Ischaemic heart disease flashcards
19 high-yield MRCP Part 1 cards from the Intellect Medicos Cardiology course. Try to answer each question before you open it — then study them properly with spaced repetition, which brings each card back just before you would forget it.
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A 58-year-old has had 40 minutes of central chest pain. ECG: horizontal ST depression in V1–V3 with tall, broad R waves in V1–V2. What is the likely diagnosis, and which extra leads would confirm it?
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Posterior myocardial infarction. Record posterior leads V7–V9 and look for ST elevation.
Why? Leads V1–V3 look at the posterior wall from the front, so posterior ST elevation and Q waves appear as their mirror image: ST depression and tall R waves.
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Four days after an inferior MI, a 70-year-old suddenly develops pulmonary oedema and hypotension. There is a new pansystolic murmur at the apex radiating to the axilla. What is the most likely mechanical complication?
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Papillary muscle rupture causing acute mitral regurgitation.
Why? The posteromedial papillary muscle usually has a single blood supply (from the posterior descending artery), so it is vulnerable in inferior or posterior MI.
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A 38-year-old smoker has recurrent chest pain at rest in the early morning. During pain the ECG shows transient ST elevation, which settles completely. Angiography shows no fixed stenosis. What is the diagnosis, and which drug class should be avoided?
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Prinzmetal (vasospastic) angina. Avoid beta-blockers.
Why? The pain is due to coronary artery spasm. Nitrates and calcium channel blockers relax the spasm; non-selective beta-blockade can leave alpha-mediated vasoconstriction unopposed.
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Name the contraindication tested for each: ivabradine, nicorandil, ranolazine.
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Ivabradine — sick sinus syndrome. Nicorandil — LV failure with low filling pressures (also hypotension, cardiogenic shock). Ranolazine — liver failure.
Why? Ivabradine needs a functioning SA node to work and can cause dangerous bradycardia if it is diseased. These are the anti-anginal contraindications listed in the course notes.
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In STEMI, when does NICE say to give fibrinolysis rather than primary PCI?
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When the patient presents within 12 hours of symptom onset and primary PCI cannot be delivered within 120 minutes of when fibrinolysis could be given.
Why? Primary PCI is better when available quickly; fibrinolysis is the fallback when delay would cost myocardium. Repeat the ECG 60–90 minutes after fibrinolysis and send for angiography if ST elevation persists.
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For a patient having primary PCI for STEMI who is not on an oral anticoagulant, which P2Y12 inhibitor does NICE prefer with aspirin?
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Prasugrel.
Why? Prasugrel gives faster, more consistent platelet inhibition in the PCI setting. Clopidogrel is used instead if the patient is already taking an oral anticoagulant.
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What is the commonest cause of death after myocardial infarction?
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Ventricular fibrillation (arrhythmia).
Why? Ischaemic and recently infarcted myocardium is electrically unstable, especially in the first hours. This is why early defibrillator access matters.
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Six weeks after an MI, a 63-year-old develops fever, pleuritic chest pain and a pericardial rub. ESR is raised. What is the diagnosis?
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Dressler syndrome (post-MI autoimmune pericarditis).
Why? Myocardial injury exposes antigens that trigger an immune response weeks to months later, causing pericarditis, pleurisy and fever. Treated with NSAIDs, high-dose aspirin or steroids.
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Persistent ST elevation several weeks after an anterior MI, with no chest pain, suggests what?
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Left ventricular aneurysm.
Why? The infarcted segment has thinned into a dyskinetic aneurysm, which leaves a persistent "injury" pattern on the ECG. Complications include heart failure, VT and mural thrombus. Echo is diagnostic.
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STEMI criteria: new ST elevation in 2 contiguous leads of at least 1 mm, except V2–V3, where the cut-off is 2 mm in men aged 40 or over, ______ in men under 40 and 1.5 mm in women.
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2.5 mm
Why? Leads V2–V3 normally show some ST elevation, especially in young men, so higher cut-offs avoid over-diagnosis.
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STEMI criteria: new ST elevation in 2 contiguous leads of at least 1 mm, except V2–V3, where the cut-off is 2 mm in men aged 40 or over, 2.5 mm in men under 40 and ______ in women.
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1.5 mm
Why? Leads V2–V3 normally show some ST elevation, especially in young men, so higher cut-offs avoid over-diagnosis.
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In NSTEMI/unstable angina, NICE suggests the ______ score; if predicted 6-month mortality is above 3%, consider angiography within 72 hours.
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GRACE
Why? Higher-risk patients gain most from early invasive management. Clinically unstable patients go for immediate angiography.
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In NSTEMI/unstable angina, NICE suggests the GRACE score; if predicted 6-month mortality is above 3%, consider angiography within ______.
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72 hours
Why? Higher-risk patients gain most from early invasive management. Clinically unstable patients go for immediate angiography.
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STEMI treated with fibrinolysis, or managed medically without reperfusion: which P2Y12 inhibitor does NICE offer with aspirin?
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Ticagrelor (clopidogrel, or aspirin alone, if bleeding risk is high).
Why? Prasugrel is reserved for patients who are going on to PCI.
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Which four drug classes does NICE recommend for secondary prevention after an MI?
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ACE inhibitor, dual antiplatelet therapy (up to 12 months), beta-blocker and statin.
Why? Each lowers recurrent events or mortality. If there is HFrEF, an aldosterone antagonist is added 3–14 days after the MI, preferably after the ACE inhibitor.
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What is the first-line regular drug treatment for stable angina (alongside sublingual GTN and secondary prevention)?
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A beta-blocker or a calcium channel blocker.
Why? Both reduce myocardial oxygen demand. If symptoms continue, switch or combine them; if both are unsuitable, use a long-acting nitrate, ivabradine, nicorandil or ranolazine.
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What is the mechanism of action of ranolazine?
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It inhibits the late inward sodium current in cardiac myocytes, reducing sodium-driven calcium overload.
Why? Less intracellular calcium improves diastolic relaxation and lowers oxygen demand, with little effect on heart rate or BP.
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Which P2Y12 inhibitor is contraindicated in a patient with a previous stroke or TIA?
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Prasugrel.
Why? In its main trial, people with prior stroke or TIA had net harm, mainly from intracranial bleeding.
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Why should omeprazole or esomeprazole be avoided with clopidogrel?
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They inhibit CYP2C19, which converts the prodrug clopidogrel to its active form, so its antiplatelet effect falls.
Why? MHRA advises against these two PPIs with clopidogrel; another PPI such as lansoprazole is used if gastroprotection is needed.
More Cardiology topics
- Physiology & haemodynamics
- Heart sounds, pulses & murmurs
- Valvular heart disease
- ECG & arrhythmias
- Inherited & sudden cardiac death syndromes
- Heart failure & cardiomyopathies
- Pericardial disease
- Endocarditis & rheumatic fever
- Congenital heart disease
- Hypertension, aorta & emboli
- Cardiovascular pharmacology
- Lipids & statins