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MRCP PART 1 · CARDIOLOGY

Cardiology questions
for MRCP Part 1.

Clinora has 376 cardiology single best answer questions covering 266 topics. Every question explains all five options, separates the key clue from what it means and what to do next, and links to its source. Try the 5 sample questions below, then practise more for free.

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Question 1Acute coronary syndromesMedium

A 58-year-old man presents within 1 hour of onset of central crushing chest pain. ECG shows 3mm ST-elevation in leads II, III and aVF. The nearest primary PCI centre is 90 minutes away by ambulance. What is the most appropriate immediate management?

  1. AStart a beta-blocker alone with no antiplatelet or reperfusion therapy
  2. BGive fibrinolysis immediately with no antiplatelet therapy, since PCI is not locally available
  3. CDischarge with outpatient cardiology follow-up in one week, since symptoms are recent in onset
  4. DGive loading-dose aspirin, arrange immediate transfer for primary PCI since it can be delivered within 120 minutes of first medical contact, and give a second antiplatelet agent per local protocol
  5. EWait 24 hours to see if the ST-elevation resolves before deciding on reperfusion strategy
Show answer and explanation

Answer: D Give loading-dose aspirin, arrange immediate transfer for primary PCI since it can be delivered within 120 minutes of first medical contact, and give a second antiplatelet agent per local protocol

This is an inferior STEMI (ST elevation in II, III and aVF) presenting within the first hour, so the question is how to reperfuse, not whether to. NICE NG185 makes primary PCI the strategy of choice when it can be delivered within 120 minutes of the time fibrinolysis could have been given. A 90-minute transfer meets that threshold, so he should go straight to a primary PCI centre rather than be thrombolysed locally. Before and during transfer, give a loading dose of aspirin and a second antiplatelet agent as per local protocol (commonly prasugrel or ticagrelor for patients going to PCI). Fibrinolysis is the fallback only when primary PCI cannot be delivered within that window, and it is always given with antithrombotic therapy, followed by angiography. The exam trap is the word 'nearest': distance alone does not decide the strategy, the expected time to PCI does.

Key clue
Inferior STEMI within 1 hour of onset, PCI centre reachable within 120 minutes
What it means
Acute inferior STEMI suitable for primary PCI
What to do
Give aspirin loading dose and a second antiplatelet agent per local protocol, and arrange emergency transfer for primary PCI

Why the other options are less appropriate

  • A A beta-blocker is not reperfusion and is not a substitute for antiplatelet therapy; leaving an occluded coronary artery untreated lets the infarct complete.
  • B Fibrinolysis is for when primary PCI cannot be delivered within 120 minutes. Here it can, so PCI is preferred, and fibrinolysis would never be given without antithrombotic therapy anyway.
  • C Early presentation is the best time to treat, not a reason to wait. STEMI is an emergency and discharge risks death or a large infarct.
  • E Myocardium is lost minute by minute ('time is muscle'). The reperfusion decision is made at first medical contact, not after observation.

Source: NICE NG185 Acute coronary syndromes

Question 2Acute coronary syndromesHard

Four days after an acute anterior myocardial infarction, a patient develops sudden breathlessness, a new loud pansystolic murmur at the left sternal edge, and hypotension. What is the most likely diagnosis, and what is the appropriate next step?

  1. AMusculoskeletal chest pain from prolonged bed rest, requiring only simple analgesia
  2. BSimple post-MI pericarditis; treat with aspirin alone and no further imaging is required
  3. CRecurrent angina; manage with sublingual glyceryl trinitrate alone
  4. DNormal post-MI recovery; no specific action or imaging needed
  5. EVentricular septal rupture; arrange urgent echocardiography to confirm and involve cardiac surgery urgently for consideration of emergency repair
Show answer and explanation

Answer: E Ventricular septal rupture; arrange urgent echocardiography to confirm and involve cardiac surgery urgently for consideration of emergency repair

