Topics of cardiology medicine davidson

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Davidson's is not in the library, so I'll give you the complete cardiology topics from Davidson's Principles & Practice of Medicine (23rd edition) from my knowledge, along with notes from the available cardiology textbooks.

Cardiology Topics in Davidson's Principles & Practice of Medicine

Davidson's covers cardiology in Chapter 16: Cardiovascular Disease. Below are all the major topics:

1. Clinical Examination of the Cardiovascular System

History taking: chest pain, dyspnoea, palpitations, syncope, oedema
Pulse: rate, rhythm, character, volume, radio-femoral delay
Jugular venous pressure (JVP) and waveforms (a, c, v waves)
Precordial examination: apex beat, thrills, heaves
Heart sounds: S1, S2, S3, S4
Murmurs: systolic, diastolic, continuous

2. Investigations in Cardiology

ECG: sinus rhythm, axis, P wave, PR interval, QRS, ST segment, T waves
Chest X-ray: cardiac silhouette, pulmonary vasculature, cardiomegaly
Echocardiography: transthoracic (TTE), transoesophageal (TOE)
Exercise (stress) testing
Cardiac CT and MRI
Coronary angiography and cardiac catheterization
Nuclear imaging: radionuclide ventriculography, myocardial perfusion scanning
Ambulatory ECG monitoring (Holter)
Electrophysiology studies
Biomarkers: troponin, BNP/NT-proBNP, CK-MB, D-dimer

3. Cardiac Arrhythmias

Sinus node dysfunction (sick sinus syndrome)
Supraventricular tachycardias (SVT): AVNRT, AVRT, atrial flutter
Atrial fibrillation (AF): classification, CHA₂DS₂-VASc score, anticoagulation, rate vs rhythm control
Ventricular tachycardia (VT) and ventricular fibrillation (VF)
Heart block: 1st, 2nd (Mobitz I/II), 3rd degree (complete)
Bundle branch blocks: LBBB, RBBB
Pre-excitation syndromes: Wolff-Parkinson-White (WPW)
Torsades de pointes
Management: antiarrhythmics, DC cardioversion, ablation, pacemakers, ICD

4. Heart Failure

Definition, types: HFrEF vs HFpEF
Causes: ischaemic, hypertensive, valvular, dilated cardiomyopathy
Pathophysiology: neurohormonal activation (RAAS, sympathetic)
NYHA functional classification (I-IV)
Investigations: BNP/NT-proBNP, echocardiography
Acute heart failure: pulmonary oedema, cardiogenic shock - management
Chronic heart failure management: ACE inhibitors/ARBs/ARNIs (sacubitril-valsartan), beta-blockers, mineralocorticoid antagonists, SGLT2 inhibitors, diuretics
Cardiac resynchronisation therapy (CRT), ICD
Cardiac transplantation

5. Coronary Artery Disease (Ischaemic Heart Disease)

Atherosclerosis: pathogenesis, risk factors (Framingham)
Stable angina: diagnosis, investigation, management (nitrates, beta-blockers, CCBs, revascularisation - PCI vs CABG)
Acute Coronary Syndromes (ACS):
- Unstable angina (UA)
- NSTEMI: ECG changes, troponin, GRACE score, management
- STEMI: reperfusion (primary PCI vs thrombolysis), adjunct therapy (aspirin, P2Y12 inhibitors, anticoagulation)
Post-MI complications: ventricular septal defect, papillary muscle rupture, free wall rupture, pericarditis (Dressler's syndrome), ventricular aneurysm
Secondary prevention: statins, antiplatelet agents, ACE inhibitors, beta-blockers

6. Hypertension

Definition (JNC/ESC/BHS guidelines: ≥140/90 mmHg)
Primary (essential) vs secondary hypertension
Causes of secondary hypertension: renal artery stenosis, primary hyperaldosteronism, phaeochromocytoma, Cushing's syndrome, coarctation of the aorta
End-organ damage: LVH, retinopathy, nephropathy, stroke
Hypertensive urgency and emergency (malignant hypertension)
Management: lifestyle modification; pharmacotherapy - ACE inhibitors, ARBs, CCBs, thiazide diuretics, alpha-blockers, beta-blockers

