTEMI to reduce thrombus propagation; withholding it increases risk of recurrent MI.

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• A) Age >65, ≥3 CAD risk factors, prior coronary stenosis >50%, ST deviation, ≥2 anginal events in 24h, aspirin use in last 7 days, elevated biomarkers
• B) Blood pressure, heart rate, age, ST changes, Killip class, creatinine
• C) Age, sex, troponin, ECG, echocardiogram result, stress test result
• D) Killip class, age, anterior ST elevation, Killip class, block on ECG
• E) LVEF, diabetes, multivessel disease, renal function, prior CABG

• B) These variables describe the GRACE score components (which uses continuous variables including BP, HR, age, creatinine, Killip class).
• C) Echocardiogram and stress test are not components of the TIMI risk score.
• D) These elements (Killip class, anterior ST elevation) are components of the TIMI risk score for STEMI, not for UA/NSTEMI.
• E) LVEF, multivessel disease, and prior CABG are considered in revascularisation planning but are not TIMI score components.

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• A) Age >70
• B) Prior ischaemic stroke (not haemorrhagic)
• C) History of haemorrhagic stroke
• D) Renal impairment (eGFR 40 mL/min)
• E) Elevated liver enzymes (2× ULN)

• A) Age >70 is not a contraindication; ticagrelor benefits elderly patients with ACS.
• B) Prior ischaemic (non-haemorrhagic) stroke is a contraindication to prasugrel but not ticagrelor; ticagrelor may still be used cautiously.
• D) Renal impairment to eGFR 40 does not contraindicate ticagrelor; it does not require dose adjustment at this level.
• E) Mild transaminase elevation is not a contraindication to ticagrelor; severe hepatic impairment is a caution, but 2× ULN elevation is not.

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• A) Discharge home with follow-up in 6 months
• B) Exercise stress test before discharge
• C) Urgent PCI within 2 hours
• D) Thrombolysis with alteplase
• E) Coronary angiography within 72 hours

• A) Discharge without further evaluation is inappropriate given the ECG changes and clinical instability.
• B) Exercise stress testing is appropriate for low-risk chest pain without ECG changes; T-wave inversions in V1–V4 mandate invasive evaluation.
• C) Urgent (within 2-hour) angiography is for very high-risk features (refractory pain, haemodynamic instability); this patient is stable.
• D) Thrombolysis is contraindicated in NSTEMI/UA — it does not improve outcomes and may be harmful.

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• A) Stable angina and ACS share the same underlying mechanism of plaque rupture
• B) ACS most commonly results from rupture or erosion of a vulnerable atherosclerotic plaque with superimposed thrombosis
• C) ACS requires >70% coronary stenosis to occur
• D) STEMI always results from plaque rupture, while NSTEMI is always due to plaque erosion
• E) Most plaques causing MI are haemodynamically significant (>70% stenosis) prior to the event

• A) Stable angina is caused by fixed obstructive stenosis limiting flow on exertion; ACS involves acute plaque disruption and thrombosis — fundamentally different mechanisms.
• C) Most culprit plaques causing ACS have <50% stenosis prior to the event because vulnerable plaques are lipid-rich with thin caps, not necessarily flow-limiting.
• D) Both rupture and erosion can cause either STEMI or NSTEMI; the ECG presentation depends on degree of flow obstruction, not plaque morphology alone.
• E) Angiographic studies show the majority of MI-causing lesions are non-obstructive (<70% stenosis) before the acute event.

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SECTION C: STEMI (Questions 14–22)

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• A) Left anterior descending (LAD)
• B) Left circumflex (LCx)
• C) Right coronary artery (RCA)
• D) Left main coronary artery
• E) Diagonal branch

• A) LAD occlusion produces anterior STEMI with ST elevation in V1–V4 (and often aVL for proximal lesions).
• B) Left circumflex occlusion causes lateral STEMI with ST elevation in I, aVL, V5–V6; it is the culprit in 15–20% of inferior MIs.
• D) Left main occlusion typically causes massive ST elevation involving anterior and lateral leads, often with haemodynamic collapse.
• E) Diagonal branch occlusion causes anterolateral changes (V4–V5, aVL), not inferior lead changes.

