IM2.1-24 | Acute Myocardial Infarction and Ischemic Heart Disease — Practice Quiz

Correct. The 12-lead ECG is the single most important and immediately actionable investigation in suspected STEMI. It must be obtained and interpreted within 10 minutes of first medical contact. STEMI criteria: new ST elevation ≥2 mm in V2–V3 (men ≥40 yr) or ≥1 mm in other leads in ≥2 contiguous leads, or new LBBB. Troponin confirms myocardial necrosis but takes hours to rise and does not determine the reperfusion strategy — the ECG does.

STEMI ECG criteria: ST elevation ≥2 mm in V2–V3 (men ≥40 yr) or ≥1 mm in ≥2 contiguous leads, or new LBBB. ECG within 10 minutes of first medical contact is the Class I time target.

In suspected STEMI, the 12-lead ECG must be obtained and read within 10 minutes of first medical contact — this is the investigation that triggers the reperfusion pathway. Troponin confirms MI but rises over hours; it does not determine the immediate reperfusion decision. The ECG drives the STEMI vs NSTEMI distinction and the choice between primary PCI and thrombolysis.

Correct. This is NSTEMI: elevated troponin (confirming myocardial necrosis) without diagnostic ST elevation in the ischaemic territory. The ECG shows ST depression and tall R waves in the inferior leads — this is a posterior STEMI pattern (ST elevation equivalent in V7–V9), but the cardinal teaching point here is that diabetic patients frequently present with atypical symptoms (epigastric pain, nausea, diaphoresis) rather than classic crushing chest pain. The troponin at 2.8 ng/mL (70× upper reference limit) confirms substantial necrosis.

ACS spectrum: STEMI (occlusion + ST elevation) vs NSTEMI (partial occlusion + troponin rise, no ST elevation) vs UA (transient ischaemia, troponin negative). Diabetics and women present atypically — consider ACS in unexplained diaphoresis, nausea, or epigastric pain.

Elevated troponin + ischaemic symptoms + no ST elevation = NSTEMI. Unstable angina is defined by the absence of troponin elevation. STEMI requires ST elevation ≥1–2 mm in ≥2 contiguous leads — ST depression here represents reciprocal change or posterior STEMI but without the ST elevation pattern that triggers immediate thrombolysis. Diabetic patients frequently present atypically with epigastric pain instead of chest pain.

Correct. Ticagrelor 180 mg loading dose (then 90 mg twice daily for 12 months) is the preferred P2Y12 inhibitor for STEMI/NSTEMI undergoing PCI, per ESC/ACC guidelines, because it provides faster and more consistent platelet inhibition than clopidogrel (which requires hepatic conversion to active metabolite and has variable response due to CYP2C19 polymorphism). Prasugrel is an alternative (60 mg load) but is contraindicated in prior stroke/TIA and age >75 years. Aspirin + P2Y12 inhibitor = dual antiplatelet therapy (DAPT), standard for 12 months post-ACS-PCI.

DAPT post-ACS: aspirin 75 mg daily + ticagrelor 90 mg BD (preferred) or clopidogrel 75 mg OD for 12 months. Ticagrelor load = 180 mg; clopidogrel load = 600 mg (for PCI) or 300 mg (for thrombolysis).

Dual antiplatelet therapy (DAPT) = aspirin + P2Y12 inhibitor for 12 months after ACS-PCI. Ticagrelor (180 mg load, then 90 mg BD) is preferred over clopidogrel because it has faster onset, higher potency, and does not require hepatic conversion. Clopidogrel 600 mg (not 300 mg) is the alternative when ticagrelor/prasugrel are contraindicated. Dipyridamole and warfarin are not first-line antiplatelet agents in ACS.

Correct. For primary PCI, the door-to-balloon (D2B) time target is ≤90 minutes. If D2B cannot be achieved within 120 minutes (including transfer time), thrombolysis should be given within 30 minutes of hospital arrival (door-to-needle ≤30 min) if there are no contraindications. The first medical contact (FMC) to balloon target is ≤120 minutes overall. Every 30 minutes of delay in STEMI reperfusion increases 1-year mortality by approximately 7.5%.