7. Valvular Heart Disease

Mitral stenosis: rheumatic fever, symptoms, Austin Flint murmur, mitral facies, mitral valvotomy/replacement
Mitral regurgitation: acute vs chronic, causes (MVP, rheumatic, ischaemic), management
Mitral valve prolapse (Barlow's disease)
Aortic stenosis: causes (bicuspid valve, calcific, rheumatic), symptoms triad (angina, syncope, dyspnoea), gradient, valve replacement (SAVR vs TAVR/TAVI)
Aortic regurgitation: causes, Corrigan's pulse, water hammer pulse, de Musset's sign, Quincke's sign, management
Tricuspid and pulmonary valve disease
Antibiotic prophylaxis for infective endocarditis

8. Infective Endocarditis

Duke criteria (major and minor)
Organisms: Streptococcus viridans, Staphylococcus aureus (IVDU), HACEK organisms
Complications: emboli, abscess, heart failure, mycotic aneurysm
Management: antibiotics (benzylpenicillin + gentamicin), surgery indications
Prophylaxis: current guidelines

9. Cardiomyopathies

Dilated cardiomyopathy (DCM): causes (alcohol, viral, idiopathic), management
Hypertrophic cardiomyopathy (HCM): LVOT obstruction, sudden cardiac death, family screening, management (disopyramide, myomectomy, alcohol septal ablation, ICD)
Restrictive cardiomyopathy: causes (amyloidosis, haemochromatosis, sarcoidosis)
Arrhythmogenic right ventricular cardiomyopathy (ARVC)
Takotsubo (stress) cardiomyopathy
Peripartum cardiomyopathy

10. Pericardial Disease

Acute pericarditis: causes, ECG changes (saddle-shaped ST elevation), management (NSAIDs + colchicine)
Pericardial effusion and cardiac tamponade: Beck's triad, pulsus paradoxus, pericardiocentesis
Constrictive pericarditis: causes (TB, post-surgical), features (Kussmaul's sign), pericardiectomy

11. Congenital Heart Disease

Acyanotic defects:
- Atrial septal defect (ASD): ostium secundum, primum; fixed split S2
- Ventricular septal defect (VSD): most common CHD; Eisenmenger's syndrome
- Patent ductus arteriosus (PDA): machinery murmur; indomethacin
- Pulmonary stenosis
- Coarctation of the aorta
Cyanotic defects (right-to-left shunts):
- Tetralogy of Fallot (ToF): 4 features, boot-shaped heart, Blalock-Taussig shunt
- Transposition of the great arteries (TGA)
- Total anomalous pulmonary venous drainage (TAPVD)
- Truncus arteriosus
- Ebstein's anomaly
Eisenmenger's syndrome

12. Diseases of the Aorta and Peripheral Vasculature

Aortic aneurysm: abdominal (AAA) and thoracic; screening; rupture risk; endovascular repair (EVAR)
Aortic dissection: Stanford (Type A, B) and DeBakey classification; D-dimer; CT aortogram; management
Peripheral arterial disease: ankle-brachial index (ABI), intermittent claudication, critical ischaemia, revascularisation
Acute limb ischaemia: 6 Ps (pain, pallor, paraesthesia, paralysis, pulselessness, perishingly cold)
Venous thromboembolism (DVT and PE): Wells score, D-dimer, anticoagulation (DOAC/heparin), thrombolysis for massive PE

13. Pulmonary Hypertension

WHO classification (Groups 1-5)
Investigations: ECHO, right heart catheterisation (gold standard)
Management: endothelin antagonists (bosentan), PDE-5 inhibitors (sildenafil), prostacyclins (epoprostenol), anticoagulation, lung transplantation

14. Cardiac Tumours

Myxoma (most common primary cardiac tumour - left atrium)
Metastatic tumours (most common overall)
Rhabdomyoma (associated with tuberous sclerosis in children)

15. Pregnancy and Heart Disease

Physiological changes in pregnancy
Management of valvular disease, arrhythmias, hypertension in pregnancy
Peripartum cardiomyopathy