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• A) Left ventricular failure
• B) Cardiogenic shock from LV dysfunction
• C) Right ventricular infarction
• D) Pulmonary embolism
• E) Tension pneumothorax

• A) LV failure causes elevated JVP AND pulmonary congestion (wet lungs); this patient has clear lungs.
• B) Cardiogenic shock from LV dysfunction is accompanied by pulmonary oedema and elevated filling pressures — not isolated raised JVP with clear lungs.
• D) Pulmonary embolism can cause hypotension and raised JVP but is not associated with STEMI or right precordial ST elevation in this context.
• E) Tension pneumothorax causes tracheal deviation and absent breath sounds; it is not related to the acute coronary syndrome presentation.

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• A) Intravenous furosemide to reduce preload
• B) Nitrates to reduce afterload
• C) Aggressive IV fluid loading (normal saline)
• D) Immediate intra-aortic balloon pump
• E) Dobutamine without fluid resuscitation

• A) Diuretics reduce preload, which would worsen hypotension in a preload-dependent RV infarction — they are contraindicated.
• B) Nitrates also reduce preload and venous return, causing precipitous hypotension in RV infarction — they are contraindicated.
• D) IABP may be needed if shock persists despite fluids, but it is not the first-line intervention.
• E) Dobutamine is used if the patient remains hypotensive after adequate volume resuscitation, not as an initial standalone measure.

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• A) Conservative management with antiplatelet therapy alone
• B) Transfer for primary PCI regardless of delay
• C) Thrombolysis now, then transfer for angiography within 24 hours (pharmacoinvasive strategy)
• D) Emergency CABG
• E) Wait for troponin result before deciding

• A) Conservative management without reperfusion in a 2-hour STEMI results in large infarcts and high mortality; reperfusion is mandatory.
• B) Transfer for primary PCI is the preferred option when achievable within 120 minutes; a 150-minute delay makes door-to-balloon time unacceptable and fibrinolysis the better immediate choice.
• D) Emergency CABG is reserved for failed PCI, cardiogenic shock with unfavourable anatomy, or mechanical complications; not first-line for reperfusion.
• E) Waiting for troponin results delays reperfusion; STEMI is a clinical and ECG diagnosis requiring immediate action — time is myocardium.

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• A) Ventricular fibrillation — immediate defibrillation
• B) Accelerated idioventricular rhythm (AIVR) — no specific treatment required
• C) Ventricular tachycardia — IV amiodarone
• D) Complete heart block — temporary pacing
• E) Torsades de pointes — IV magnesium

• A) Ventricular fibrillation is chaotic, pulseless, and immediately life-threatening; it requires immediate defibrillation — AIVR has a regular, slow rate and the patient has a pulse.
• C) Ventricular tachycardia is defined as rate >100 bpm with broad complexes; rates of 60–80 bpm are below the VT threshold.
• D) Complete heart block causes bradycardia with dissociated P and QRS waves; the described rhythm is regular and broad without conduction block.
• E) Torsades de pointes is a polymorphic VT associated with QT prolongation; it is not a regular broad complex rhythm at 60–80 bpm.

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• A) It carries the same poor long-term prognosis as VF occurring days after MI
• B) Primary VF occurring within the first 48 hours carries a similar long-term survival to MI without VF, if successfully resuscitated
• C) Survivors require ICD implantation before discharge in all cases
• D) This event indicates severe LV dysfunction requiring mechanical support
• E) Beta-blockers should be discontinued after primary VF

• A) Late VF (after 48 hours) reflects myocardial scarring and is associated with poor long-term prognosis; early primary VF carries a better long-term outcome.
• C) ICD implantation is indicated for secondary prevention in those with sustained VT/VF due to a fixed substrate (reduced EF after ≥40 days); early primary VF alone is not an automatic ICD indication.
• D) Primary VF can occur in haemodynamically preserved patients; it does not invariably indicate severe LV dysfunction.
• E) Beta-blockers are protective after MI and should be continued (unless contraindicated); they reduce the risk of recurrent arrhythmia.

