Aortic stenosis — clinical presentation, diagnosis and management

Epidemiology and aetiology. Acquired calcific degenerative aortic stenosis is the commonest valve disease in the elderly, with a prevalence of 2.8% in those aged 75 and over, and it is found at autopsy in about 4–6% of those over 65. Aortic valve cusp sclerosis or calcification is present in 26–29% of adults older than 65. Isolated aortic stenosis is commoner in men except over the age of 80, where women predominate. Degenerative calcification was formerly thought to be passive calcium deposition, but is now known to share the pathophysiology of vascular atherosclerosis — lipid deposition, inflammatory cell infiltration, basement membrane disruption and calcification, a concept termed "valvulo-metabolic risk". Other causes: bicuspid valve (presents in the 50s–60s) and rheumatic disease, still important in India.

Clinical presentation. The usual presentation in older adults is fatigue, syncope, angina pectoris and congestive heart failure; exertional dyspnoea is often the earliest symptom. The development of symptoms — angina, syncope or heart failure — identifies the critical point in the natural history, because symptomatic aortic stenosis without intervention has only a 20% three-year survival. Other features: exertional dizziness, sudden death, and gastrointestinal bleeding from angiodysplasia with acquired von Willebrand disease (Heyde's syndrome). Note that the asymptomatic state is difficult to establish in the elderly because of a gradual reduction in activity or a sedentary lifestyle — patients unconsciously limit themselves.

Physical signs and their unreliability in the old. The classical findings are a slow-rising, low-volume pulse (pulsus parvus et tardus), a narrow pulse pressure, a heaving sustained apex beat, a soft or absent second heart sound, an S4, and an ejection systolic murmur radiating to the carotids. However, the typical murmur and pulse of aortic stenosis may be modified in older adults: systemic hypertension may shorten the systolic murmur, giving it the character of an aortic sclerosis murmur, and loss of vascular elasticity may modify the pulse pressure so that the typical pulse contour is absent. The murmur may also be maximal at the apex and fail to radiate (Gallavardin phenomenon), mimicking mitral regurgitation. Physical examination alone is therefore not reliable for diagnosing aortic stenosis in older adults, and because systolic murmurs are so common in this age group, differentiating mitral regurgitation, aortic sclerosis and aortic stenosis by auscultation is a genuine challenge.

Diagnosis. The addition of Doppler flow studies to echocardiography has greatly improved diagnostic accuracy. Severe aortic stenosis is defined by an aortic valve area < 1.0 cm² (or < 0.6 cm²/m² indexed), a peak transvalvular velocity ≥ 4.0 m/s, and a mean gradient ≥ 40 mmHg. Be alert to low-flow, low-gradient severe aortic stenosis (small valve area with a low gradient) — with a reduced ejection fraction, use dobutamine stress echocardiography to distinguish true severe stenosis from pseudo-severe; with a preserved ejection fraction, use the calcium score on CT. Left ventricular catheterisation remains the most reliable method of assessing aortic stenosis in older adults but should be reserved for patients who are symptomatic (angina, syncope or dyspnoea) and in whom surgery is contemplated. An exercise test is recommended to determine whether an apparently asymptomatic patient is truly asymptomatic — but is contraindicated once symptoms are present. Add BNP and coronary angiography before intervention.

Management — general. There is no effective medical therapy that alters the natural history; valve replacement is the only definitive treatment. Medical care is supportive: cautious diuretics for congestion, control of hypertension (avoid excessive vasodilatation), rate control and prompt cardioversion of atrial fibrillation, and treatment of coexisting coronary disease. Avoid nitrates and high-dose vasodilators in severe stenosis because a fixed cardiac output makes profound hypotension likely. Statins do not slow progression. Follow asymptomatic patients with serial echocardiography and educate them to report symptoms immediately.

Intervention — SAVR versus TAVI. Survival of the elderly patient after successful surgical aortic valve replacement is similar to that of the general population and enables return to an independent, active life. Operative mortality approaches that of younger patients, and it is not until patients reach their 80s that age alone becomes a risk factor; five-year survival for UK octogenarians undergoing SAVR is about 65% (about 55% with concomitant CABG). Once symptomatic aortic valve disease is diagnosed in a patient aged 80 or more, early referral for valve replacement avoids the hazards of falling LV function, loss of contractile reserve, urgent surgery and sudden death. TAVI improves five-year survival compared with medical treatment in inoperable patients, is equivalent to SAVR in high-risk patients with possible peri-procedural advantage, and is now used in intermediate and lower-risk patients; the choice between SAVR and TAVI must be made by the Heart Team on clinical, anatomical and technical grounds. Considerations favouring one over the other include the lower rate of paravalvular leak with SAVR, the higher pacemaker requirement with TAVI, and uncertain long-term TAVI valve durability. A bioprosthesis is generally preferred over a mechanical valve above 65 years, since mortality from thromboembolism and anticoagulant-related haemorrhage is three times higher with mechanical valves in this group. Balloon aortic valvuloplasty is no longer a definitive option — mortality 3–10%, stroke 10–25%, 66% restenosis within six months, and fewer than 20% surviving a year — but retains a role as a bridge in very sick patients. Finally, identify futility: life expectancy under two years from malignancy, severe airways disease, established dementia or severe frailty, an STS score > 15%, dialysis dependence or home oxygen dependence all predict that even TAVI will not benefit the patient.

EARLY TAVR (NEJM 2024) challenged the long-standing rule of watchful waiting in asymptomatic disease. In patients with asymptomatic severe aortic stenosis and a normal ejection fraction, early TAVI significantly reduced the composite of death, stroke or unplanned cardiovascular hospitalisation compared with clinical surveillance, driven largely by fewer unplanned hospitalisations — and notably 26% of the surveillance group required valve replacement within six months, underlining how quickly these patients declare themselves. This supports a strategy of earlier intervention in selected asymptomatic patients, and is particularly relevant in older adults in whom, as the textbook notes, the "asymptomatic" state is unreliable because activity is self-limited.