Chronic AR causes gradual left ventricular volume overload that leads to a series of compensatory changes, including LV enlargement and eccentric hypertrophy. LV dilation occurs through the addition of sarcomeres in series (resulting in longer myocardial fibers), as well as through the rearrangement of myocardial fibers. As a result, the LV becomes larger and more compliant, with greater capacity to deliver a large stroke volume that can compensate for the regurgitant volume. The resulting hypertrophy is necessary to accommodate the increased wall tension and stress that result from LV dilation (Laplace law).¹
Aortic incompetence often has a long asymptomatic period with increasing ;eft ventricular dilatation before symptoms in the 4th-5th decade. prognosis is 75% 5-years and 50% 10-years, even when moderately severe.
Symptoms:
- exertional dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea
- nocturnal angina
- cardiovascular collapse, pulmonary oedema (acute aortic regurgitation)
- severe:
- collapsing pulse, wide pulse pressure
- long decrescendo diastolic murmur – ultimately becomes shorter again due to ↑ LVEDP
- LV S3, soft A2
- Austin-Flint murmur
- signs of left ventricular failure (LVF)
Signs / Examination:
General
- Marfanoid appearance, seronegative
- Argyle -Robertson pupil, etc
Pulse
- collapsing
- wide pulse pressure (Corrigan’s neck)
Palpation
- displaced, hyperkinetic
- ± diastolic thrill left sternal edge (LSE): “up and out”
Auscultation
- soft AI, decrescendo high-pitched murmur in 3rd-4th LICS/RICS
- length of murmur ∝ severity
- + SEM for associated aortic stenosis or torrential flow murmur
- ± Austin-Flint murmur: similar to mitral stenosis but without loud S1 and no opening snap
Differential Diagnosis:
- aortic incompetence
- pulmonary incompetence
Causes of Aortic Incompetence:
Valvular
- rheumatic – rarely isolated
- congenital bicuspid valve
- seronegative arthropathy – especially ankylosing spondylitis, SLE, Psoriatic arthritis, Reiter’s syndrome
Aortic root
- Marfan’s syndrome
- Aortitis – seronegative, rheumatoid arthritis, tertiary syphilis
- dissecting aneurysm
Acute AI
- valvular – infective endocarditis, (trauma)
- aortic root – Marfan’s syndrome, hypertension, dissecting aneurysm, (elderly)
Investigations:
- ECG: left ventricular hypertrophy (LVH)
- CXR: LVH, valve calcification, aortic root dilatation → cor bovinum
- ECHO: aortic root dimensions, LV dimensions, LV function (ejection fraction), regurgitation (estimation of amount with Doppler)
Treatment:
- treat concomitant hypertension
- Prazosin
- Nitrates
- regular echocardiography
- endocarditis prophylaxis
- ± digoxin and diuretics – since atrial fibrillation and bradycardias are poorly tolerated
- surgery – indicated because once symptomatic / reduced LVF, prognosis rapidly decreases and most are dead within2 years without surgical intervention
- symptomatic: exertional angina, dyspnoea, syncope
- reduced LVF: low EF (since high till late)
References
- Wang, Stanley S. and O’Brien, Terrence X. Aortic Regurgitation: Background, Pathophysiology, Etiology (medscape.com). Nov 19, 2018.
- Cheitlin, Melvin D. Surgery for Chronic Aortic Regurgitation: When Should It Be Considered? – American Family Physician (aafp.org). Am Fam Physician. 2001 Nov 15;64(10):1709-1716.