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• A) Right coronary artery (proximal)
• B) Left main coronary artery
• C) Proximal left anterior descending artery
• D) Left circumflex artery
• E) Posterior descending artery

• A) Proximal RCA causes inferior ST elevation (II, III, aVF), not anterior-lateral changes.
• B) Left main occlusion typically causes even more extensive changes, often presenting with haemodynamic collapse and a very broad ST elevation pattern; isolated proximal LAD occlusion is more common and explains this distribution.
• D) LCx occlusion typically produces lateral STEMI (I, aVL, V5–V6) without V1–V3 changes.
• E) Posterior descending artery occlusion causes inferior MI, not the extensive anterior pattern seen here.

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• A) Sinus tachycardia
• B) New left bundle branch block (LBBB)
• C) First-degree AV block
• D) Isolated T-wave flattening in V5–V6
• E) PR interval of 180 ms

• A) Sinus tachycardia is a non-specific response to pain, anxiety, or haemodynamic compromise; it is not an indication for reperfusion.
• C) First-degree AV block (PR >200 ms) does not alter the acute reperfusion decision.
• D) Isolated T-wave flattening is a non-specific change that may reflect ischaemia but does not mandate immediate reperfusion without other criteria.
• E) A PR of 180 ms is within the upper limit of normal; it is not an indication for reperfusion.

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• A) Active peptic ulcer disease
• B) Age >75 years
• C) Previous haemorrhagic stroke at any time
• D) Diabetic retinopathy
• E) Blood pressure 150/90 mmHg on arrival

• A) Active peptic ulcer is a relative contraindication (risk of GI bleeding), not absolute, and must be weighed against reperfusion benefit.
• B) Age >75 is a relative contraindication; advanced age increases bleeding risk but does not absolutely preclude thrombolysis in the absence of other options.
• D) Diabetic retinopathy is listed as a relative (not absolute) contraindication in older guidelines and is not universally considered contraindicated.
• E) Uncontrolled hypertension (>180/110 mmHg) is a relative contraindication; 150/90 mmHg does not reach that threshold.

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SECTION D: COMPLICATIONS OF MI (Questions 23–36)

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• A) Acute mitral regurgitation due to papillary muscle rupture
• B) Ventricular septal defect (VSD) due to septal rupture
• C) Aortic regurgitation
• D) Left ventricular free wall rupture
• E) Dressler syndrome

• A) Papillary muscle rupture also causes a new pansystolic murmur but the murmur radiates to the axilla, and echocardiography shows severe mitral regurgitation (not a VSD shunt) — though both can cause acute pulmonary oedema.
• C) Aortic regurgitation causes a diastolic murmur, not a pansystolic murmur, and is not a direct complication of MI.
• D) LV free wall rupture typically causes pulseless electrical activity and cardiac tamponade; it does not produce an intracardiac shunt.
• E) Dressler syndrome presents with fever, pericarditis, and pleuritis; it does not cause a new cardiac murmur or intraventricular shunt.

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• A) Systemic anticoagulation with heparin
• B) Repeat thrombolysis
• C) Emergency surgical repair of the VSD
• D) IV diuretics alone
• E) Percutaneous VSD closure via cardiac catheterisation as first-line

• A) Anticoagulation alone does not close the VSD or restore haemodynamics.
• B) Thrombolysis plays no role in mechanical complications of MI.
• D) Diuretics reduce preload but do not address the structural defect; they are inadequate definitive therapy.
• E) Percutaneous closure is considered for post-MI VSD in select stable patients, but emergency surgical repair remains the standard definitive treatment in haemodynamic compromise.

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• A) Acute VSD
• B) Pericardial tamponade
• C) Papillary muscle rupture causing acute mitral regurgitation
• D) Mitral annular calcification
• E) LV free wall rupture

• A) Acute VSD produces a murmur at the left lower sternal border with echocardiographic demonstration of interventricular flow — not a flail mitral leaflet.
• B) Cardiac tamponade presents with Beck's triad (hypotension, elevated JVP, muffled heart sounds) and pulsus paradoxus; it does not produce a new murmur or mitral pathology.
• D) Mitral annular calcification is a chronic degenerative condition that does not cause acute MR in the setting of MI.
• E) Free wall rupture causes haemopericardium and cardiac arrest, not an acute MR murmur.