Reperfusion windows: primary PCI D2B ≤90 min; if PCI not feasible within 120 min of FMC, give thrombolysis with door-to-needle ≤30 min. Symptom-to-reperfusion ideally <12 hours for STEMI.

Primary PCI door-to-balloon target = ≤90 minutes. If D2B >120 minutes (including transfer), fibrinolysis is preferred with door-to-needle ≤30 minutes. First medical contact to balloon ≤120 minutes is the overall system target. Time is muscle — each 30-minute delay in reperfusion increases 1-year mortality by ~7.5%.

Correct. ACE inhibitors (e.g., ramipril, lisinopril) are a Class I recommendation post-MI with LVEF ≤40% (HFrEF). They reduce LV remodelling, prevent progressive HF, and reduce all-cause mortality and reinfarction. Beta-blockers (metoprolol, carvedilol) should also be added — they reduce sudden cardiac death. The discharge medication bundle post-MI with reduced EF: aspirin + P2Y12 inhibitor + high-intensity statin + ACE inhibitor + beta-blocker + mineralocorticoid receptor antagonist (spironolactone/eplerenone if LVEF ≤35% with HF symptoms).

Post-MI mandatory medications: aspirin + P2Y12 (12 months) + high-intensity statin + ACE inhibitor (all LVEF ≤40%, or diabetes/HF) + beta-blocker (LVEF ≤40% or ongoing ischaemia). Add MRA if LVEF ≤35% + HF symptoms.

Post-MI with LVEF ≤40%, ACE inhibitors are mandatory (Class I) to prevent LV remodelling and reduce mortality. Diltiazem is contraindicated post-MI with LV dysfunction. Amiodarone has no mortality benefit for primary prevention. Beta-blockers should also be initiated. The complete discharge bundle: aspirin + P2Y12 + high-intensity statin + ACE inhibitor + beta-blocker ± MRA.

Correct. Nitrates are CONTRAINDICATED in RV infarction. The right ventricle in RV infarction is completely dependent on preload (venous return) to maintain output to the left side of the heart. Nitrates cause venodilation, dramatically reducing preload and precipitating catastrophic hypotension. The classic triad of RV infarction is: hypotension + raised JVP + clear lung fields, with ST elevation in right precordial leads (V3R/V4R). Management: IV fluid loading to maintain RV preload + urgent reperfusion of the RCA + avoid all preload-reducing agents (nitrates, diuretics, morphine with caution).

RV infarction triad: hypotension + elevated JVP + clear lungs. ECG: ST elevation V3R/V4R. Management: IV fluids (increase preload) + reperfusion. CONTRAINDICATED: nitrates, diuretics (any preload-reducing agent).

RV infarction: hypotension + raised JVP + clear lungs = the classic triad. Nitrates are absolutely contraindicated — they reduce venous return (preload), which the RV-infarcted heart is critically dependent on to fill the left side. Treatment is the opposite: IV fluid boluses to increase preload. ST elevation in V3R/V4R diagnoses RV infarction.

Correct. Anterior STEMI (ST elevation in V1–V4) with ST elevation in aVR and diffuse lateral ST depression indicates proximal LAD occlusion before the first septal perforator and first diagonal. Proximal LAD occlusion causes the largest infarct territory (anterior wall + septum + sometimes apex) and carries the highest mortality. ST elevation in aVR with lateral ST depression is also the pattern of left main or proximal LAD equivalents when the territory is large enough to produce this 'global subendocardial ischaemia' appearance. The key localisation: V1–V4 = anterior = LAD; II/III/aVF = inferior = RCA or LCx; I/aVL/V5–V6 = lateral = LCx or diagonal.

ECG localisation: anterior (V1–V4) = LAD; inferior (II, III, aVF) = RCA (80%) or LCx (20%); lateral (I, aVL, V5–V6) = LCx or diagonal; posterior = tall R in V1–V2 with ST depression (obtain V7–V9). ST elevation in aVR + lateral depression = LMCA or proximal LAD equivalent.

ECG localisation: V1–V4 elevation = anterior territory = LAD. RCA occlusion causes inferior STEMI (II, III, aVF). LCx causes lateral STEMI (I, aVL, V5–V6) or posterior MI. Proximal LAD occlusion produces the largest MI territory, involving anterior wall, septum, and apex — this is the highest-risk STEMI pattern.

