Aortic Stenosis and Valve Disease

Aortic stenosis is asymptomatic for years while the valve narrows, and then declares itself. Once the classical symptoms appear, average survival without valve replacement is short and well characterised: approximately 5 years after angina, 3 years after syncope, and 2 years after heart failure. This is why symptom status, not valve gradient alone, drives the decision to intervene, and why every patient with known aortic stenosis must be told explicitly which symptoms to report urgently rather than mention at a routine annual review.

Transcatheter aortic valve implantation was introduced for patients considered inoperable, then proved non-inferior or superior to surgery sequentially in high-risk (PARTNER, CoreValve), intermediate-risk (PARTNER 2, SURTAVI) and low-risk (PARTNER 3, Evolut Low Risk) populations. It is now the default approach for most patients over approximately 75, with surgery preferred in younger patients, bicuspid valves in some anatomies, when concomitant coronary or other valve surgery is needed, or where anatomy is unsuitable. The critical unknown remains long-term valve durability in younger patients, and lifetime management — planning for a future second or third valve procedure — is now an explicit part of the initial decision.

Rheumatic heart disease affects over 40 million people worldwide and causes several hundred thousand deaths annually, overwhelmingly in low- and middle-income countries and among disadvantaged populations in wealthy ones. It results from an autoimmune response to group A streptococcal infection, predominantly damaging the mitral and aortic valves in children and young adults. Every stage is preventable: primary prevention through treating streptococcal pharyngitis; secondary prevention through regular benzathine penicillin injections to prevent recurrent rheumatic fever, which is highly effective yet undermined by penicillin supply shortages; and tertiary care through surgery, which is largely inaccessible where the disease is commonest.

The murmur of aortic stenosis is an ejection systolic murmur at the right upper sternal edge radiating to the carotids, with a slow-rising, low-volume pulse and a soft or absent second heart sound in severe disease. Echocardiography defines severity by valve area, mean gradient and peak velocity. The important trap is LOW-FLOW, LOW-GRADIENT severe aortic stenosis: when the left ventricle is failing, it cannot generate a high gradient across even a severely narrowed valve, so the gradient looks reassuring while the disease is critical. Dobutamine stress echocardiography distinguishes true severe stenosis from pseudo-severe, and calcium scoring on CT provides a flow-independent measure.

Watchful waiting was standard for asymptomatic severe aortic stenosis, but this position has weakened. The RECOVERY and AVATAR trials showed benefit from early surgery in asymptomatic patients with very severe or severe stenosis compared with conservative management, and guidelines now support intervention in asymptomatic patients with left ventricular systolic dysfunction, an abnormal exercise test, very severe stenosis, rapid progression, or markedly raised natriuretic peptides. Exercise testing is genuinely useful in this group, because many patients described as asymptomatic have simply limited their activity unconsciously to avoid symptoms.

No drug slows the progression of calcific aortic stenosis. Statins were tested specifically for this and failed (SEAS, SALTIRE, ASTRONOMER), despite the biological plausibility of a lipid-driven process — though lipoprotein(a) remains implicated and is an active therapeutic target. Management is therefore mechanical. Practical caution: in severe aortic stenosis, cardiac output is relatively fixed, so vasodilators, nitrates, high-dose ACE inhibitors and diuretics can precipitate profound hypotension and syncope, and require careful introduction and monitoring. Antibiotic prophylaxis for endocarditis is indicated only in the highest-risk groups, principally those with prosthetic valves or previous endocarditis.