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• A) Right ventricular infarction
• B) Cardiac tamponade from LV free wall rupture
• C) Tension pneumothorax
• D) Massive pulmonary embolism
• E) Cardiogenic shock from LV dysfunction

• A) RV infarction also causes hypotension and elevated JVP but with clear lungs and ST elevation in V4R — it does not cause muffled heart sounds or electrical alternans.
• C) Tension pneumothorax causes tracheal deviation, absent ipsilateral breath sounds, and hyperresonance; it is not a complication of MI.
• D) Massive PE can cause hypotension and raised JVP but does not produce the electrical alternans or occur specifically after anterior STEMI.
• E) LV cardiogenic shock typically presents with pulmonary oedema and no pericardial effusion; muffled sounds and pulsus paradoxus are not features.

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• A) Reinfarction
• B) Pulmonary embolism
• C) Dressler syndrome (post-MI syndrome)
• D) Infarct pericarditis
• E) Aortic dissection

• A) Reinfarction presents acutely with new ischaemic chest pain and ECG/biomarker changes, not 4 weeks later with pleuritic features and fever.
• B) PE causes pleuritic pain and dyspnoea but is associated with risk factors (DVT, immobility) and does not cause fever with pericardial effusion in this setting.
• D) Infarct pericarditis occurs in the first 1–3 days after transmural MI, not at 4 weeks — onset is the key distinguishing feature.
• E) Aortic dissection presents with tearing chest pain radiating to the back, BP differential between arms, and is not associated with prior MI at 4 weeks.

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• A) True left ventricular aneurysm
• B) False aneurysm (pseudoaneurysm)
• C) Apical HCM
• D) Mural thrombus without aneurysm
• E) Ventricular non-compaction

• B) A false aneurysm (pseudoaneurysm) results from contained myocardial rupture with a narrow neck; it has a high risk of complete rupture and requires urgent surgery — it lacks a smooth fibrous wall.
• C) Apical HCM is a hereditary cardiomyopathy with hypertrophied (not thinned/akinetic) apical myocardium.
• D) Mural thrombus can form on an akinetic wall without aneurysm formation; the presence of a distinct bulge indicates true aneurysm.
• E) Non-compaction is a congenital cardiomyopathy with prominent trabeculations; it is not an MI complication.

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• A) Spironolactone
• B) Digoxin
• C) ACE inhibitor (e.g., ramipril)
• D) Warfarin
• E) Calcium channel blocker (e.g., amlodipine)

• A) Spironolactone (or eplerenone) provides additional mortality benefit in post-MI heart failure with EF ≤40%, but it is added on top of an ACE inhibitor, not instead of one.
• B) Digoxin improves symptoms and reduces hospitalisations in heart failure but does not reduce mortality after MI.
• D) Warfarin is indicated in specific situations (large apical aneurysm with LV thrombus, AF, hypercoagulable state) but not routinely after MI.
• E) Calcium channel blockers have no mortality benefit post-MI; non-dihydropyridine CCBs (diltiazem, verapamil) are relatively contraindicated with reduced EF.

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• A) Aspirin and clopidogrel only
• B) Anticoagulation with warfarin (target INR 2–3) for 3–6 months
• C) Urgent surgical thrombectomy
• D) IV heparin indefinitely
• E) No treatment needed as most LV thrombi resolve spontaneously

• A) Dual antiplatelet therapy alone is inadequate for LV thrombus; antiplatelet agents are less effective than anticoagulants for preventing arterial thromboembolism from an intracardiac source.
• C) Surgical thrombectomy is not indicated for an intracavitary LV thrombus without haemodynamic compromise.
• D) Long-term IV heparin is impractical; oral anticoagulation is the appropriate strategy.
• E) While some small thrombi may resolve, leaving a large apical thrombus untreated risks systemic embolism; treatment is mandatory.

