Aortic valve

What it normally does

• Three thin cusps open to roughly 3 to 4 cm² in an adult — a door wide enough that blood crosses it with almost no resistance, so left ventricular and aortic pressure during ejection are within a few mmHg of each other.

  when the orifice narrows, any pressure difference measured across the valve has to be generated by the ventricle itself — that gradient, and the hypertrophy the ventricle builds to sustain it, is aortic stenosis.

• It shuts at the start of diastole, when aortic pressure exceeds the falling ventricular pressure. That closure is the first and normally the louder component of the second heart sound (A2), and it is what holds the column of blood up in the aorta through diastole.

  a valve whose cusps no longer meet lets that column fall back into the ventricle (aortic regurgitation), while a valve too calcified and immobile to snap shut makes A2 soft or inaudible in severe stenosis.

• The coronary ostia open from the right and left aortic sinuses, above the cusp attachments, and left ventricular myocardium is perfused almost entirely in diastole, when the muscle is relaxed and the shut valve is holding aortic pressure up. Left coronary flow therefore tracks aortic diastolic pressure much more closely than systolic — the thinner-walled right ventricle, at far lower wall tension, keeps some perfusion through systole.

  anything that raises left ventricular diastolic pressure, or drops aortic diastolic pressure, starves the subendocardium — which is why aortic stenosis and aortic regurgitation both cause angina with angiographically clean coronaries.

• Each beat pushes a stroke volume of roughly 70 mL into the aorta, which stretches and then recoils. The pulse pressure (systolic minus diastolic, normally around 40 mmHg) is set by three things: the size of that stroke volume, the compliance of the aorta, and how fast blood runs off during diastole.

  the pulse changes shape in valve disease — narrow and slow-rising when a stenosed valve limits stroke volume, wide and collapsing when a leaking valve inflates stroke volume and drains the aorta in diastole — but because arterial stiffness moves it independently, the pulse raises the question rather than answering it.

• The cusps are thin and avascular, and competence depends on broad coaptation of their free edges within an aortic root of normal calibre, with commissures that stay unfused. Damaged valve tissue is not regenerated.

  calcification, congenital bicuspid geometry, rheumatic commissural fusion, root dilatation and endocarditic destruction all end in stenosis, regurgitation or both — and none of them is reversed by drugs, which is why the definitive treatment is mechanical.

What goes wrong

• Aortic stenosis← from “Three thin cusps open to roughly 3 to 4 cm² in…”

  Decades of calcium deposition on the cusps (or a bicuspid valve, or old rheumatic damage) stiffen them so they no longer open fully. The wide, free door becomes a narrow hole, so the ventricle must generate a large pressure gradient to push the same stroke volume out. It responds with concentric hypertrophy, and thick muscle working at high pressure demands more oxygen while the raised diastolic pressure inside the ventricle squeezes the subendocardial bed it depends on. Hence the triad: angina from supply-demand mismatch even with normal coronary arteries; exertional syncope, largely because the obstruction is fixed, so when exercising muscle vasodilates the heart cannot raise output to match and cerebral perfusion falls (an exercise-triggered vasodepressor reflex and arrhythmia can contribute); and breathlessness and heart failure, because a stiff hypertrophied ventricle fills at high pressure and that pressure backs up into the lungs.

  Severity on echo: mean gradient ≥40 mmHg, peak velocity ≥4 m/s, or valve area ≤1.0 cm² — but low-flow, low-gradient severe stenosis exists, so a gradient under 40 mmHg with a small stroke volume does not exclude severe disease. Symptoms change everything: the classic quoted mean survival untreated is about 5 years after angina, 3 after syncope and 2 after heart failure, and symptomatic severe stenosis is a referral for valve replacement (surgical or TAVI), not a prescription.

  You would find: A harsh ejection systolic murmur at the right second intercostal space radiating to the carotids, classically with a slow-rising, low-volume pulse (pulsus parvus et tardus), a narrow pulse pressure, and a soft or absent A2 — the tighter and more immobile the valve, the quieter A2. Those pulse signs have a real limit: stiff arteries in an older patient can keep the upstroke brisk and the pulse pressure normal or even wide despite severe stenosis, so a normal-feeling pulse does not exclude it in exactly the age group where the disease is commonest. The symptom history — angina, blackouts on exertion, breathlessness — is the turning point, and echocardiography is what settles severity.

• Chronic aortic regurgitation← from “It shuts at the start of diastole, when aortic…”

  The cusps no longer meet in diastole — a bicuspid valve, rheumatic scarring, or an aortic root that has dilated and pulled the cusps apart — so blood falls back into the ventricle. The ventricle ejects its normal filling plus the regurgitant volume, so total stroke volume becomes very large and the chamber dilates over years to hold it (eccentric hypertrophy), which is why the patient can stay asymptomatic for a long time. Two consequences follow directly: systolic pressure rises because the ejected volume is large, and diastolic pressure falls because blood leaks backwards out of the aorta instead of staying in it. That gives the wide pulse pressure and the collapsing pulse. Low aortic diastolic pressure and a high ventricular diastolic pressure also narrow the coronary perfusion gradient, so angina can occur. Eventually the dilated ventricle decompensates and the patient becomes breathless.