Summary Table of Key Davidson's Cardiology Topics

Category	Key Topics
Symptoms & Signs	Angina, dyspnoea, syncope, JVP, murmurs
Investigations	ECG, Echo, Angiography, Biomarkers
Arrhythmias	AF, SVT, VT/VF, Heart block, WPW
Heart Failure	HFrEF/HFpEF, NYHA, medical/device therapy
IHD	Stable angina, ACS, STEMI, NSTEMI
Hypertension	Essential, Secondary, Malignant
Valvular Disease	MS, MR, AS, AR, endocarditis
Cardiomyopathies	DCM, HCM, Restrictive, ARVC, Takotsubo
Pericardial Disease	Pericarditis, Tamponade, Constrictive
Congenital HD	ASD, VSD, ToF, TGA, Eisenmenger
Aorta & Vessels	Aneurysm, Dissection, PAD, DVT/PE
Pulmonary HTN	Groups 1-5, targeted therapy

Davidson's cardiology chapter is one of the most comprehensive in any internal medicine textbook. The topics above represent all the major sections in the 23rd edition (2018). For exam purposes, highest-yield areas are typically: AF, heart failure (especially HFrEF management), ACS/STEMI, aortic stenosis, infective endocarditis (Duke criteria), and HCM sudden cardiac death risk.

Make a 40 question quiz of coronary artery disease covering every aspect of it

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Coronary Artery Disease - 40 Question Quiz

Format: Single best answer (A-E) | Answers with explanations at the end

SECTION 1: Pathophysiology & Risk Factors (Q1-8)

Q1. Which of the following is the MOST accurate description of the earliest lesion in atherosclerosis?

A) Fibrous plaque
B) Foam cell accumulation (fatty streak)
C) Calcified plaque
D) Complicated plaque with thrombus
E) Intimal hyperplasia after endothelial injury

Q2. A 52-year-old man has a 10-year ASCVD risk of 14%. His LDL is 4.1 mmol/L (158 mg/dL). He smokes 20 cigarettes/day and has a BMI of 32. Which single risk factor, if modified, would produce the GREATEST reduction in his cardiovascular risk?

A) Weight loss
B) Statin therapy
C) Smoking cessation
D) Aspirin prophylaxis
E) Blood pressure control

Q3. Which lipoprotein particle is most directly atherogenic and is the primary target of statin therapy?

A) HDL
B) VLDL
C) LDL (specifically apoB-containing particles)
D) IDL
E) Chylomicrons

Q4. A vulnerable atherosclerotic plaque most commonly ruptures at which location?

A) The central core of the lipid pool
B) The shoulder region of the fibrous cap
C) The adventitia overlying the plaque
D) Areas of calcification within the plaque
E) The media of the coronary artery

Q5. Which of the following is a NON-modifiable risk factor for coronary artery disease?

A) Hypertension
B) Dyslipidaemia
C) Diabetes mellitus
D) Family history of premature CAD (first-degree relative <55M / <65F)
E) Obesity

Q6. Diabetes mellitus increases the risk of CAD primarily through which mechanism?

A) Direct myocardial toxicity of insulin
B) Endothelial dysfunction, advanced glycation end-products, and accelerated atherogenesis
C) Increased platelet count
D) Coronary artery vasospasm
E) Reduced fibrinolysis only

Q7. Which of the following inflammatory markers is an independent risk factor for CAD and is used in the Reynolds Risk Score?

A) ESR
B) Interleukin-6
C) High-sensitivity C-reactive protein (hsCRP)
D) Ferritin
E) TNF-alpha

Q8. The JUPITER trial demonstrated cardiovascular benefit of rosuvastatin in patients with:

A) High LDL and established CAD
B) Normal LDL but elevated hsCRP (>2 mg/L)
C) Familial hypercholesterolaemia
D) Hypertriglyceridaemia only
E) Diabetes with CKD

SECTION 2: Stable Angina (Q9-14)

Q9. A 62-year-old man develops central chest tightness on walking uphill that resolves within 3 minutes of rest. This most accurately describes:

A) Unstable angina
B) Prinzmetal's (vasospastic) angina
C) Chronic stable angina (CCS Class II)
D) NSTEMI
E) Musculoskeletal chest pain

Q10. According to the Canadian Cardiovascular Society (CCS) classification, angina that occurs with ordinary activity such as walking >2 blocks on the level or climbing >1 flight of stairs is classified as:

A) CCS Class I
B) CCS Class II
C) CCS Class III
D) CCS Class IV
E) CCS Class V

Q11. A patient with stable angina is started on sublingual glyceryl trinitrate (GTN). Which mechanism explains its anti-anginal effect?

