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

Correct. This is inferior STEMI where primary PCI is unavailable within 120 minutes. The correct approach is the pharmacoinvasive strategy: thrombolysis with a fibrin-specific agent (tenecteplase or alteplase, preferred over streptokinase because they are bolus-administered, have lower bleeding risk, and are more effective), given with aspirin + clopidogrel 300 mg (not ticagrelor/prasugrel with thrombolysis — increased bleeding risk) + enoxaparin (not UFH with tenecteplase in most protocols). Transfer to a PCI-capable centre for angiography at 3–24 hours (pharmacoinvasive strategy). Successful thrombolysis = >50% ST resolution at 60–90 minutes, reperfusion arrhythmia (accelerated idioventricular rhythm — AIVR), relief of pain. Failed thrombolysis (<50% ST resolution) = rescue PCI immediately.

Pharmacoinvasive strategy: fibrin-specific thrombolysis (tenecteplase/alteplase) within 30 min (door-to-needle) when PCI >120 min → transfer for angiography 3–24 hr. Antiplatelet with lysis: aspirin + clopidogrel 300 mg (NOT ticagrelor). Assess reperfusion at 60–90 min: >50% ST resolution = success; <50% = rescue PCI.

PCI unavailable within 120 min from FMC → fibrinolysis (tenecteplase preferred) + aspirin + clopidogrel 300 mg (NOT ticagrelor — increased bleeding with thrombolysis). Transfer for pharmacoinvasive PCI within 3–24 hours after successful thrombolysis. Streptokinase is older, less effective, infusion-based, and not preferred. Waiting for spontaneous reperfusion or heparin-only management is inappropriate in STEMI.

Correct. Proximal RCA occlusion causes both inferior STEMI (II, III, aVF) and RV infarction. The ECG clues for RV infarction are ST elevation in V1 and right precordial leads (V3R/V4R). The tall R wave with ST depression in V2 here represents posterior MI (posterior wall infarction = mirror image of anterior STEMI). The clinical triad: hypotension + elevated JVP + clear lung fields (no LV failure). Management: IV fluids to maintain RV preload; AVOID nitrates (contraindicated — reduce preload and precipitate cardiovascular collapse); urgent reperfusion. This patient has triple-vessel territory involvement of the RCA: inferior + posterior + RV.

RV infarction: proximal RCA occlusion, inferior STEMI + ST elevation V3R/V4R. Clinical: hypotension + high JVP + CLEAR lungs. AVOID: nitrates, diuretics, morphine (preload-reducers). GIVE: IV fluids + reperfusion. Concurrent posterior MI: tall R + ST depression V1–V2.

Inferior STEMI + hypotension + clear lungs (no pulmonary oedema) = RV infarction until proven otherwise. ECG: ST elevation in V1 and V3R/V4R confirms RV involvement. Key: LV failure causes pulmonary oedema; RV infarction causes hypotension with CLEAR lungs and raised JVP. Management reversal: RV infarction needs IV fluids (increase preload); LV failure needs diuretics. Nitrates are lethal in RV infarction.

Correct. Failed thrombolysis is defined as <50% ST resolution at 60–90 minutes after thrombolytic administration, with persistent symptoms. The correct management is immediate rescue PCI — urgent transfer for coronary angiography and PCI of the infarct-related artery. Re-administration of thrombolytics (repeat dose) is not recommended — it increases bleeding risk without improving outcomes. Ticagrelor is NOT added when thrombolytics have been given (increased intracranial bleeding risk; only clopidogrel or aspirin are used with lysis). Continued observation allows further myocardial loss.

Thrombolysis success: >50% ST resolution at 60–90 min + pain relief + reperfusion arrhythmia (AIVR). Failure (<50% ST resolution): rescue PCI urgently. NEVER re-dose thrombolytics. Routine PCI (pharmacoinvasive) = 3–24 hr after SUCCESSFUL lysis.

Failed thrombolysis (<50% ST resolution at 60–90 min + persistent pain) = rescue PCI immediately. Do NOT re-dose thrombolytics (ineffective, dangerous). Do NOT add ticagrelor (contraindicated within 24 hours of thrombolysis — intracranial bleeding risk). Time is still muscle — every minute of delay after failed lysis represents continued infarction.

