Ischaemic and valvular heart disease
Coronary, valvular, structural and congenital heart disease; heart failure
Heart disease questions link a time course or a murmur to a structural change. Know how an infarct evolves and fails, what each valve lesion does to the chambers and lungs, the main cardiomyopathies and congenital defects, and how echo, MRI and the chest film show them.
Ischaemic heart disease: mechanisms
- Stable angina: a fixed stenosis (often over 70%) exhausts coronary flow reserve, so pain appears only when demand rises. Thick-capped plaque.
- Acute coronary syndrome: rupture of a thin-capped plaque with thrombosis.
- Vasospastic (Prinzmetal) angina: rest pain in the early morning, transient ST elevation, normal angiogram; avoid non-selective β-blockers (unopposed α vasoconstriction).
- Adenosine stress imaging dilates normal arterioles and steals flow from the territory beyond a stenosis; caffeine blocks it.
- Aortic stenosis with heavy hypertrophy causes angina with normal coronaries (high demand, compressed subendocardial flow).
- Other causes of infarction without atheroma: takotsubo (catecholamine stunning, ballooned apex), spontaneous coronary dissection (young, often postpartum women), allograft vasculopathy (diffuse concentric narrowing; denervated heart, so no angina).
- Stunned myocardium recovers after reperfusion; hibernating myocardium recovers after revascularisation of a chronic stenosis and shows no late enhancement on MRI.
Evolution of an infarct
| Time | Microscopy | Clinical correlate |
|---|---|---|
| 0–24 h | Wavy fibres, then coagulative necrosis (outlines kept, nuclei lost) | Arrhythmias, sudden death |
| 1–3 days | Neutrophils | Fibrinous pericarditis |
| 3–7 days | Macrophages; wall softest | Rupture of papillary muscle, septum or ventricular wall |
| 7–14 days | Granulation tissue from the margins inwards | — |
| Weeks–months | Collagen scar | True aneurysm, Dressler syndrome (2–10 weeks) |
- Reperfusion produces contraction band necrosis and a haemorrhagic infarct.
- MRI late gadolinium enhancement: scar has a larger extracellular space, so gadolinium washes out slowly; infarcts enhance from the subendocardium outwards in a coronary territory. Myocarditis enhances patchily in the subepicardium; HCM in the septum.
Mechanical complications
| Complication | Key finding |
|---|---|
| Papillary muscle rupture | Acute MR, flail leaflet; the jet aimed at the right upper pulmonary vein can cause right upper lobe oedema |
| Septal rupture | New pansystolic murmur and thrill; oxygen step-up in the right ventricle |
| Ventricular wall rupture | Tamponade, electromechanical dissociation |
| True aneurysm | Wide neck, dyskinetic apex, persistent ST elevation |
| Pseudoaneurysm | Narrow neck; wall of pericardium and organised haematoma |
| RV infarction (inferior MI, RCA) | Hypotension with nitrates; needs preload |
- Lead territories: inferior II, III, aVF (RCA); anterior V1–V4 (LAD); posterior shows reciprocal ST depression with tall R waves in V1–V3.
Valve disease
- Rheumatic mitral stenosis: commonest valve lesion in Pakistan. Left atrial enlargement, AF, pulmonary venous hypertension; haemosiderin-laden macrophages (heart failure cells, Perls' positive) and, after repeated bleeds, tiny dense lung nodules (pulmonary haemosiderosis). Aschoff bodies are acute; a MacCallum plaque is chronic regurgitant jet injury on the left atrial wall.
- Mitral valve prolapse: mid-systolic click and late systolic murmur; myxomatous degeneration; linked with Marfan and hypermobility.
- Bicuspid aortic valve: ejection click and stenosis in mid life; associated with coarctation and aortic dilatation or dissection.
- Aortic regurgitation with heart block suggests ankylosing spondylitis aortitis.
- Carcinoid heart disease affects the tricuspid and pulmonary valves, only once liver metastases exist.
- Mechanical valves cause fragmentation haemolysis (schistocytes, high LDH, low haptoglobin).
Infective and non-infective endocarditis
| Setting | Valve or site | Organism or type |
|---|---|---|
| Injecting drug user | Tricuspid; septic lung emboli | *Staphylococcus aureus* |
| Damaged native valve, dental work | Mitral, aortic | Viridans streptococci |
| Small VSD | Right ventricular side of the defect (high-velocity jet) | Viridans streptococci |
| Prosthetic valve, early | Paravalvular abscess | *S. epidermidis* |
| SLE, antiphospholipid | Both surfaces of mitral leaflets, sterile | Libman–Sacks |
Cardiomyopathy and pericardium
| Condition | Basis | Imaging |
|---|---|---|
| Hypertrophic | Autosomal dominant sarcomere protein mutations; myocyte disarray | Asymmetric septal thickening (often 15 mm or more), patchy septal enhancement; athlete's heart is symmetric and regresses |
| Dilated | Alcohol, viral, peripartum, anthracycline; trastuzumab (reversible, HER2 blockade) | Dilated, globally hypokinetic LV |
| Arrhythmogenic RV | Fibrofatty replacement of RV muscle | RV dilatation, fat and scar; VT with LBBB pattern |
| Non-compaction | Arrested compaction of embryonic myocardium | Thick trabeculated inner layer |
- Constrictive pericarditis (TB in Pakistan): raised JVP rising on inspiration (Kussmaul), early diastolic knock, ascites out of proportion; pericardial calcification on the film.