A) Increased heart rate
B) Coronary vasoconstriction
C) Venodilation reducing preload, and arterial dilation reducing afterload
D) Negative chronotropy via beta-1 blockade
E) Direct myocardial oxygen consumption increase

Q12. For a patient with stable angina, which first-line pharmacological agent has been shown to improve prognosis (reduce MI and death) in addition to relieving symptoms?

A) Long-acting nitrate
B) Ranolazine
C) Ivabradine
D) Beta-blocker
E) Amlodipine (dihydropyridine CCB)

Q13. Exercise stress testing in a patient with stable angina shows 2 mm horizontal ST depression in leads V4-V6 at 4 METs. This is considered:

A) A normal test result
B) A low-risk result
C) A high-risk result requiring urgent coronary angiography
D) A positive test but warrants only repeat testing
E) Non-diagnostic due to insufficient heart rate

Q14. A 67-year-old woman has stable angina with triple-vessel disease and reduced LV function (EF 35%). The most appropriate revascularisation strategy is:

A) Medical therapy alone
B) Percutaneous coronary intervention (PCI) with drug-eluting stents
C) Coronary artery bypass grafting (CABG)
D) Transmyocardial laser revascularisation
E) Enhanced external counterpulsation

SECTION 3: Acute Coronary Syndromes (ACS) (Q15-24)

Q15. A 58-year-old man presents with 45 minutes of crushing chest pain radiating to his left arm. His ECG shows ST elevation in leads II, III, and aVF with reciprocal ST depression in I and aVL. Which coronary artery is most likely occluded?

A) Left anterior descending (LAD)
B) Left circumflex (LCx)
C) Right coronary artery (RCA)
D) Left main stem
E) Ramus intermedius

Q16. In STEMI, the current gold standard treatment and the preferred reperfusion strategy is:

A) Thrombolysis with alteplase within 12 hours
B) Primary PCI within 90 minutes of first medical contact (or within 120 minutes if transfer required)
C) Emergency CABG in all cases
D) IV heparin infusion alone
E) Fondaparinux and watchful waiting

Q17. A patient with STEMI arrives at a non-PCI-capable hospital. PCI cannot be performed within 120 minutes of first medical contact. Thrombolysis is administered. After 90 minutes, the patient has persistent ST elevation >50% and ongoing chest pain. What is the next step?

A) Repeat thrombolysis
B) Emergency rescue PCI
C) IV amiodarone for presumed arrhythmia
D) IABP insertion
E) Conservative management with IV heparin

Q18. Which ECG finding in STEMI indicates posterior MI and warrants posterior leads (V7-V9)?

A) ST elevation in V1-V4
B) Tall R waves and ST depression in V1-V3
C) Q waves in aVL
D) ST elevation in aVR
E) Right bundle branch block

Q19. A 70-year-old woman presents with chest pain and her ECG shows new LBBB. Troponin I is elevated at 2.8 ng/mL. The most appropriate diagnosis and management is:

A) NSTEMI - conservative management
B) STEMI equivalent - urgent primary PCI
C) Unstable angina - medical management only
D) Pericarditis - NSAIDs and colchicine
E) Takotsubo cardiomyopathy - supportive care

Q20. In NSTEMI, the GRACE score is used to predict:

A) Bleeding risk from anticoagulation
B) 6-month mortality risk and guide timing of angiography
C) Likelihood of re-infarction
D) Response to thrombolytic therapy
E) Need for CABG versus PCI

Q21. A patient with NSTEMI and a GRACE score >140 should undergo coronary angiography within:

A) 24 hours (early invasive strategy)
B) 72 hours
C) 1 week
D) Immediately on admission (within 2 hours)
E) Only if medical therapy fails

Q22. Which of the following is an absolute contraindication to thrombolytic therapy in STEMI?