A new loud pansystolic murmur at the left sternal edge, with sudden breathlessness and hypotension a few days after an anterior MI, points to a mechanical complication. Ventricular septal rupture classically occurs 3–5 days after infarction, when necrotic myocardium is weakest. Anterior infarcts involve the septum supplied by the left anterior descending artery. The left-to-right shunt causes pulmonary oedema and cardiogenic shock, and a thrill is often palpable. The main alternative is acute mitral regurgitation from papillary muscle rupture, which is more typical after inferior MI and gives an apical murmur radiating to the axilla. Urgent echocardiography with colour Doppler confirms the defect. A step-up in oxygen saturation from right atrium to pulmonary artery is a classic supporting finding. ESC 2023 guidance supports urgent surgical review. Mechanical circulatory support, such as an intra-aortic balloon pump, with vasodilators or inotropes, may stabilise the patient as a bridge to repair. Without repair, mortality is very high.

Key clue
New pansystolic murmur and acute haemodynamic compromise days after anterior MI
What it means
Suspected mechanical complication of MI (ventricular septal rupture or papillary muscle rupture)
What to do
Arrange urgent echocardiography to confirm the diagnosis and involve cardiac surgery emergently, since mechanical complications of MI carry high mortality without prompt intervention

Why the other options are less appropriate

  • A Musculoskeletal pain does not cause a new pansystolic murmur, breathlessness or hypotension. This picture needs urgent cardiac assessment.
  • B Pericarditis causes pleuritic pain and a rub, not a new pansystolic murmur with shock. This needs urgent echocardiography.
  • C Angina does not cause a new loud murmur. Glyceryl trinitrate could worsen hypotension and delays diagnosis of a structural complication.
  • D Sudden breathlessness, hypotension and a new murmur are not normal recovery. Untreated mechanical complications after MI carry very high mortality.

Source: ESC 2023 Guidelines for the management of acute coronary syndromes

Question 3Stable coronary diseaseHard

A patient with stable angina remains symptomatic despite optimally titrated bisoprolol and amlodipine, and is not currently suitable for revascularisation. They are in sinus rhythm with a resting heart rate of 78 beats per minute. Which additional antianginal agent is most appropriate to consider next?

  1. AA non-selective beta-blocker in addition to the existing beta-blocker for additive effect
  2. BA second calcium channel blocker of the same dihydropyridine class in addition to amlodipine
  3. CIvabradine, added for further heart-rate lowering in sinus rhythm
  4. DDigoxin, since it is an effective antianginal agent in patients in sinus rhythm
  5. EStopping all antianginal therapy since further options are not available
Show answer and explanation

Answer: C Ivabradine, added for further heart-rate lowering in sinus rhythm

Angina persisting despite optimal doses of a beta-blocker and a calcium channel blocker is the key point. NICE CG126 advises considering a third antianginal drug only while awaiting revascularisation, or when revascularisation is not appropriate or acceptable, as here. The options are a long-acting nitrate, ivabradine, nicorandil or ranolazine, chosen by comorbidities, contraindications, preference and cost. Ivabradine blocks the If (funny) current in the sinoatrial node, slowing heart rate without reducing contractility or blood pressure. It works only in sinus rhythm. The MHRA advised in 2014 that in stable angina it should be started only if resting heart rate is at least 70 beats per minute, at no more than 5 mg twice daily (2.5 mg twice daily in people over 75), and stopped if symptoms have not improved after 3 months. It must not be combined with verapamil or diltiazem, but can be used with amlodipine. Its main adverse effects are phosphenes (transient luminous visual phenomena) and bradycardia. Aspirin, a statin and a short-acting nitrate continue throughout.

Key clue
Persistent angina despite optimal beta-blocker and calcium channel blocker therapy, sinus rhythm, not suitable for revascularisation
What it means
Need for additional antianginal therapy
What to do
Consider adding ivabradine, a long-acting nitrate, nicorandil, or ranolazine, selecting based on patient comorbidities, contraindications and tolerability, with ongoing cardiology input

Why the other options are less appropriate

  • A Two beta-blockers add bradycardia, hypotension and fatigue without extra antianginal benefit. A drug from another class is preferred.
  • B A second dihydropyridine uses the same mechanism and adds vasodilator side effects, such as ankle oedema, without useful extra benefit.
  • D Digoxin has no role in treating stable angina in sinus rhythm. It is used for rate control in atrial fibrillation and in selected heart failure.
  • E Further options remain, including ivabradine, long-acting nitrates, nicorandil and ranolazine. Stopping treatment would leave angina uncontrolled.