Correct. Cardiac rehabilitation (CR) after MI reduces all-cause mortality by approximately 20–26% and cardiac mortality by approximately 26% (Cochrane meta-analysis of exercise-based CR). CR also reduces hospital readmissions, improves exercise capacity, health-related quality of life, and lipid profiles, and aids smoking cessation. CR is a Class I recommendation post-MI. It is NOT contraindicated in reduced LVEF — exercise training is beneficial even in patients with LVEF ≤35–40% (supervised). The optimal timing for CR initiation is within 1–2 weeks of hospital discharge; it is typically structured as 12–36 supervised sessions over 3–6 months, with an ongoing home exercise prescription.

Cardiac rehabilitation (Class I, post-MI): reduces all-cause mortality 20–26%, cardiac mortality 26%. Not contraindicated in reduced LVEF. Components: aerobic exercise + resistance training + smoking cessation + dietary counselling + psychosocial support + medication adherence. Start within 1–2 weeks of discharge.

Cardiac rehabilitation has Class I evidence post-MI: ~20–26% reduction in all-cause mortality, ~26% reduction in cardiac mortality (Cochrane). It is NOT contraindicated in reduced EF — supervised CR is beneficial even for HFrEF. CR components: exercise training + risk factor modification + psychosocial support + education. Initiate within 1–2 weeks of discharge. Not restricted to those who complete a fixed number of sessions.

Correct. Smoking cessation is the single most impactful secondary prevention intervention post-MI — it reduces 1-year mortality by approximately 36% (independent of other interventions). Abrupt cessation is preferred over gradual reduction. Pharmacological support (nicotine replacement therapy — NRT, varenicline, bupropion) should be offered alongside behavioural counselling. Varenicline (Champix) was previously thought to have cardiovascular risk, but the EAGLES trial and subsequent data show it is safe in patients with established cardiovascular disease and is more effective than NRT or bupropion. Empathic, non-judgmental counselling is the evidence-based communication approach.

Post-MI secondary prevention priority: smoking cessation (36% mortality reduction > any single medication). Method: abrupt cessation + pharmacotherapy (varenicline preferred — safe post-MI per EAGLES trial; NRT or bupropion as alternatives) + behavioural support. Counsel empathically; avoid judgmental language.

Smoking cessation post-MI is the strongest secondary prevention intervention — ~36% mortality reduction. Abrupt cessation is recommended, not gradual reduction. Varenicline is SAFE post-MI (EAGLES trial) and more effective than NRT. Empathic counselling + pharmacotherapy = most effective combination. Never tell a post-MI patient that cessation is not worth the effort.

Correct. Tall, broad R waves in V1 with ST depression and upright T waves represent the mirror image of posterior ST elevation — this is a posterior STEMI equivalent. In posterior STEMI, the ECG shows ST depression in V1–V3 (the 'reciprocal' of posterior ST elevation); placing posterior leads (V7–V9) would show direct ST elevation. Combined with inferior ST elevation (II, III, aVF), this is an inferior + posterior STEMI — a larger territory than isolated inferior MI, typically from proximal RCA or LCx occlusion. This is distinguished from RBBB (which has a rSR' pattern in V1 with wide QRS >0.12 s). The management — urgent reperfusion — is the same as for any STEMI.

Posterior STEMI signs in standard 12-lead: ST depression + tall R (R>S) + upright T in V1–V3. Confirm with V7/V8/V9 leads. Often concurrent with inferior STEMI (RCA). Don't miss this STEMI equivalent — it mandates reperfusion.

Posterior STEMI: ST depression V1–V3 + tall R (>R wave width = R) + upright T = posterior wall infarction (mirror image of posterior ST elevation). Place V7–V9 to confirm. Combined with inferior ST elevation = inferior + posterior STEMI from proximal RCA or dominant LCx. Not a normal variant; not RBBB (normal QRS width here). This is a STEMI equivalent requiring urgent reperfusion.

Correct. Current evidence (COMPLETE, PRAMI, CvLPRIT trials) supports complete revascularisation in haemodynamically stable STEMI patients, but NOT routinely in the same primary PCI session unless haemodynamic instability warrants it. The current ESC 2023 position: staged non-culprit PCI is recommended, ideally during the index hospitalisation or within 45 days, based on the COMPLETE trial which showed reduced cardiovascular death and MI. Immediate complete revascularisation in a stable patient carries additional risks (contrast load, procedure duration). CABG is not the first choice at the acute stage unless there is left main disease or anatomy unsuitable for PCI.

