Aortic stenosis and aortic regurgitation

Overview

The aortic valve normally has three cusps and opens fully in systole. It can become narrowed (aortic stenosis, AS), obstructing left ventricular outflow, or leaky (aortic regurgitation, AR), letting blood fall back into the ventricle in diastole.

Both are important because they are silent for years and then become dangerous: symptomatic AS carries a high risk of death without valve replacement, and AR damages the ventricle before symptoms appear. The pulse and blood pressure often give the diagnosis before the stethoscope does.

Aortic stenosis

Causes

Other causes of LV outflow obstruction to distinguish:

• Supravalvular stenosis: Williams syndrome (elfin face, hypercalcaemia, learning difficulty).
• Subvalvular membrane or ridge.
• Hypertrophic cardiomyopathy (dynamic obstruction).

Pathophysiology

• Obstruction raises LV systolic pressure → concentric LV hypertrophy (thick wall, normal cavity).
• The thick muscle needs more oxygen while coronary flow (which occurs in diastole) is reduced → angina even with normal coronaries.
• Output is fixed: on exercise the vessels dilate but output cannot rise, so BP falls → exertional syncope.
• Eventually the ventricle fails → breathlessness and heart failure.
• Tachycardia shortens diastole and further reduces coronary flow.

Symptoms

• Angina, syncope on exertion and exertional breathlessness (heart failure).
• Fatigue, sudden death.
• Heyde syndrome: GI bleeding from angiodysplasia with AS.

Physical signs

Signs of severe AS

• Slow-rising, low-volume pulse and narrow pulse pressure.
• Soft or absent A2, reversed splitting.
• Late-peaking, long murmur.
• S4, LV failure.
• Thrill.

Diagnosis: auscultatory, ECG and radiological findings

• Auscultation: ejection systolic murmur to the carotids, soft A2, ejection click (mobile bicuspid valve), S4.
• ECG: LVH with a "strain" pattern (ST depression and T inversion in I, aVL, V5–V6), left atrial enlargement; sometimes LBBB or heart block (calcium extending into the conducting tissue). Usually sinus rhythm.
• Chest X-ray: often a normal-sized heart (hypertrophy without dilatation), post-stenotic dilatation of the ascending aorta, calcified valve on the lateral film; cardiomegaly only once failure develops.
• Echocardiography: thickened, calcified, restricted cusps; LVH; LV function; severity by Doppler:

• Coronary angiography is required before surgery (coexisting coronary disease is common).
• CT/MRI for the aorta in bicuspid valves; CT also plans TAVI.

Management

• Asymptomatic: regular review with echo; warn the patient to report symptoms. An exercise test can unmask symptoms in apparently asymptomatic patients.
• Symptomatic severe AS: aortic valve replacement (AVR).
• Asymptomatic severe AS – AVR advised if:
  • symptoms or a fall in BP on exercise testing;
  • LVEF below 50%;
  • other cardiac surgery is planned (e.g. CABG);
  • very severe disease (e.g. peak velocity above 5.5 m/s) or rapid progression.
• TAVI (transcatheter aortic valve implantation): a stent-mounted valve is placed via the femoral artery; used in elderly or high-risk patients and increasingly in others.
• Balloon valvuloplasty: young patients with a non-calcified congenital valve; in adults only as a bridge or when unfit for other options.
• Medical: treat hypertension and heart failure cautiously; avoid dehydration and large doses of vasodilators (nitrates, ACE inhibitors) in severe AS, as they can cause hypotension and syncope because output is fixed.
• Bicuspid valve: consider surgery if the ascending aorta is over 50 mm or enlarging quickly.

Aortic regurgitation

Causes

Pathophysiology

• Blood leaks back into the LV in diastole, so the LV must pump the forward volume plus the regurgitant volume: volume overload → LV dilates and hypertrophies (eccentric).
• Large stroke volume → high systolic pressure; rapid run-off back into the LV → low diastolic pressure → wide pulse pressure and collapsing pulse.
• Low diastolic pressure reduces coronary filling → angina.
• In acute AR the normal-sized LV cannot cope: sudden pulmonary oedema and shock, often without the classic wide pulse pressure.