- Tamponade: pericardial pressure exceeds RV diastolic pressure, so the RV collapses in early diastole; pulsus paradoxus. The commonest cardiac tumour is a metastasis (lung, breast, melanoma).
- Ruptured sinus of Valsalva aneurysm gives a sudden continuous murmur.
Congenital heart disease
- Tetralogy of Fallot: VSD, overriding aorta, RV outflow obstruction, RV hypertrophy; 'boot-shaped' heart with oligaemic lungs. Right-to-left shunting bypasses the lung filter, causing cerebral abscess and paradoxical emboli.
- Coarctation: usually just distal to the left subclavian artery near the ductus. The 'figure 3' sign (prestenotic dilatation, indentation, post-stenotic dilatation) and rib notching of ribs 3–8 from collateral intercostal arteries, usually after age 5.
- Left-to-right shunts (ASD, VSD, PDA) give plethoric lungs and may reverse (Eisenmenger).
- Congenital heart block: maternal anti-Ro antibodies; the AV node is replaced by fibrosis, so it is permanent.
- Fetal hydrops in severe anaemia is high-output failure.
Heart failure
- Low output activates sympathetic and renin–angiotensin systems, retaining salt and water.
- Chest film sequence: upper lobe venous diversion, then interstitial oedema (Kerley B lines, peribronchial cuffing), then alveolar 'bat-wing' oedema and effusions.
- Septic shock can depress the myocardium through cytokines (dilated LV, low ejection fraction).
Remember Time after MI tells the complication: arrhythmia first, rupture at 3–7 days, aneurysm and Dressler weeks later.
Exam trap A narrow neck means pseudoaneurysm (contained rupture); a wide neck means true aneurysm.
Exam trap Coagulase-negative staphylococci in a patient with a prosthetic valve are pathogens, not contaminants.
Test yourself on this topic
5 of the 55 questions in our bank on this topic. Choose an answer to see why every option is right or wrong.
A 30-year-old man has sudden chest pain and breathlessness while lifting weights, followed by a new loud continuous murmur at the lower left sternal edge. An aneurysm of the right coronary sinus has burst into the right ventricular outflow tract. What is the diagnosis?
Answer: Ruptured sinus of Valsalva aneurysm
A sinus of Valsalva aneurysm is a congenital weakness at the junction of the aortic media and the valve annulus, most often in the right coronary sinus. When it ruptures, usually into the right ventricle or right atrium, there is a sudden aorta-to-right-heart shunt. Because aortic pressure exceeds right heart pressure in both systole and diastole, the murmur is continuous. It is associated with VSD and aortic regurgitation.
Sinus of Valsalva aneurysm
- Often the right coronary sinus
- Ruptures into RV or RA
- Sudden continuous murmur
- Linked to VSD, AR
Remember A sudden continuous murmur after strain: think ruptured sinus aneurysm.
Exam trap A continuous murmur is not always a PDA; site and onset matter.
Why the other options are wrong
- Acquired ventricular septal defect Would give a pansystolic murmur and arise from the septum, not the sinus.
- Patent ductus arteriosus Gives a continuous murmur below the left clavicle and connects the aorta to the pulmonary artery.
- Coronary arteriovenous fistula Arises from a coronary artery, not the aortic sinus itself.
- Type A aortic dissection Gives tearing pain and an aortic regurgitation murmur, not a continuous one.
A 23-year-old man has palpitations and a run of ventricular tachycardia with left bundle branch block morphology. His right ventricle is dilated and contracts poorly, and his brother died suddenly while playing football. What is the underlying pathology?
Answer: Fibrofatty replacement of RV muscle
Arrhythmogenic right ventricular cardiomyopathy is usually caused by mutations in desmosome proteins such as plakophilin-2, inherited as autosomal dominant. Poor cell-to-cell adhesion leads to myocyte death and replacement by fat and fibrous tissue, mainly in the right ventricular free wall. The right ventricle dilates and contracts poorly, and the scarred muscle generates ventricular tachycardia from the right ventricle, hence the left bundle branch block pattern. It is a cause of sudden death in young people and athletes.
ARVC
- Desmosome gene mutations
- Fibrofatty replacement of RV wall
- VT with LBBB pattern
- Sudden death in young athletes
Remember Fat in a failing right ventricle: ARVC.