Correct. Papillary muscle rupture causing acute severe mitral regurgitation (MR) typically occurs 2–7 days post-MI, most often after inferior MI (posteromedial papillary muscle, supplied by a single artery — the PDA from RCA — unlike the anterolateral papillary muscle which has dual supply). It presents with sudden-onset pulmonary oedema, a new loud pansystolic murmur at the apex (MR), and cardiogenic shock. VSR also causes a new pansystolic murmur but at the lower left sternal edge (VSD murmur) with a step-up in oxygen saturation in the RV on catheterisation. Echocardiography (urgent TOE) distinguishes them. Management: emergency surgical repair (MV replacement/repair) ± IABP.

Mechanical complications of MI (days 2–7): papillary muscle rupture = acute MR (apex murmur, pulmonary oedema); VSR = VSD murmur (LLSE, RV O2 step-up); free wall rupture = electromechanical dissociation. All require emergency surgery. Papillary muscle rupture most often complicates inferior MI (posteromedial PM, single blood supply).

Papillary muscle rupture: sudden pulmonary oedema + loud pansystolic murmur at the apex (MR) + cardiogenic shock on day 2–7 post-MI. This is different from VSR (murmur at lower left sternal border, step-up in O2 saturation on RV catheterisation). Both are mechanical complications requiring urgent cardiac surgery. Dressler syndrome occurs weeks later with pleuritic chest pain and fever.

Correct. For very high cardiovascular risk (established ASCVD — post-ACS, post-MI, prior stroke, PAD), the ESC 2019 guidelines set LDL-C target <1.8 mmol/L (70 mg/dL) AND ≥50% reduction from baseline untreated LDL. If LDL remains ≥1.8 mmol/L on maximum-tolerated statin, add ezetimibe. If still above target, add a PCSK9 inhibitor (evolocumab, alirocumab). The patient's current LDL of 2.4 mmol/L is above target — the statin should be intensified or ezetimibe added. Note: for recurrent ACS within 2 years on statin therapy, the even lower target of <1.4 mmol/L (55 mg/dL) applies (ESC 2019).

LDL-C targets (ESC 2019): very high risk (ASCVD) = <1.8 mmol/L AND ≥50% reduction; recurrent ACS within 2 years on statin = <1.4 mmol/L. Statin dose-response plateau: each doubling adds only ~6% further LDL reduction. Add ezetimibe, then PCSK9 inhibitor if needed.

Very high CV risk (established ACS/ASCVD): LDL target <1.8 mmol/L (70 mg/dL) AND ≥50% from baseline. LDL 2.4 mmol/L is above target — add ezetimibe to maximise statin therapy. For recurrent ACS within 2 years on statin therapy, the target is even lower: <1.4 mmol/L. Statins: doubling the dose gives only a further ~6% LDL reduction (the '6% rule') — switching to ezetimibe or PCSK9 inhibitor is more effective for residual LDL.

Correct. Stable angina is defined by predictable, reproducible chest pain on exertion (or emotional stress) that is consistently relieved by rest or sublingual nitrate within 5 minutes, with no rest pain and negative serial troponins. This distinguishes it from unstable angina (rest pain/new onset/accelerating pattern) and NSTEMI (elevated troponin). The first investigation of choice for stable angina is an exercise stress test (treadmill ECG/TMT) — it evaluates ischaemic ECG changes, symptoms, exercise capacity, and BP response. Coronary angiography is reserved for stress test-positive cases, high-risk features, or diagnostic uncertainty.

Stable vs unstable angina: stable = predictable exertional pain, relieved by rest, troponin negative; unstable = rest pain/new/accelerating, higher-risk. Investigation sequence: stable angina → TMT → if positive/high-risk → coronary angiogram → revascularisation (PCI or CABG) based on anatomy.

Stable angina = exertional chest pain consistently relieved by rest, negative troponins, no rest pain. First investigation: exercise stress test (TMT). Unstable angina = rest pain or new-onset or crescendo pattern — requires acute hospital management. NSTEMI requires positive troponin. TMT detects inducible ischaemia; positive test leads to coronary angiography.