Aortic Regurgitation

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Aortic Regurgitation

Dr Pukar Ghimire
MBBS, MD
Causes
Primary valve disease
• A rheumatic origin is much less common in
patients with isolated AR who do not have
associated rheumatic mitral valve disease.
• Patients with congenital BAV disease may
develop predominant AR
• The coexistence of hemodynamically significant
AS with AR usually excludes all the rarer forms
of AR because it occurs almost exclusively in
patients with rheumatic or congenital AR.
Primary aortic root disease
• AR also may be due entirely to marked
• aortic annular dilation, i.e., aortic root disease,
without primary involvement of the valve
leaflets; widening of the aortic annulus and
separation of the aortic leaflets are
responsible for the AR
Pathophysiology of
chronic AR
Clinical features: History
• Approximately 3/4 of patients with pure or
predominant valvular AR are men; women
predominate among patients with primary
valvular AR who have associated rheumatic
mitral valve disease.
• Acute severe AR
– May occur in infective endocarditis, aortic
dissection, or trauma,
– the LV cannot dilate sufficiently to maintain stroke
volume, and LV diastolic pressure rises rapidly with
associated marked elevations of LA and PA wedge
pressures.
– Pulmonary edema and/or cardiogenic shock may
develop rapidly.
Chronic AR: Symptoms
• Long latent period
• Relative Asymptomatic for 10-15 yrs
• However, uncomfortable awareness of the heartbeat, especially on lying
down, may be an early complaint.
• Sinus tachycardia, during exertion or with emotion, or premature ventricular
contractions may produce particularly uncomfortable palpitations as well as
head pounding.
• Yrs later, exertional SOB develop, which is the 1st symptom of
dimininished cardiac reserve
• Followed by orthopnea, PND
• Anginal chest pain during rest or exertion
• Nocturnal angina is particularly troublesome
• Late in course of diseaem congestive hepatomegaly and edema
Signs
Treatment
• Acute AR
– Patients with acute severe AR may respond to
intravenous diuretics and vasodilators (such as
sodium nitroprusside), but stabilization is usually
short-lived and operation is indicated urgently.
Chronic AR
• Medical management
– Diuretics
– Vasodilators (ACE inhibitors, dihydropyridine calcium channel
blockers, or hydralazine)

• It is often difficult to achieve adequate BP control


because of the increased stroke volume that
accompanies severe AR.
• Cardiac arrhythmias and systemic infections are poorly
tolerated in patients with severe AR and must be treated
promptly and vigorously.
Surgical management
• In deciding on the advisability and proper
timing of surgical treatment, two points
should be kept in mind:
– Patients with chronic severe AR usually do not
become symptomatic until after the development
of myocardial dysfunction;
– When delayed too long (defined as >1 year from
onset of symptoms or LV dysfunction), surgical
treatment often does not restore normal LV
function.
• Therefore, in patients with chronic severe AR,
careful clinical follow-up and noninvasive
testing with echocardiography at
approximately 6- to 12-month intervals are
necessary if operation is to be undertaken at
the optimal time, i.e., after the onset of LV
dysfunction but prior to the development of
severe symptoms.
• Surgeries
– Aortic Valve Replacement with mechanical or
tissue prosthesis
– Valve-sparing aortic root reconstruction can be
possible when AR is due to aneurysmal dilation of
the root or proximal ascending aorta rather than
to primary valve involvement

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