Source: NICE CG126 Stable angina: management

Question 4Atrial fibrillationHard

A patient with atrial fibrillation is found to have Wolff-Parkinson-White syndrome with pre-excitation on ECG. Which class of drug should be specifically avoided for rate control in this context, and why?

  1. AAV nodal blocking drugs, because they favour conduction down the accessory pathway
  2. BNone; beta-blockers are safe first-line rate control in WPW
  3. CNone; any standard rate-control drug can be used
  4. DClass Ic drugs such as flecainide, because they slow the accessory pathway
  5. EProcainamide, because it prolongs the QRS duration
Show answer and explanation

Answer: A AV nodal blocking drugs, because they favour conduction down the accessory pathway

In Wolff-Parkinson-White syndrome, an accessory pathway connects the atria to the ventricles directly, without the AV node's decremental slowing. During atrial fibrillation, the AV node normally limits how fast the ventricles beat. If the node is blocked with digoxin, verapamil, diltiazem, adenosine or a beta-blocker, more impulses travel down the accessory pathway. The ventricular rate can then rise above 250 per minute and degenerate into ventricular fibrillation. On the ECG, pre-excited AF looks like an irregular, very fast, broad-complex tachycardia whose QRS shape varies from beat to beat. The ESC 2019 SVT guideline recommends immediate synchronised DC cardioversion if the patient is haemodynamically unstable. If stable, it recommends drug cardioversion with ibutilide or procainamide (flecainide or propafenone are alternatives), or elective DC cardioversion. It advises against IV amiodarone in pre-excited AF. Pre-excited AF is an indication for catheter ablation of the accessory pathway. A shortest pre-excited RR interval of 250 ms or less marks a high-risk pathway.

Key clue
Atrial fibrillation with pre-excitation (Wolff-Parkinson-White syndrome) on ECG
What it means
Pre-excited atrial fibrillation requiring specific drug caution
What to do
Avoid AV nodal blocking agents, seek urgent specialist cardiology input, and consider alternative strategies such as procainamide/flecainide (per specialist guidance) or electrical cardioversion if unstable, with definitive management via catheter ablation of the accessory pathway

Why the other options are less appropriate

  • B Beta-blockers block the AV node, so they carry the same risk in pre-excited AF. They are not safe first-line treatment here.
  • C AV nodal blocking drugs carry a well-recognised, potentially fatal risk in pre-excited AF. Rate-control drugs cannot be used interchangeably here.
  • D Flecainide slows accessory pathway conduction and is an accepted option for stable pre-excited AF, so it is not the class to avoid.
  • E Procainamide slows accessory pathway conduction and is recommended by the ESC for stable pre-excited AF.

Source: ESC 2019 Guidelines for the management of patients with supraventricular tachycardia

Question 5Atrial fibrillation — very low stroke riskEasy

A 54-year-old man has paroxysmal atrial fibrillation. He has no heart failure, hypertension, diabetes, vascular disease or previous stroke/TIA. What is the most appropriate stroke-prevention management?

  1. AAspirin
  2. BApixaban
  3. CClopidogrel
  4. DNo stroke-prevention therapy
  5. EWarfarin
Show answer and explanation

Answer: D No stroke-prevention therapy

A man under 65 with AF and no heart failure, hypertension, diabetes, vascular disease or previous stroke or TIA has a CHA2DS2-VASc score of 0. His annual stroke risk is very low, so the bleeding risk of anticoagulation outweighs any benefit. NICE NG196 advises against offering stroke prevention therapy to people aged under 65 with AF and no risk factors other than their sex. The same score applies whether AF is paroxysmal, persistent or permanent, because stroke risk depends on the risk factors, not the pattern. NICE advises considering anticoagulation in men with a score of 1 and offering it to anyone with a score of 2 or more, with a DOAC as first choice. Aspirin is not recommended for stroke prevention in AF at any score, because it is less effective and still causes bleeding. Stroke risk should be reassessed when he turns 65 or if he develops hypertension, diabetes, heart failure or vascular disease. Bleeding risk is assessed with ORBIT, which NICE now prefers to HAS-BLED. Symptom control with rate or rhythm treatment is a separate decision.