A) Age >75 years
B) Haemorrhagic stroke at any time in the past
C) Uncontrolled hypertension (BP 160/100)
D) Active menstruation
E) Prior CABG >1 year ago

Q23. Dual antiplatelet therapy (DAPT) after ACS with PCI using a drug-eluting stent (DES) typically consists of aspirin plus a P2Y12 inhibitor for:

A) 1 month
B) 3 months
C) 6 months
D) 12 months (minimum)
E) Indefinitely with no stopping point

Q24. A 55-year-old man with STEMI develops sudden hypotension, elevated JVP, clear lung fields, and ST elevation in inferior leads. The right-sided ECG shows ST elevation in V4R. The diagnosis is:

A) Left ventricular free wall rupture
B) Acute mitral regurgitation from papillary muscle rupture
C) Right ventricular infarction
D) Ventricular septal defect (post-MI VSD)
E) Cardiogenic shock from LV failure

SECTION 4: Post-MI Complications (Q25-28)

Q25. A loud pansystolic murmur appears 3-5 days after an anterior STEMI. Echocardiography shows a left-to-right shunt at the ventricular level. The most likely diagnosis is:

A) Acute mitral regurgitation
B) Aortic stenosis
C) Post-MI ventricular septal defect
D) Pericardial friction rub
E) Tricuspid regurgitation

Q26. Dressler's syndrome (post-cardiac injury syndrome) typically presents:

A) Within 24 hours of MI with ST elevation
B) 2-10 weeks after MI with fever, pleuritis, and pericarditis
C) Immediately after PCI with chest pain
D) As a late complication (>1 year) with constrictive pericarditis
E) With Kussmaul's sign and equalization of diastolic pressures

Q27. A patient develops sudden-onset pulmonary oedema 5 days after an inferior MI. Echo shows severe mitral regurgitation with a flail leaflet. The most likely cause is:

A) Rheumatic mitral valve disease
B) Posterior papillary muscle rupture (supplied by RCA/LCx)
C) Mitral valve prolapse
D) Anterior papillary muscle rupture
E) Infective endocarditis

Q28. A ventricular aneurysm developing after anterior MI is most commonly associated with:

A) Intermittent fever and night sweats
B) Persistent ST elevation on ECG, thrombus formation, and ventricular arrhythmias
C) Loud systolic murmur at the lower sternal border
D) Pulsus paradoxus
E) Elevated JVP with Kussmaul's sign

SECTION 5: Secondary Prevention & Long-Term Management (Q29-33)

Q29. Which of the following four drug classes have demonstrated mortality reduction in post-MI patients with reduced ejection fraction (HFrEF)?

A) Nitrates, digoxin, calcium channel blockers, aspirin
B) Beta-blockers, ACE inhibitors/ARBs, mineralocorticoid antagonists, SGLT2 inhibitors
C) Statins, beta-blockers, loop diuretics, aspirin
D) ACE inhibitors, fibrates, amiodarone, ivabradine
E) ARBs, nitrates, diuretics, antiplatelet agents

Q30. In patients with stable CAD, which statin intensity is recommended and what is the LDL target for very-high-risk patients (established ASCVD)?

A) Low-intensity statin; LDL <3.0 mmol/L
B) Moderate-intensity statin; LDL <2.6 mmol/L
C) High-intensity statin (e.g. atorvastatin 40-80 mg); LDL <1.4 mmol/L (<55 mg/dL)
D) Any statin; LDL <2.0 mmol/L
E) No specific LDL target; treat based on risk score alone

Q31. Ezetimibe and PCSK9 inhibitors (e.g. evolocumab, alirocumab) are used in patients with CAD who:

A) Have LDL <1.0 mmol/L on statin
B) Cannot tolerate aspirin
C) Do not achieve LDL target on maximally tolerated statin therapy
D) Have TG >5 mmol/L
E) Have elevated Lp(a) only

Q32. Which intervention is most effective in reducing all-cause mortality in post-MI patients with EF <35% who have survived a haemodynamically significant VT/VF?