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• A) Low CO, low PCWP, low SVR
• B) High CO, low PCWP, high SVR
• C) Low CO, high PCWP, high SVR
• D) High CO, high PCWP, low SVR
• E) Normal CO, normal PCWP, normal SVR

• A) Low CO, low PCWP, low SVR is the profile of distributive (septic) shock.
• B) High CO with low PCWP and high SVR does not fit any classic shock state.
• D) High CO, high PCWP, and low SVR is seen in high-output states (e.g., early sepsis, anaemia, AV fistula).
• E) Normal haemodynamics do not constitute cardiogenic shock.

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• A) Intra-aortic balloon pump (IABP) insertion
• B) Early coronary revascularisation (PCI or CABG)
• C) High-dose noradrenaline alone
• D) Thrombolysis instead of PCI
• E) Intravenous sodium bicarbonate for lactic acidosis

• A) IABP improves coronary perfusion and reduces afterload but the IABP-SHOCK II trial showed no mortality benefit over medical therapy alone; it remains a bridge to revascularisation.
• C) Vasopressors (noradrenaline is preferred over dopamine) support BP but do not address the underlying ischaemia; they are adjuncts.
• D) Thrombolysis is specifically shown NOT to reduce mortality in cardiogenic shock (unlike non-shock STEMI) — the fibrinolytic agents have poor tissue penetration in low-flow states.
• E) Treating metabolic acidosis is supportive but does not improve outcomes; the priority is restoring myocardial blood flow.

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• A) AV node supplied by the RCA — usually transient, good prognosis
• B) Bundle branches below the AV node — often permanent, poor prognosis
• C) Sinoatrial node — transient, responds to atropine
• D) Pulmonary valve — structural complication, requires surgery
• E) Left circumflex territory — always transient

• A) AV nodal CHB occurs in inferior STEMI (supplied by RCA) and is typically transient, atropine-responsive, and carries a better prognosis.
• C) SA node injury causes sinus bradycardia or sick sinus syndrome, not complete heart block.
• D) Pulmonary valve pathology is unrelated to STEMI complications.
• E) LCx territory infarction primarily causes lateral wall damage; it does not characteristically produce complete heart block.

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• A) Killip Class I indicates pulmonary oedema with S3 gallop
• B) Killip Class II is cardiogenic shock
• C) Killip Class III is defined as frank pulmonary oedema
• D) Killip Class IV is defined as mild heart failure with basal crepitations
• E) Killip Class I carries a 30% in-hospital mortality

• A) Killip Class I is no evidence of heart failure — no crepitations, no S3; in-hospital mortality ~5%.
• B) Killip Class IV (not II) represents cardiogenic shock (hypotension <90 mmHg, signs of peripheral hypoperfusion) with mortality exceeding 80%.
• D) Killip Class II is mild-to-moderate heart failure with S3 gallop and basal crepitations (<50% of lung fields), with mortality ~10–15%.
• E) Killip Class I carries approximately 5% in-hospital mortality, not 30%.

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• A) Oral amiodarone indefinitely as the only therapy
• B) Implantable cardioverter-defibrillator (ICD)
• C) Ablation alone without ICD
• D) Repeat revascularisation to prevent VT
• E) Beta-blockers alone; ICD is not needed

• A) Amiodarone reduces VT burden and may be used as adjunctive therapy, but as monotherapy it is inferior to ICD for preventing sudden cardiac death.
• C) Catheter ablation reduces VT burden and ICD shocks but does not replace ICD for secondary prevention in ischaemic cardiomyopathy.
• D) Revascularisation addresses ischaemia-driven arrhythmias (like primary VF) but does not treat scar-mediated re-entrant VT occurring >48 hours post-MI.
• E) Beta-blockers are essential adjuncts post-MI but provide insufficient protection against sustained VT/SCD compared to ICD.