Symptoms

• Often none for many years.
• Exertional breathlessness, orthopnoea and PND once the LV fails.
• Palpitations (awareness of a forceful heartbeat), angina.
• Arrhythmias are uncommon.

Physical signs

Pulse and blood pressure (hyperdynamic circulation):

• Large-volume, collapsing ("water-hammer") pulse: sharp rise and quick fall, felt best at the radial artery with the arm raised.
• Wide pulse pressure (e.g. 160/40 mmHg).

Eponymous signs:

Precordium:

• Apex displaced down and out, forceful and diffuse (volume-loaded).

Auscultation:

• High-pitched, blowing early diastolic murmur at the left sternal edge (3rd–4th space), heard best with the diaphragm, patient sitting forward, breath held in expiration. In aortic root disease it may be louder at the right sternal edge.
• Ejection systolic flow murmur at the base (high stroke volume); does not mean AS.
• Austin Flint murmur: a mid-diastolic rumble at the apex, caused by the AR jet striking the anterior mitral leaflet and partly closing it.
• Soft A2 if the valve is diseased; S3 if the LV is failing.

Diagnosis: auscultatory, ECG and radiological findings

• Auscultation: early diastolic murmur at the left sternal edge, flow systolic murmur, Austin Flint murmur.
• ECG: LVH from volume overload: tall R waves and deep T inversion in left chest leads, deep S waves in right chest leads; usually sinus rhythm.
• Chest X-ray: LV enlargement (cardiomegaly), dilated ascending aorta; calcified ascending aorta suggests syphilis; valve calcification if valve disease is the cause.
• Echocardiography: dilated, vigorously contracting LV; the regurgitant jet on colour Doppler; vena contracta width and pressure half-time; diastolic flow reversal in the descending aorta in severe AR; aortic root size; fluttering of the anterior mitral leaflet.
• CT or MRI of the aorta if root dilatation or dissection is suspected; MRI can measure regurgitant volume.
• Cardiac catheterisation or CT coronary angiography before surgery.
• Serology for syphilis where relevant.

Treatment

• Treat the cause: endocarditis (antibiotics), syphilis (penicillin), dissection (surgery).
• Acute severe AR: urgent valve surgery; vasodilators and inotropes as a bridge. Avoid an intra-aortic balloon pump (it worsens AR).
• Chronic AR:
  • ACE inhibitors or other vasodilators for LV dysfunction or hypertension.
  • Beta-blockers (or ARBs) can slow aortic root dilatation in Marfan syndrome.
  • Regular echo to watch LV size and function.
• Surgery (aortic valve replacement, with root repair if needed) is indicated for:
  • acute severe AR (e.g. endocarditis);
  • symptomatic severe chronic AR;
  • asymptomatic severe AR with LVEF of 50% or less;
  • asymptomatic severe AR with a dilated LV: end-diastolic diameter above 70 mm or end-systolic diameter above 50 mm;
  • patients having other cardiac or aortic surgery.

Choice of replacement valve

Aortic stenosis and regurgitation compared

Quick revision

• AS: elderly calcific, bicuspid in middle age (coarctation link), rheumatic with mitral disease.
• AS triad: angina, exertional syncope, breathlessness; survival 2–3 years once symptomatic without surgery.
• AS signs: slow-rising small pulse, narrow pulse pressure, thrill, heaving apex, ESM to carotids, soft A2, reversed split, S4.
• Severe AS: velocity >4 m/s, mean gradient >40 mmHg, area <1 cm².
• AS treatment: AVR or TAVI if symptomatic; avoid big vasodilator doses.
• AR: collapsing pulse, wide pulse pressure, Corrigan, de Musset, Quincke, Duroziez, pistol-shot.
• AR murmur: early diastolic at left sternal edge, sitting forward, expiration; Austin Flint at apex.
• AR surgery: acute, symptomatic, EF ≤50%, LVEDD >70 mm or LVESD >50 mm.

Written by The House Job from standard references (Kumar and Clark's Clinical Medicine).

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