Valvular Heart Disease and Murmurs — MS, MR, AS, AR, TR, Manoeuvres and Eponymous Signs

A murmur is the sound of turbulent flow across a valve that is either too narrow (stenosis) or fails to close (regurgitation). The first step is timing: systolic murmurs lie between S1 and S2, diastolic murmurs between S2 and the next S1. Stenotic valves make noise when they should be open; leaky valves make noise when they should be shut.

Mitral stenosis narrows the mitral orifice, raising left atrial pressure, which is transmitted back to the pulmonary veins and capillaries, causing congestion and eventually pulmonary hypertension and right ventricular strain. It is mostly rheumatic — commissural fusion, leaflet thickening and subvalvular fibrosis — and about 80% of patients worldwide are women, with symptoms typically starting in the third or fourth decade.

• Loud S1 (sometimes palpable — the 'tapping apex').
• Opening snap shortly after A2; the A2–opening snap interval shortens as stenosis worsens — the best bedside marker of severity.
• Low-pitched mid-diastolic rumble with presystolic accentuation, heard with the bell at the apex in the left lateral decubitus position or after isometric exercise.
• Presystolic accentuation disappears in atrial fibrillation (no atrial kick).
• Haemoptysis from rupture of engorged bronchial veins; atrial fibrillation and thromboembolism are the major complications.

The normal mitral orifice is about 4–6 cm². Suitability for percutaneous balloon mitral valvotomy (PBMV) is judged with the Wilkins score, which grades leaflet mobility, thickness, calcification and subvalvular thickening from 1 to 4 each (total 4–16). A score below 8 with less than moderate MR predicts a good PBMV result; a score above 12 favours surgery.

Aortic stenosis (AS) has a long latent period of about 10–20 years. Once symptoms appear — the classic triad of angina, syncope and dyspnoea/heart failure — average survival without valve replacement is only 1–3 years. Angina comes from a hypertrophied myocardium needing more oxygen while coronary flow is compressed; exertional syncope comes from vasodilation that a fixed cardiac output cannot match.

• Ejection systolic, crescendo–decrescendo murmur at the right 2nd intercostal space, radiating to the right side of the neck; it becomes softer in LV failure as stroke volume falls.
• Pulsus parvus et tardus — a slow-rising, late-peaking, low-amplitude carotid pulse — is specific for severe AS.
• S2 may be single, or paradoxically split when aortic closure is delayed.
• Causes: bicuspid aortic valve (commonest under 70 in developed countries), calcific degeneration (elderly), rheumatic disease (commonest in developing countries).
• Definitive treatment: aortic valve replacement, surgical or percutaneous (TAVR).

Aortic regurgitation (AR) lets blood leak back into the left ventricle in diastole. Chronic AR is compensated by eccentric hypertrophy and LV dilatation, producing a large stroke volume and a wide pulse pressure. Acute AR — from infective endocarditis, aortic dissection or trauma — gives the ventricle no time to adapt and can present as cardiogenic shock needing urgent surgery.

Mitral regurgitation produces a holosystolic murmur at the apex radiating to the left axilla. It is classified as primary (a structural problem of the leaflets, chordae, papillary muscles or annulus — degeneration, prolapse, flail leaflet, rheumatic disease, endocarditis, chordal rupture) or secondary (normal leaflets that fail to meet because the left ventricle or atrium has remodelled). Myxomatous degeneration with mitral valve prolapse is the leading cause in developed countries.

Tricuspid regurgitation is most commonly secondary (functional) — right ventricular dilatation, annular dilatation and leaflet tethering from pulmonary hypertension or RV overload. Primary causes include infective endocarditis (intravenous drug use, infected catheters), rheumatic disease, carcinoid syndrome, trauma and Ebstein anomaly (the commonest congenital tricuspid lesion).

• TR murmur: high-pitched pansystolic, loudest in the 4th intercostal space parasternally.
• It increases with inspiration, exercise and leg raising (more venous return) and decreases on standing and with Valsalva.
• JVP shows a prominent V wave; severe cases have pulsatile neck veins, ascites, oedema and a right ventricular heave.

The tumour plop is an early-diastolic sound that can accompany a diastolic murmur in atrial myxoma; findings can change with body position. A left-sided myxoma causes mitral valve obstruction or regurgitation (exertional dyspnoea, orthopnoea, pulmonary oedema), while a right-sided one produces features of tricuspid stenosis with a prominent jugular a wave. Clues that point away from true valve disease are systemic embolisation, fever, weight loss or malaise, and the first test is transthoracic echocardiography, with transoesophageal echo for attachment site. Treatment is prompt surgical excision.

American physician Austin Flint described his murmur in 1862. Because it mimics mitral stenosis, the distinction is classic: amyl nitrite inhalation (which lowers afterload) softens the Austin Flint murmur, whereas the murmur of true MS becomes louder and longer. The early diastolic murmur of pulmonary incompetence caused by pulmonary hypertension is eponymously linked with the Manchester physician Graham Steell.

Rheumatic heart disease is the chronic valvular sequel of acute rheumatic fever, an abnormal immune response that follows group A β-haemolytic streptococcal (Streptococcus pyogenes) pharyngitis by about 2–3 weeks. Rheumatic carditis is characterised histologically by Aschoff bodies and MacCallum plaques (in the left atrial subendocardium). It predominantly affects people living in poverty with poor access to health care.