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• A) No — ICD is only for secondary prevention (prior VT/VF)
• B) Yes — MADIT-II criteria justify ICD for primary prevention
• C) No — LVEF must be ≤25% for primary prevention ICD
• D) Yes — but only if the patient has diabetes
• E) No — a wearable defibrillator is always used first for 12 months

• A) ICD is indicated for both primary (EF ≤35%, optimal therapy, ≥40 days post-MI) and secondary prevention — the concept that it is "only secondary" is incorrect.
• C) The LVEF threshold for primary prevention ICD is ≤35%, not ≤25%.
• D) Diabetes is not a criterion for primary prevention ICD indication.
• E) A wearable cardioverter-defibrillator (LifeVest) is used as a bridge during the waiting period (before 40 days post-MI) but does not preclude ICD assessment at reassessment.

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SECTION E: INVESTIGATIONS — ECG, ENZYMES, IMAGING (Questions 37–44)

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• A) Q waves → ST elevation → T inversion → hyperacute T waves
• B) Hyperacute T waves → ST elevation → T inversion → Q waves
• C) ST elevation → hyperacute T waves → Q waves → T inversion
• D) T inversion → ST elevation → hyperacute T waves → Q waves
• E) Q waves appear immediately then resolve within 24 hours

• A) This sequence is reversed; Q waves and T inversion are late findings, not the earliest.
• C) Hyperacute T waves precede ST elevation — they do not follow it.
• D) T inversion is a late finding occurring after ST elevation, not before.
• E) Pathological Q waves develop hours to days after STEMI and are usually permanent markers of necrosis; they do not appear immediately and resolve.

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• A) LAD; ST elevation in aVL confirms RV involvement
• B) RCA; ST elevation in V4R confirms RV infarction
• C) LCx; ST depression in V1 confirms posterior involvement
• D) Left main; broad ST elevation in all leads
• E) RCA; ST depression in V4R confirms RV involvement

• A) ST elevation in aVL reflects high lateral wall ischaemia (diagonal/circumflex territory), not RV involvement.
• C) ST depression in V1–V3 reflects posterior wall ischaemia (mirror image of posterior ST elevation) — a different finding from RV infarction.
• D) Left main occlusion causes diffuse ST elevation and profound haemodynamic collapse affecting a much broader territory.
• E) ST elevation (not depression) in V4R is the key finding for RV infarction; depression in V4R is a non-diagnostic or normal finding.

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• A) CK-MB: rises at 3–6h, peaks 12h, normalises 48–72h
• B) Myoglobin: rises at 1–2h, peaks 4–6h, normalises 24h
• C) Troponin I or T: rises at 3–6h, peaks 24h, normalises 7–14 days
• D) LDH: rises at 8–12h, peaks 3–6 days, normalises 8–14 days
• E) AST: rises at 8–12h, peaks 18–36h, normalises 3–4 days

• A) CK-MB is less specific than troponin (present in skeletal muscle) and normalises faster (48–72h), limiting its use for late presentation — however, its faster normalisation makes it useful for diagnosing reinfarction.
• B) Myoglobin is the earliest rising marker but is non-specific for myocardium (also in skeletal muscle); it is no longer routinely used.
• D) LDH (particularly LDH1) is very late-rising and was used before troponin era for late presentations; it is no longer the preferred biomarker.
• E) AST was historically used but is non-specific and not recommended in current practice.

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• A) CK-MB
• B) Myoglobin
• C) High-sensitivity troponin
• D) LDH (LDH-1 isoform)
• E) BNP

• A) CK-MB normalises within 48–72 hours and is no longer reliably elevated at 9 days.
• B) Myoglobin normalises within 24 hours and cannot be used for diagnosis at 9 days.
• C) High-sensitivity troponin typically normalises by 7–14 days; at 9 days, it may still be mildly elevated, but LDH specifically peaks late and its elevation is more reliably persistent at this time point.
• E) BNP is a marker of ventricular wall stress and heart failure; while it may be elevated post-MI due to reduced EF, it does not specifically confirm MI timing.

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• A) Mitral valve prolapse
• B) Regional wall motion abnormality (RWMA) in the anterior wall
• C) Diastolic dysfunction grade 1
• D) Mild tricuspid regurgitation
• E) Left atrial enlargement

• A) Mitral valve prolapse is a chronic structural finding unrelated to acute MI.
• C) Diastolic dysfunction grade 1 is a non-specific finding common in elderly and hypertensive patients; it is not diagnostic of acute MI.
• D) Mild tricuspid regurgitation is common and non-specific; it does not localise MI.
• E) Left atrial enlargement is a chronic finding associated with diastolic dysfunction or AF, not acute MI.