A) Amiodarone
B) Implantable cardioverter-defibrillator (ICD)
C) Cardiac resynchronisation therapy (CRT)
D) Catheter ablation of VT circuit
E) Beta-blocker dose escalation

Q33. Cardiac rehabilitation after MI has been shown to:

A) Increase re-infarction rate
B) Have no effect on mortality
C) Reduce cardiovascular mortality by approximately 20-25% and improve functional capacity
D) Be contraindicated in patients post-PCI
E) Only benefit patients with EF >50%

SECTION 6: Special Scenarios, Investigations & Pharmacology (Q34-40)

Q34. Prinzmetal's (vasospastic) angina is characterised by:

A) ST depression during episodes occurring at rest
B) Transient ST elevation at rest, usually in the early morning hours, due to coronary vasospasm
C) Fixed stenosis on angiography with reproducible exertional symptoms
D) Normal ECG during all episodes
E) Association with hyperlipidaemia as the primary cause

Q35. A 45-year-old woman with no cardiac history presents with ACS. Coronary angiography reveals smooth coronary arteries with no obstructive disease. CT shows a linear filling defect in the LAD. The most likely diagnosis is:

A) Plaque erosion without obstructive disease
B) Spontaneous coronary artery dissection (SCAD)
C) Coronary artery spasm
D) Myocarditis
E) Takotsubo cardiomyopathy

Q36. A patient on clopidogrel after PCI is found to be a CYP2C19 poor metaboliser. The clinical implication is:

A) Increased risk of bleeding from excessive drug effect
B) Reduced conversion to active metabolite, leading to inadequate platelet inhibition and higher thrombotic risk
C) Faster onset of action requiring dose reduction
D) No clinical significance; clopidogrel is not a prodrug
E) Increased efficacy of clopidogrel in this group

Q37. Which of the following antiplatelet agents acts by irreversibly blocking the P2Y12 ADP receptor and has a faster onset of action than clopidogrel?

A) Aspirin
B) Dipyridamole
C) Ticagrelor (note: ticagrelor is reversible; prasugrel is irreversible and faster than clopidogrel)
D) Prasugrel
E) Cangrelor

Q38. Fractional flow reserve (FFR) measurement during coronary angiography is used to:

A) Measure LV ejection fraction during the procedure
B) Assess the haemodynamic significance of an intermediate coronary stenosis (typically 40-70%) to guide PCI
C) Detect coronary artery spasm
D) Quantify myocardial scar tissue
E) Replace echocardiography for valve assessment

Q39. A patient with ACS is started on ticagrelor. Which side effect unique to ticagrelor (not seen with clopidogrel or prasugrel) should be counselled about?

A) Thrombocytopenia
B) Rash and urticaria
C) Dyspnoea (not related to heart failure, often benign and self-limiting)
D) Hepatotoxicity
E) Peripheral neuropathy

Q40. The ISCHEMIA trial (2019-2020) changed management of stable CAD by demonstrating that:

A) All patients with stable CAD should undergo immediate revascularisation
B) In patients with stable CAD and moderate-to-severe ischaemia, routine invasive strategy did NOT reduce death or MI compared to optimal medical therapy alone
C) PCI is superior to CABG in all stable CAD patients
D) CABG should be avoided in patients >70 years
E) DAPT for 3 years reduces MI in stable CAD

ANSWERS WITH EXPLANATIONS

Q1. B - Fatty streaks (foam cells = lipid-laden macrophages) are the earliest visible lesion. They appear in the intima and are present even in young adults and children.

Q2. C - Smoking cessation produces the single largest reduction in CVD risk. Within 1 year of quitting, excess coronary risk is halved.

Q3. C - LDL (via apoB-containing particles) penetrates the arterial intima and is oxidised, driving foam cell formation. Statins reduce LDL by inhibiting HMG-CoA reductase.

Q4. B - Plaque rupture occurs at the shoulder region where the fibrous cap is thinnest and macrophage activity (MMP secretion) is highest.

Q5. D - Family history of premature CAD is non-modifiable. All others (HTN, dyslipidaemia, DM, obesity) can be treated or modified.

Q6. B - Diabetes drives atherosclerosis through endothelial dysfunction, advanced glycation end-products (AGEs), oxidative stress, and pro-inflammatory pathways.

Q7. C - hsCRP is the inflammatory marker incorporated into the Reynolds Risk Score and validated as an independent CVD predictor. The JUPITER trial used hsCRP >2 mg/L as a selection criterion.

Q8. B - JUPITER enrolled patients with LDL <3.4 mmol/L but hsCRP ≥2 mg/L and showed rosuvastatin 20 mg significantly reduced CV events vs placebo.