Key clue
Male, under 65, no comorbidity
What it means
CHA₂DS₂-VASc = 0
What to do
No stroke-prevention therapy

Why the other options are less appropriate

  • A Aspirin is not recommended for AF stroke prevention. It gives little protection while still increasing bleeding risk.
  • B A DOAC such as apixaban is first choice when anticoagulation is indicated, but it is not offered at a score of 0.
  • C Clopidogrel, like other antiplatelet monotherapy, is not an effective or recommended way to prevent stroke in AF.
  • E Warfarin carries bleeding risk and monitoring burden, and is not indicated when the CHA2DS2-VASc score is 0.

Source: NICE NG196: Atrial fibrillation — recommendations

That is 5 of 376. Carry on with cardiology in the practice bank, with progress tracking, flashcards and timed sessions.

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Topics covered

Show all 266 cardiology topics
  • A drug option after unsuccessful claudication exercise therapy
  • A high clinic reading without emergency features
  • A hostile abdomen changes the elective approach
  • A low peptide with continuing suspicion
  • A nondiagnostic bedside scan does not close rupture concern
  • A peptide does not classify ejection fraction
  • A raised ankle–brachial index in diabetes
  • A third anti-anginal while awaiting intervention
  • A threatened limb needs a team decision
  • A well-controlled older thiazide prescription
  • AAA assessment in an older woman
  • AAA repair strategy
  • AAA screening
  • ACE inhibition in stable angina with diabetes
  • ACE-inhibitor continuation after MI with preserved ejection fraction
  • ACE-inhibitor intolerance without angioedema
  • Acute aortic dissection
  • Acute aortic syndrome
  • Acute coronary syndromes
  • Acute myocarditis activity restriction
  • Acute pericarditis
  • Acute severe mitral regurgitation
  • Additional rate control with reduced ejection fraction
  • Adult congenital disease
  • AF during acute decompensated HF
  • Alcohol-induced cardiomyopathy
  • Alternative when both usual anti-anginal classes are unsuitable
  • Amiodarone is not routine long-term rate control
  • Amiodarone is not set-and-forget
  • An asymptomatic response to carotid sinus massage
  • An inadequate ambulatory recording
  • Andersen-Tawil syndrome
  • Angioedema changes the HFrEF pathway
  • Angiography despite symptom control when ischaemia is extensive
  • Anticoagulation after apparent rhythm resolution
  • Aortic coarctation in adulthood
  • Aortic stenosis
  • Aortic syndromes
  • Aortic valve disease
  • Aortitis
  • ARNI washout
  • Arrhythmic mitral-valve prolapse
  • Arrhythmogenic mitral-valve prolapse
  • Arrhythmogenic right-ventricular cardiomyopathy
  • Aspirin allergy after MI
  • Atrial fibrillation
  • Atrial septal defect
  • Blackout with a conduction abnormality
  • Blood pressure measurement with an irregular pulse
  • Bone scintigraphy in transthyretin cardiac amyloidosis
  • Bradyarrhythmia
  • Brief jerking during a vasovagal faint
  • Brugada syndrome
  • Bypass is not the first procedural shortcut
  • Calculate the index from the highest pressures
  • Cancer therapy-related cardiotoxicity
  • Cardiac amyloidosis
  • Cardiac memory T waves
  • Cardiac resynchronisation therapy
  • Cardiac sarcoidosis
  • Cardiac sarcoidosis evaluation
  • Catecholaminergic polymorphic ventricular tachycardia
  • Choosing a calcium-channel blocker alongside a beta-blocker
  • Chronic thromboembolic pulmonary hypertension
  • Class Ic treatment with ischaemic scar
  • Coarctation collateral flow
  • Complex coronary anatomy and team selection
  • Compression hosiery can expose occult arterial disease
  • Confirmed stage 1 in a younger adult
  • Confirming a new diagnosis
  • Confirming hypertension with ABPM
  • Congestion and the purpose of diuretics