STEMI + multivessel disease (stable): PCI culprit vessel acutely → staged non-culprit PCI within 45 days (COMPLETE trial). Haemodynamic instability = exception (may do culprit-only or complete). Urgent CABG: left main or complex multivessel anatomy not suitable for PCI.

Primary PCI strategy: treat the culprit vessel acutely. For stable STEMI with 3-vessel disease: staged non-culprit PCI within 45 days (COMPLETE trial: reduced composite of CV death + MI vs culprit-only). Immediate complete revascularisation in the same session is NOT standard for stable patients — adds procedure time and contrast load without additional acute benefit. Urgent CABG is reserved for left main or complex anatomy unsuitable for PCI.

Correct. Dressler syndrome (post-cardiac injury syndrome, PCIS) typically occurs 2–10 weeks after MI (some definitions extend to months). It is an autoimmune/immune-mediated inflammatory reaction to myocardial and pericardial antigens released at infarction. Features: pleuritic chest pain, fever, pericardial friction rub, diffuse saddle-shaped ST elevation (pericarditis pattern), bilateral pleural effusions, mildly elevated inflammatory markers and troponin. Treatment: NSAIDs + colchicine (first-line for recurrence prevention); corticosteroids for refractory cases. Contrast with early post-MI pericarditis (fibrinous, first 24–72 hours, localised ST elevation in infarct territory, usually mild). Reinfarction would cause territory-specific ST elevation in the infarct leads, not diffuse saddle-shaped changes.

Dressler syndrome (PCIS): 2–10 weeks post-MI; autoimmune pericarditis/pleuritis; saddle ST elevation (diffuse), friction rub, fever, bilateral pleural effusion. Treatment: NSAIDs + colchicine. Early post-MI pericarditis: 24–72 hr, fibrinous, localised to infarct territory, usually mild and self-limiting.

Dressler syndrome: 2–10 weeks post-MI, autoimmune pericarditis + pleuritis. Features: fever + pleuritic pain + pericardial rub + diffuse saddle ST + bilateral effusions. Distinguish from reinfarction (territory-specific ST elevation, no friction rub) and early pericarditis (first 72 hr, fibrinous, no systemic features). Treat: NSAIDs + colchicine; avoid anticoagulation if significant effusion.

Correct. Statin-associated muscle symptoms (SAMS) with CK 3–10× ULN but no severe muscle weakness or myoglobinuria: temporarily hold the statin, recheck CK in 2–4 weeks after resolution of symptoms. Once CK normalises, reintroduce at a lower dose (e.g., atorvastatin 40 mg) or switch to a lower myopathy-risk statin (e.g., pravastatin, rosuvastatin). If symptoms recur at low dose, add ezetimibe and consider a PCSK9 inhibitor. Stopping statin permanently without a re-challenge deprives a post-MI patient of life-saving therapy — the LDL target must still be met. Rhabdomyolysis (CK >10× ULN + myoglobinuria + renal impairment) requires immediate discontinuation + IV fluids.

Statin SAMS management: CK <4× ULN + mild symptoms = continue, monitor. CK 4–10× ULN = hold statin, recheck, reintroduce low dose or alternate statin. CK >10× ULN (rhabdomyolysis) = stop immediately + hydration + monitor renal function. Never abandon statin post-MI without re-challenge.

SAMS with CK 3–10× ULN: hold statin temporarily → recheck CK → reintroduce at lower dose or switch statin. CK >10× ULN = rhabdomyolysis risk → stop immediately. Never permanently abandon statins post-MI without exhausting lower-dose and statin-switch options. PCSK9 inhibitors are added when statin + ezetimibe insufficient, not as first replacement for SAMS.

Correct. High-risk NSTEMI (GRACE score >140) requires an early invasive strategy: coronary angiography within 24 hours of presentation. This is supported by the TIMACS and VERDICT trials. Very high-risk features (haemodynamic instability, ongoing ischaemia, acute HF, life-threatening arrhythmia) require immediate angiography (<2 hours — same as STEMI). Low-to-intermediate risk: selective invasive (angiography guided by non-invasive stress testing). The GRACE score >140 is the key threshold for the early (24-hour) invasive approach. Anticoagulation (fondaparinux preferred; or enoxaparin/UFH) should be given while awaiting angiography.