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• A) No significant coronary artery disease
• B) Low 10-year cardiovascular risk; no further testing needed
• C) High atherosclerotic plaque burden; high likelihood of obstructive CAD
• D) The patient has had a prior MI
• E) Calcification confirms haemodynamically significant stenosis

• A) A score of 520 indicates significant calcified plaque; a score of 0 (zero calcium) effectively rules out significant obstructive CAD.
• B) A high CAC score is associated with high (not low) cardiovascular risk; a CAC of 0 allows risk reclassification downward.
• D) CAC scoring quantifies calcified atherosclerotic plaque; it does not diagnose prior MI or indicate which segments are ischaemic.
• E) Calcification correlates with plaque burden but not necessarily with haemodynamic significance; a calcified stenosis may be 50% or 90% — functional assessment (FFR, iFR, stress testing) is needed to determine physiological severity.

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• A) Anterior STEMI (LAD occlusion)
• B) Posterior STEMI (RCA or LCx occlusion)
• C) Brugada pattern
• D) Normal variant (early repolarisation)
• E) Pulmonary embolism pattern (S1Q3T3)

• A) Anterior STEMI shows ST elevation in V1–V4, not ST depression; this patient's V1–V2 changes are the reciprocal (mirror) of a posterior injury current.
• C) Brugada pattern is a right precordial coved ST elevation with RBBB morphology in V1–V2, occurring in the absence of ischaemia.
• D) Early repolarisation shows concave (saddle-shaped) ST elevation diffusely, not localised ST depression in V1–V3.
• E) S1Q3T3 (deep S in lead I, Q and inverted T in lead III) is seen in large PE with right heart strain; it does not cause the described V1–V3 pattern.

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• A) Inferior STEMI
• B) Pericarditis
• C) Left main coronary artery occlusion or severe proximal LAD stenosis
• D) Normal variant
• E) Hyperkalaemia

• A) Inferior STEMI produces ST elevation in II, III, aVF with reciprocal depression in I and aVL — not ST elevation in aVR with diffuse depression.
• B) Pericarditis causes diffuse saddle-shaped ST elevation (not depression) in most leads, with PR depression.
• D) ST elevation in aVR is never a normal variant; it always requires a clinical explanation.
• E) Hyperkalaemia causes peaked T waves, widened QRS, and P wave flattening — not ST elevation in aVR with diffuse depression.

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SECTION F: MANAGEMENT — DRUGS, PCI, CABG (Questions 45–50)

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• A) 1 month
• B) 3 months
• C) 6 months
• D) 12 months (minimum), may extend in high ischaemic risk
• E) Indefinitely without review

• A) 1 month of DAPT is insufficient even for bare-metal stents in stable CAD.
• B) 3 months is acceptable for short DAPT protocols in stable CAD (DES-LATE, STOPDAPT), not post-ACS.
• C) 6 months DAPT may be considered in ACS patients with very high bleeding risk (using PRECISE-DAPT), but 12 months is the standard.
• E) Indefinite DAPT without review is not guideline-recommended; it must be reassessed at 12 months balancing ischaemic vs. bleeding risk.

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• A) Low-dose pravastatin 20 mg at discharge only if LDL >3.0 mmol/L
• B) High-intensity statin (atorvastatin 40–80 mg or rosuvastatin 20–40 mg) initiated as early as possible regardless of baseline LDL
• C) Statin is not needed if patient has no prior history of hyperlipidaemia
• D) Moderate-intensity statin only; high-intensity statins are too risky post-MI
• E) Ezetimibe alone if patient is intolerant of statins

• A) Statin initiation should not be based on arbitrary LDL thresholds in ACS; all patients benefit from early high-intensity statin therapy.
• C) History of hyperlipidaemia is irrelevant to the indication; the ACS event itself mandates statin therapy for plaque stabilisation and secondary prevention.
• D) High-intensity statins are the standard of care post-ACS; moderate intensity provides inferior LDL reduction and MACE prevention.
• E) Ezetimibe is used as an add-on when LDL target is not achieved on maximum statin, not as monotherapy.