  • Consciousness after cardiac arrest and STEMI reperfusion eligibility
  • Constrictive pericarditis
  • Continuing a beta-blocker during an acute heart-failure admission
  • Contraception counselling in ACHD
  • Coronary steal
  • Coronary vasospasm
  • Coronary–subclavian steal
  • Counselling about repeat intervention after PCI or CABG
  • De Winter ECG pattern
  • Delayed STEMI with continuing pain
  • Digoxin in sedentary non-paroxysmal AF
  • Dissection/aneurysm
  • Double-chambered right ventricle
  • Dressler syndrome
  • Early post-MI aldosterone antagonism
  • Early specialist escalation for potentially reversible severe heart failure
  • Ebstein anomaly
  • Echocardiography before rhythm control
  • Effusive-constrictive pericarditis
  • Eisenmenger physiology
  • Electrical alternans
  • Endocarditis prophylaxis in ACHD
  • Escalation after two short-acting nitrate doses
  • Fabry disease cardiomyopathy
  • Familial hypercholesterolaemia
  • Fasting for risk assessment
  • First-line arterial imaging before planned revascularisation
  • Fluids during suspected rupture transfer
  • Follow-up of severe asymptomatic valve disease
  • Fontan circulation
  • Giant-cell myocarditis
  • Growth can matter below 5.5 cm
  • Heart failure and iron deficiency
  • Heart failure referral by NT-proBNP
  • HFpEF
  • HFpEF congestion treatment
  • HFrEF
  • HFrEF disease-modifying therapy
  • High INR excursions despite acceptable TTR
  • Home oxygen is not routine HF palliation
  • Hypertension
  • Hypertension before age forty
  • Hypertension in older adults
  • Hypertension in pregnancy
  • Hypertensive emergency
  • Hypertrophic cardiomyopathy
  • ICD goals must be revisited
  • Imaging after duplex when more anatomy is needed
  • Implantable loop recorder
  • Individualising fluid advice in stable euvolaemic heart failure
  • Infective endocarditis
  • Inferior myocardial infarction
  • Inherited/acquired cardiomyopathy
  • Initial anticoagulation in acute new-onset AF
  • Inter-arm blood pressure difference
  • Inter-arm discrepancy
  • Interpreting an intermediate coronary stenosis
  • Intolerance of first-step calcium-channel blockade
  • Intramural aortic haematoma
  • Investigation after optimal angina therapy fails
  • Iron deficiency in heart failure
  • Irregular pulse and blood-pressure technique
  • Isolated systolic hypertension
  • Kidney function affects titration
  • Kounis syndrome
  • Kussmaul sign
  • Lambl excrescences
  • Left ventricular non-compaction
  • Left-ventricular non-compaction
  • Low TTR despite a normal current INR
  • Low-flow low-gradient aortic stenosis
  • Markedly raised cholesterol without obvious familial history
  • Mechanical-valve anticoagulation
  • Mid-ventricular Takotsubo syndrome
  • MINOCA diagnostic pathway
  • Missing valve disease because ECG is normal
  • Mitral valve disease
  • Monitoring infrequent suspected paroxysmal AF
  • Multivessel STEMI with cardiogenic shock: extent of index PCI
  • Murmur and a quiet second sound
  • Murmur with exertional syncope
  • Myocardial bridging
  • Natriuretic peptides cannot determine ejection fraction
  • New diabetes during effective BP treatment
  • Next combination step
  • No chemical sympathectomy shortcut
  • No third anti-anginal when symptoms are controlled
  • Non-healing wound and weak pulses are a cardiovascular warning
  • Observation after restarting a beta-blocker in hospital
  • ORBIT assessment of anticoagulant bleeding risk
  • Pain persists after successful revascularisation
  • Papillary fibroelastoma
  • Paradoxical low-flow, low-gradient aortic stenosis
  • Patent ductus arteriosus
  • PCI when CABG is not appropriate
  • Pericardial effusion
  • Pericardial tamponade physiology
  • Pericarditis/tamponade
  • Peripartum cardiomyopathy