NSTEMI angiography timing (ESC): very high risk (shock, refractory ischaemia, acute HF) = <2 hr; high risk (GRACE >140) = <24 hr; intermediate = <72 hr; low risk = non-invasive testing. Start anticoagulation (fondaparinux preferred; or enoxaparin) + DAPT while waiting.

NSTEMI risk stratification drives angiography timing: very high risk (haemodynamic instability, refractory ischaemia) = <2 hours; high risk (GRACE >140, NSTEMI with ongoing symptoms) = <24 hours; intermediate risk = <72 hours; low risk = non-invasive testing first. GRACE >140 in this patient = early invasive (24 hours), not immediate (<2 hr) unless additional very-high-risk features present.

Correct. His LDL-C is 2.2 mmol/L, above the post-ACS target of <1.8 mmol/L (with ≥50% reduction from baseline). He is already on high-intensity statin (atorvastatin 80 mg). The next step per ESC guidelines is to add ezetimibe 10 mg, which reduces LDL by a further 18–20%. If still above target, a PCSK9 inhibitor would be the third agent. DAPT (aspirin + ticagrelor) must continue for 12 months post-ACS-PCI — stopping at 1 month would substantially increase the risk of stent thrombosis and recurrent MI. ACE inhibitor should continue in HFmrEF (LVEF 41–49%) — it remains beneficial. Diltiazem (a non-dihydropyridine CCB) is contraindicated in HF with reduced/mid-range EF as it is negatively inotropic. Aspirin 75–100 mg is the correct dose for long-term secondary prevention; higher doses increase GI bleeding without additional cardioprotection.

Secondary prevention post-ACS at 1 month: DAPT continues to 12 months; LDL target <1.8 mmol/L — add ezetimibe if not at goal on max statin; ACE inhibitor continues regardless of EF recovery; beta-blocker continues if EF ≤40–49%. Diltiazem is contraindicated in HFrEF and HFmrEF.

Post-ACS management checklist: DAPT for 12 months (do not stop at 1 month); atorvastatin 80 mg + add ezetimibe if LDL still above target (<1.8 mmol/L); continue ACE inhibitor even if EF improves to 41–49% (HFmrEF still benefits); beta-blocker (metoprolol is correct — diltiazem is contraindicated in HF); aspirin 75–100 mg (not 325 mg long-term — higher GI risk, no added cardioprotection).

Correct. Familial hypercholesterolaemia (FH) is characterised by markedly elevated LDL-C (typically >4.9 mmol/L in heterozygous FH), tendinous xanthomata (pathognomonic — LDL deposits in tendons), and a strong family history of premature IHD. The mechanism: loss-of-function mutation in the LDL receptor (LDLR) gene reduces hepatic uptake of LDL, causing LDL accumulation in plasma. Other FH mutations: ApoB-100 (reduces LDL binding to LDLR) or PCSK9 gain-of-function (increases LDLR degradation). Metabolic syndrome dyslipidaemia presents with elevated TG + low HDL + modestly elevated LDL (not LDL 4.6 mmol/L in isolation with xanthomata). This patient needs high-intensity statin immediately (LDL target <2.5 mmol/L for FH without ASCVD, or <1.8 mmol/L if additional ASCVD risk factors present) and family cascade screening.

Familial hypercholesterolaemia: LDLR loss-of-function → elevated LDL >4.9 mmol/L + tendinous xanthomata + premature IHD family history. Dutch Lipid Clinic criteria for diagnosis. Treatment: high-intensity statin + ezetimibe + PCSK9 inhibitor if target not met. Family cascade screening mandatory. Secondary causes (hypothyroidism, nephrotic syndrome, DM) must be excluded before labelling as primary FH.

Tendinous xanthomata + LDL-C >4.9 mmol/L + premature family IHD = familial hypercholesterolaemia (heterozygous FH) until proven otherwise. Mechanism: LDL receptor loss-of-function mutation → impaired hepatic LDL clearance → LDL accumulation. Metabolic syndrome has a different lipid triad (elevated TG + low HDL). Chylomicronaemia is caused by LPL deficiency presenting with TG >11 mmol/L and eruptive (not tendinous) xanthomata.