Q9. C - Classic stable angina: predictable, exertional, relieved within 5 minutes of rest or GTN. CCS Class II = slight limitation of ordinary activity.

Q10. B - CCS Class II: angina with ordinary activity (walking >2 blocks on level, >1 flight of stairs). Class I = only with strenuous activity. Class III = marked limitation. Class IV = rest angina.

Q11. C - GTN causes venodilation (reducing preload/wall stress) and some arterial dilation. This reduces myocardial O2 demand. It does NOT increase HR (it can reflexively increase HR slightly if BP drops).

Q12. D - Beta-blockers are the only anti-anginals with proven prognostic benefit (mortality reduction) in CAD, especially post-MI. Nitrates, CCBs, ranolazine, and ivabradine are purely symptom-relieving.

Q13. C - High-risk features on exercise testing: ST depression ≥2 mm, at low workload (<5 METs or Bruce Stage 2), widespread leads, ST depression lasting >5 min in recovery, hypotension during exercise, VT.

Q14. C - CABG is superior to PCI in triple-vessel disease with reduced LV function (EF <35%), as demonstrated by the SYNTAX and STICH trials. PCI has higher rates of incomplete revascularisation in this group.

Q15. C - ST elevation in II, III, aVF = inferior STEMI = RCA occlusion in ~80% of cases. Reciprocal changes in I and aVL confirm inferior distribution.

Q16. B - Primary PCI is the gold standard. The target is door-to-balloon (or first medical contact to balloon) within 90 minutes at a PCI centre, or within 120 minutes if transfer is needed.

Q17. B - Failed thrombolysis (defined as <50% ST resolution at 90 min + ongoing symptoms) requires emergency rescue PCI. Re-thrombolysis is NOT recommended.

Q18. B - Posterior MI shows reciprocal changes anteriorly: tall broad R waves (= posterior Q waves reflected) and horizontal ST depression in V1-V3. Confirm with posterior leads V7-V9 showing ST elevation.

Q19. B - New LBBB with a clinical presentation of ACS and elevated troponin = STEMI equivalent requiring urgent primary PCI, per ESC/ACC/AHA guidelines (Sgarbossa criteria can help confirm ischaemia within LBBB).

Q20. B - The GRACE (Global Registry of Acute Coronary Events) score predicts 6-month all-cause mortality and guides timing of invasive strategy: >140 = high risk, early invasive (<24h); 109-140 = intermediate (<72h).

Q21. A - ESC 2020 ACS guidelines: GRACE score >140 = high risk = early invasive strategy within 24 hours. Immediate PCI (<2h) is reserved for very high risk (refractory ischaemia, haemodynamic instability, life-threatening arrhythmia, STEMI).

Q22. B - Absolute contraindications to thrombolysis include: haemorrhagic stroke ever, ischaemic stroke <6 months, CNS neoplasm, recent major surgery/trauma (<3 weeks), active internal bleeding, suspected aortic dissection. Age >75 is a relative contraindication only.

Q23. D - Standard DAPT after ACS + DES = aspirin + P2Y12 inhibitor (ticagrelor or prasugrel preferred) for at least 12 months. Can be modified based on bleeding vs ischaemic risk assessment (PRECISE-DAPT, DAPT score).

Q24. C - RV infarction: triad of hypotension + elevated JVP + clear lung fields in inferior STEMI. ST elevation in V4R is the key diagnostic finding. Management: IV fluids (preload dependent), avoid nitrates/diuretics.

Q25. C - Post-MI VSD: occurs 3-5 days after MI (earlier with thrombolysis), causes a new harsh pansystolic murmur with left-to-right shunt. Echo with colour Doppler is diagnostic. Carries high mortality; requires surgical repair or catheter-based closure.

Q26. B - Dressler's syndrome (post-cardiac injury syndrome) occurs 2-10 weeks post-MI due to autoimmune pericarditis. Features: fever, pleuritic chest pain, pericardial/pleural effusion. Treat with NSAIDs + colchicine; avoid corticosteroids if possible.

Q27. B - Posterior papillary muscle has single blood supply (from RCA/LCx) making it more vulnerable to infarction than the anterior papillary muscle (dual supply from LAD + LCx). Rupture causes acute severe MR.

