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Aortic Regurgitation

Aortic regurgitation results in volume overload of the left ventricle and dilation. Severe aortic regurgitation can occur with a normal ejection fraction due to eccentric left ventricular hypertrophy that allows ejection of a large stroke volume without increased myocardial shortening. The primary causes of aortic regurgitation are rheumatic heart disease, congenital bicuspid aortic valve disease, infective endocarditis, and primary aortic root diseases such as syphilis or ankylosing spondylitis that cause aortic dilation and annular enlargement.

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Justine Castillo
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47 views2 pages

Aortic Regurgitation

Aortic regurgitation results in volume overload of the left ventricle and dilation. Severe aortic regurgitation can occur with a normal ejection fraction due to eccentric left ventricular hypertrophy that allows ejection of a large stroke volume without increased myocardial shortening. The primary causes of aortic regurgitation are rheumatic heart disease, congenital bicuspid aortic valve disease, infective endocarditis, and primary aortic root diseases such as syphilis or ankylosing spondylitis that cause aortic dilation and annular enlargement.

Uploaded by

Justine Castillo
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AORTIC REGURGITATION  Produces volume overload w/ dilation and LVH; w/

subsequent dilation of the MV annulus


 LA may also dilate and hypertrophy depending on the
ETIOLOGY severity

Primary Valve Disease


Rheumatic Disease PATHOPHYSIOLOGY
 Results in thickening, deformity, and shortening of the
 Mechanism: the retrograde flow of a portion of the LV
individual aortic valve cusps
stroke volume into the LV during diastole, producing
 Much less common in patients with isolated AR or does not
volume overload
have assoc. rheumatic mitral valve disease
 The total stroke volume (SV) of LV is increased
 Patients with congenital BAV disease may develop
 Severe AR: regurgitant flow volume = SV
predominant AR; ~20% of these pts will require aortic valve
surgery between 10 - 40 y/o of age.  In AR, the entire LV stroke volume is delivered into the high-
pressure zone (i.e., aorta)
 Congenital fenestrations of the aortic valve occasionally
produce mild AR.  Increased LV end-diastolic volume (preload) constitutes the
major hemodynamic compensation for AR
 Membranous subaortic stenosis >> high velocity systolic jet
>> valve thickening and scarring >> 2ry AR >> aortic  Dilation and eccentric LVH:
prolapse  Allows ejection of large SV
 Dilation of the aortic annulus may occur secondarily and  Does not require increase in the relative shortening of
lead to worsening regurgitation each myofibril
 Result = severe AR may occur with a normal effective
forward stroke volume and a normal LV ejection fraction
Infective Endocarditis
 Laplace’s Law:
 Can develop on a valve affected by:
 “the inward pressure that is exerted by the vessel wall on
 rheumatic disease the blood is directly proportional to the tensional stress in
 congenitally deformed valve the wall but inversely proportional to the radius of the
 normal aortic valve wall”
 Valve become scarred and retracted during the course of  LV dilation increases the LV systolic tension
syphilis or ankylosing spondylitis  Chronic AR = LV preload and afterload are both
increased
Traumatic rupture or avulsion  As LV function deteriorates:
 Uncommon cause of acute AR  end-diastolic volume rises further
 Most frequent serious lesion in patients surviving  forward stroke volume and EF decline
nonpenetrating cardiac injuries.  thickening of LV wall; large heart (>1000g)
 development of symptoms
Primary Aortic Root Disease  The reverse pressure gradient from aorta to LV:
 AR may be due to entirely to marked aortic annular dilation  Drives the AR flow
 Widening of the aortic annulus + lack of diastolic coaptation  Falls progressively during diastole
of the aortic leaflets = AR  Causes decrescendo diastolic murmur
 Medial degeneration of the ascending aorta
 May be caused by retrograde dissection of the aorta
involving the aortic annulus.
 Syphilis and ankylosing spondylitis:
 may be assoc. with cellular infiltration and scarring of
the media of the thoracic aorta
 May lead to aortic dilation, aneurysm formation, and
severe regurgitation.
 Takayasu’s aortitis and giant cell aortitis can also result in
aneurysm formation and secondary AR.

PATHOLOGY
References:

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