  Wide pulse pressure plus early diastolic murmur; echo defines severity and, just as importantly, the aortic root. Timing of surgery is driven by symptoms, or in asymptomatic severe regurgitation by falling left ventricular systolic function or progressive dilatation — the ACC/AHA threshold is an ejection fraction of 55% or less, the ESC 50% or less, with left ventricular end-systolic dimension above about 50 mm as the other trigger. Vasodilator drugs treat blood pressure and the failing ventricle; they do not remove the indication for surgery.

  You would find: A soft early diastolic murmur at the left sternal edge, best heard with the patient sitting forward in held expiration, with a wide pulse pressure and a collapsing (water hammer) pulse. The peripheral eponyms are the same physiology restated — head nodding (de Musset), nail bed capillary pulsation (Quincke), a visibly pulsating carotid (Corrigan) — and they are insensitive, so their absence proves little.

• Acute severe aortic regurgitation← from “It shuts at the start of diastole, when aortic…”

  A cusp is destroyed suddenly — a vegetation perforates it in infective endocarditis, or a type A aortic dissection tears the root apart. The ventricle has had no time to dilate, so the regurgitant volume arrives in a normal-sized, relatively non-compliant chamber; its diastolic pressure climbs steeply and that pressure is transmitted back into the pulmonary circulation. Because total stroke volume never has the chance to become large, the wide pulse pressure and collapsing pulse of the chronic form are typically absent, and the murmur is short and quiet because ventricular and aortic diastolic pressures equalise early.

  Acute severe regurgitation = pulmonary oedema with an unimpressive pulse and an unimpressive murmur. Endocarditis or dissection until proven otherwise; management is urgent surgery, and vasodilators or inotropes are only a bridge to it.

  You would find: Sudden breathlessness, pulmonary oedema, tachycardia and shock, sometimes with fever, and only a short soft murmur — occasionally a soft first heart sound from premature mitral valve closure. A normal-looking pulse pressure does not exclude it. The trap is expecting it to look like chronic regurgitation; this is a surgical emergency needing urgent echocardiography and cardiothoracic involvement.

• Bicuspid aortic valve← from “The cusps are thin and avascular, and competen…”

  The valve forms with two functional cusps instead of three, in roughly 1 to 2% of people and about two to three times more often in men — the commonest congenital valve lesion (ventricular septal defect is the commonest congenital heart defect diagnosed in infancy). Two cusps means asymmetric, turbulent flow and abnormal leaflet mechanics, and that stress accelerates calcification, so these valves tend to become stenotic one to two decades earlier than three-cusp valves: bicuspid disease dominates severe aortic stenosis presenting in the fifties and sixties, while calcific stenosis of a three-cusp valve typically presents in the seventies and eighties. Bicuspid valves may also be regurgitant. The associated aortopathy affects the wall of the ascending aorta, which can dilate and dissect independently of how the valve itself is functioning.

  Young-to-middle-aged aortic stenosis, or an incidental click and murmur: think bicuspid, then image the aorta and screen the family. Valve severity and aortic diameter are followed separately.

  You would find: An ejection click followed by a systolic murmur (with or without an early diastolic murmur) in a young or middle-aged person, often found incidentally. Imaging of the ascending aorta and root matters as much as the valve, because the aorta can be the lesion that kills. Because it clusters in families, guidelines recommend echocardiographic screening of first-degree relatives.

• Rheumatic aortic valve disease← from “The cusps are thin and avascular, and competen…”

  After group A streptococcal infection — classically pharyngitis, and in high-burden Australian settings skin infection (impetigo) is also implicated — the immune response cross-reacts with valve tissue. Repeated episodes of acute rheumatic fever fuse the cusps at their commissures and scar and retract them, so the valve both fails to open fully and fails to close fully: mixed stenosis and regurgitation, usually alongside mitral disease, which is the valve most often affected. In Australia this is not a historical curiosity — Aboriginal and Torres Strait Islander peoples carry among the highest rates of acute rheumatic fever and rheumatic heart disease in the world, and it presents in children and young adults rather than the elderly.

  Mixed aortic stenosis and regurgitation with mitral disease in a young Aboriginal or Torres Strait Islander patient = rheumatic until proven otherwise. Diagnosis of the acute episode is clinical plus echo; the long game is register-based secondary prophylaxis, because it is the repeat attacks that fix the valve damage.

  You would find: A young patient with both a systolic and a diastolic murmur, usually with mitral involvement. A child or young adult with a new murmur, fever and migratory joint pain needs acute rheumatic fever actively excluded (Jones criteria, echocardiography, streptococcal serology). Acute rheumatic fever and rheumatic heart disease are notifiable in the Australian jurisdictions that run register-based control programs, and confirmed cases are entered on those registers so that secondary prophylaxis is delivered and tracked.

What we give, and how it works

Open a drug to see what it binds, what that does to the cell, and what you then see in the patient.