  • Persistent chest pain after treatment needs diagnostic review
  • Persistent clinical suspicion despite low natriuretic peptide
  • PFO/cryptogenic stroke
  • Post-dissection surveillance
  • Posterior myocardial infarction
  • Postural symptoms change the target
  • Potassium-containing salt substitutes with RAAS blockade
  • Pre-excitation and atrial fibrillation
  • Pre-exertional use of prescribed short-acting nitrate
  • Pregnancy planning and statins
  • Pregnancy risk stratification (mWHO)
  • Primary aldosteronism screening
  • Primary mitral regurgitation
  • Primary stenting has an anatomical exception
  • Primary-prevention offer
  • Primary/secondary hypertension
  • Prosthetic valve thrombosis
  • Prosthetic-valve dysfunction
  • Prosthetic-valve endocarditis with abscess
  • Pseudoresistant hypertension
  • Pulsus bisferiens
  • Pulsus paradoxus
  • Rate-control drug choice
  • Reassessing AF stroke risk after a new diagnosis
  • Recording serial clinic blood pressures
  • Recording syncope occurring every 10 days
  • Recurrent pericarditis
  • Referral urgency for a newly found large AAA
  • Renal denervation evidence
  • Renal liaison during HFrEF optimisation
  • Renovascular hypertension
  • Resistant hypertension
  • Resistant hypertension and potassium
  • Resistant hypertension with potassium above 4.5
  • Response to primary-prevention statin
  • Restrictive cardiomyopathy
  • Review after changing an anti-anginal
  • Reviewing beta-blocker need beyond one year after MI
  • Rheumatic mitral stenosis and atrial fibrillation
  • Rhythm restoration with uncertain duration
  • Risk below 10% is not an absolute prohibition
  • Risk tools in established CVD
  • Ruptured AAA
  • Same-day referral for accelerated hypertension
  • Scimitar syndrome
  • Secondary hypertension
  • Secondary prevention irrespective of baseline lipid
  • Secondary-prevention biochemical target
  • Selecting a pill-in-the-pocket strategy
  • Severe asymptomatic BP without organ damage
  • Severe symptoms with a murmur
  • Sexual activity following uncomplicated MI
  • Shock after infarction
  • Short QT syndrome
  • Sinus rhythm after ablation
  • Spontaneous coronary artery dissection
  • Stable coronary disease
  • Stage 1 plus target-organ damage
  • Standardising ultrasound diameter
  • STEMI reperfusion clock
  • Stroke prevention
  • Stroke prevention in atrial flutter
  • Suggestive orthostatic symptoms with normal initial measurements
  • Supervised exercise before intervention for claudication
  • Surveillance interval in uncomplicated mild aortic stenosis
  • Suspected endoleak after EVAR
  • Suspected outflow obstruction before an exercise test
  • Switching after beta-blocker intolerance
  • Syncope after stopping exercise
  • Tachyarrhythmia
  • Tachycardia-induced cardiomyopathy
  • Takotsubo syndrome
  • The selected role of tilt testing in recurrent reflex syncope
  • Timing echocardiography in new acute heart failure
  • TOE-guided elective cardioversion
  • Transfer after vascular acceptance
  • Transition of care in ACHD
  • Transposition of the great arteries (atrial switch)
  • Traumatic aortic injury
  • Type 1 diabetes and prevention
  • Type 2 endoleak with sac expansion
  • Type 2 myocardial infarction
  • Uncontrolled treatment is not yet resistant hypertension
  • Uninterpretable transthoracic echocardiogram
  • Upstream glycoprotein inhibitor
  • Uraemic pericarditis
  • Vein conduit is more than a technical afterthought
  • Ventricular arrhythmia in long-QT syndrome
  • Ventricular septal defect
  • Very high natriuretic peptide
  • Very low peptide in acute breathlessness
  • Warfarin maintenance TTR
  • Wellens pattern
  • White-coat and masked hypertension
  • Wide-complex tachycardia

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