Exam trap Some fat in the RV wall is normal in older adults; it must go with dysfunction and scar to mean ARVC.
Why the other options are wrong
- Myocyte disarray in a thick septum Describes hypertrophic cardiomyopathy, mainly of the left ventricle.
- Amyloid deposits in both ventricles Causes thick walls, mainly in the elderly.
- Non-caseating granulomas in the septum Describes cardiac sarcoidosis.
- Lymphocytic myocarditis of the LV Affects mainly the left ventricle, without fat replacement.
A woman with a malignant pericardial effusion becomes hypotensive. The right atrium and right ventricular free wall are pushed inwards during diastole before the left-sided chambers are affected. What explains this?
Answer: Pericardial pressure exceeds RV diastolic pressure
In tamponade, fluid raises intrapericardial pressure until it exceeds the filling pressure of the thin-walled, low-pressure right heart chambers. In early diastole, right ventricular pressure is at its lowest, so the free wall is pushed inwards: right ventricular diastolic collapse. The right atrium collapses even earlier. Filling of all chambers becomes limited, stroke volume falls and pulsus paradoxus develops.
Tamponade
- Pericardial pressure rises
- Exceeds right heart filling pressure
- RA and RV collapse in diastole
- Filling falls: pulsus paradoxus
Remember The weakest, lowest-pressure chamber is squeezed first.
Exam trap A thick-walled or hypertensive right ventricle may not collapse even when tamponade is present.
Why the other options are wrong
- Right ventricular infarction weakens the wall An infarcted wall does not collapse in diastole.
- Pulmonary hypertension pushes the septum Pulmonary hypertension makes the RV thick and dilated, resisting collapse.
- Left ventricular pressure exceeds RV pressure Septal motion depends on interventricular pressures, not free-wall collapse.
- Inspiration lowers pericardial pressure Inspiration lowers intrathoracic pressure and increases right filling.
Two weeks after an inferior myocardial infarction, a 70-year-old man is found to have a false aneurysm (pseudoaneurysm) of the inferolateral left ventricular wall, joined to the cavity by a narrow neck. What forms the wall of this outpouching?
Answer: Pericardium and organised haematoma
This is a false aneurysm (pseudoaneurysm) of the left ventricle: the free wall has ruptured, but adherent pericardium and clot have contained the leak. Its wall has no myocardium, and it joins the cavity through a narrow neck. It is commoner after inferior and lateral infarcts and has a high risk of rupture, so it needs surgery. A true aneurysm is a wide-necked bulge of thinned scar, usually anterior or apical, and rarely ruptures.
False vs true LV aneurysm
- False: contained rupture
- Wall = pericardium + clot
- Narrow neck, high rupture risk
- True: wide neck, scar, anterior
Remember Narrow neck means the wall has burst and is only held by pericardium.
Exam trap A narrow neck relative to the sac separates a false aneurysm from a true one.
Why the other options are wrong
- Thinned, scarred myocardium This is the wall of a true aneurysm, which has a wide neck.
- All three layers of the heart wall No layer of the heart wall survives in a contained rupture.
- Endocardium with fibrous tissue only Endocardium is lost at the rupture site.
- Calcified mural thrombus Thrombus may line the sac but does not form its wall.
A 70-year-old with severe aortic stenosis and marked LV hypertrophy has exertional angina despite a normal coronary angiogram. What best explains it?
Answer: Hypertrophy raises demand and squeezes subendocardial flow
Pressure overload from aortic stenosis causes concentric hypertrophy, which increases muscle mass and wall stress and so raises oxygen demand. At the same time the high left ventricular diastolic pressure compresses subendocardial vessels, the lower aortic diastolic pressure reduces perfusion pressure, and a longer systole shortens diastolic filling time. Capillary density also fails to keep up with the hypertrophy. The result is subendocardial ischaemia and angina even with normal coronary arteries.
Angina in aortic stenosis
- More muscle, higher wall stress
- High LVEDP compresses subendocardium
- Lower aortic diastolic pressure
- Shorter diastole for coronary filling
Remember A thick muscle that needs more and gets less.
Exam trap Normal coronary arteries do not exclude ischaemia when the ventricle is severely hypertrophied.
Why the other options are wrong
- Calcium emboli from the valve block small arteries Calcific emboli are rare and cause acute events, not stable angina.
- Coronary ostia are covered by the calcified cusps The ostia lie above the cusps and are not normally covered.
- Coronary vasospasm triggered by the stenotic jet The jet does not cause coronary spasm.
- Anaemia from valve haemolysis cuts oxygen supply Significant haemolysis is unusual with native aortic stenosis.
Where this sits in the CPSP syllabus
- Diagnostic Radiology, Paper 2: Lungs, heart and vessels, Coronary, valvular, structural and congenital heart disease; heart failure
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