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• A) Digoxin
• B) Amiodarone
• C) Eplerenone (mineralocorticoid receptor antagonist)
• D) Diltiazem
• E) Ivabradine as first-line addition

• A) Digoxin improves symptoms and reduces HF hospitalisations but has not been shown to reduce mortality post-MI.
• B) Amiodarone does not improve mortality in post-MI patients without arrhythmia indications; it has significant toxicity.
• D) Diltiazem and other non-dihydropyridine CCBs are contraindicated in patients with reduced LVEF due to negative inotropic effects.
• E) Ivabradine reduces resting heart rate and may reduce HF hospitalisations (SHIFT trial) but has not demonstrated mortality reduction post-MI; it is an add-on, not a priority over eplerenone.

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• A) PCI to the most stenosed vessel only
• B) Medical therapy only — revascularisation is not indicated above SYNTAX score 22
• C) CABG is preferred over PCI for intermediate-to-high SYNTAX score disease
• D) PCI with DES to all three vessels
• E) Bilateral internal mammary artery (BIMA) CABG only if the patient is under 60

• A) Culprit-only PCI is appropriate for cardiogenic shock (STEMI), not stable triple-vessel disease.
• B) Revascularisation (specifically CABG) improves outcomes in triple-vessel CAD — SYNTAX score threshold for recommending PCI is low (<22), not <22 for medical therapy alone.
• D) PCI to all three vessels is acceptable for low SYNTAX scores (<22) but inferior to CABG at intermediate-high scores.
• E) BIMA grafting is beneficial for long-term patency but the decision for CABG is not age-restricted to <60 years; elderly patients can benefit from CABG.

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• A) Beta-blockers should be withheld in all patients with MI as they worsen cardiac output
• B) Oral beta-blockers should be started within 24 hours and continued long-term in all patients without contraindications
• C) IV beta-blockers should be given to all STEMI patients immediately on arrival
• D) Beta-blockers are only indicated if the patient develops arrhythmia post-MI
• E) Beta-blockers are contraindicated if LVEF is below 40%

• A) Beta-blockers improve cardiac outcomes post-MI by reducing myocardial oxygen demand, heart rate, and arrhythmia risk; they are beneficial unless specific contraindications exist (acute decompensated heart failure, severe bradycardia, cardiogenic shock).
• C) Routine IV beta-blockers on arrival for STEMI are not universally recommended; current guidelines favour early oral administration; IV use is restricted to specific situations (e.g., rapid AF, uncontrolled hypertension, persistent ischaemia) after confirming haemodynamic stability.
• D) Beta-blockers are a cornerstone of post-MI therapy for all patients (anti-ischaemic and antiarrhythmic), not only those with arrhythmias.
• E) Reduced LVEF is actually a stronger indication for long-term beta-blocker therapy (metoprolol succinate, carvedilol, bisoprolol); the original concern was about starting during acute decompensated failure, not chronic use.

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• A) Clopidogrel monotherapy 75 mg daily
• B) Ticagrelor 90 mg BD monotherapy as aspirin replacement
• C) Aspirin desensitisation is mandatory before proceeding
• D) No antiplatelet therapy — anticoagulation with heparin is sufficient
• E) Warfarin as antiplatelet substitute

• A) Clopidogrel monotherapy is also an acceptable alternative to aspirin in true allergy, but ticagrelor has superior efficacy (PLATO trial) and is the preferred P2Y12 inhibitor in ACS.
• C) Aspirin desensitisation is appropriate for aspirin-intolerant patients in a planned/elective setting; in acute STEMI requiring urgent PCI, there is no time to complete desensitisation safely.
• D) Anticoagulation alone without antiplatelet therapy is inadequate in ACS/PCI; antiplatelet agents are essential to prevent stent thrombosis.
• E) Warfarin has no role as an antiplatelet substitute; it acts on coagulation factors, not platelets, and does not prevent stent thrombosis.

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Summary: Subtopic Coverage

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