Q28. B - LV aneurysm after anterior MI: persistent ST elevation (even weeks later), risk of mural thrombus (anticoagulate), ventricular tachycardia, and reduced EF. Distinct from pseudoaneurysm (contained rupture).

Q29. B - The four pillars of HFrEF post-MI management with mortality benefit: beta-blockers (carvedilol, bisoprolol), ACE inhibitors/ARBs (or ARNI if stable), mineralocorticoid antagonists (spironolactone/eplerenone), and SGLT2 inhibitors (empagliflozin/dapagliflozin per recent trials - EMPEROR-Reduced, DAPA-HF).

Q30. C - ESC 2019/2021 Dyslipidaemia Guidelines: very-high-risk patients (established ASCVD) require high-intensity statin AND LDL target <1.4 mmol/L (<55 mg/dL) with ≥50% LDL reduction from baseline. If ACS within 2 years: target <1.0 mmol/L.

Q31. C - Ezetimibe (IMPROVE-IT trial) and PCSK9 inhibitors (FOURIER, ODYSSEY trials) are added when maximal statin therapy fails to achieve LDL targets. PCSK9 inhibitors reduce MACE by ~15% on top of statin therapy.

Q32. B - ICD is superior to amiodarone for secondary prevention of SCD in patients with haemodynamically significant VT/VF and EF <35% (AVID, CASH, CIDS trials). Amiodarone does not reduce all-cause mortality in this group.

Q33. C - Multiple meta-analyses show cardiac rehabilitation reduces CV mortality by ~20-25%, reduces hospital readmissions, improves exercise capacity, QoL, and risk factor profile. It is underutilised globally.

Q34. B - Prinzmetal's angina: ST elevation (not depression) during episodes at rest (often 2-4 AM), due to focal coronary artery spasm on angiographically normal or near-normal arteries. Treat with CCBs (verapamil/diltiazem) and long-acting nitrates. Beta-blockers may worsen spasm.

Q35. B - SCAD predominantly affects young women, often peripartum or with fibromuscular dysplasia. Angiography shows a radiolucent intimal flap or linear filling defect. Conservative management preferred (PCI has high failure rates in SCAD).

Q36. B - Clopidogrel is a prodrug requiring CYP2C19 activation. Poor metabolisers (10-15% of Caucasians, higher in Asians) cannot activate it adequately, resulting in reduced antiplatelet effect and higher stent thrombosis risk. Switch to prasugrel or ticagrelor.

Q37. D - Prasugrel is an irreversible P2Y12 blocker with faster onset and more consistent platelet inhibition than clopidogrel (not a prodrug requiring as many metabolic steps). Ticagrelor is reversible and also faster than clopidogrel but is NOT irreversible - so D is the best answer here.

Q38. B - FFR ≤0.80 indicates haemodynamically significant stenosis requiring PCI. FFR >0.80 = defer PCI (DEFER, FAME, FAME-2 trials). It is the physiological gold standard for intermediate lesion assessment.

Q39. C - Ticagrelor's unique side effects: dyspnoea (in ~15%, benign, often resolves spontaneously - mechanism unclear, possibly adenosine-mediated) and ventricular pauses (especially in first week). Neither is seen with clopidogrel or prasugrel.

Q40. B - ISCHEMIA trial (NEJM 2020, n=5,179): in stable CAD with moderate-to-severe ischaemia on stress testing, routine invasive management (angiography + revascularisation) did NOT reduce death or MI vs optimal medical therapy over ~3.2 years. This was a landmark finding that shifted practice towards conservative management for stable CAD.

Quiz Summary by Section

Section	Questions	Focus
Pathophysiology & Risk Factors	Q1-8	Atherogenesis, risk scoring, lipids
Stable Angina	Q9-14	CCS class, anti-anginals, revascularisation
Acute Coronary Syndromes	Q15-24	STEMI, NSTEMI, UA, reperfusion
Post-MI Complications	Q25-28	VSD, MR, RV infarct, aneurysm, Dressler's
Secondary Prevention	Q29-33	Pharmacotherapy, ICD, rehab, LDL targets
Special Scenarios & Pharm	Q34-40	SCAD, vasospasm, drug mechanisms, ISCHEMIA trial

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