Aortic Regurgitation
The causes of aortic regurgitation can be divided into those occurring
because of (1) primary aortic valve leaflet disease and (2) aortic root disease.
The most common causes of primary disease of the valve leaflets leading to aortic
regurgitation are rheumatic fever, infective endocarditis, loss of commissural support
with cusp collapse, and congenital bicuspid aortic valves. If bicuspid aortic valves
result in aortic regurgitation, it is usually associated with aortic stenosis. Common
causes of root-mediated aortic regurgitation are degenerative diseases of the aorta,
cystic medial necrosis (Marfan's and related syndromes), dissection, and several
rare conditions, including syphilitic disease and ankylosing spondylitis.
Aortic regurgitation can develop chronically or acutely. In chronic
aortic regurgitation, the left ventricle undergoes progressive dilatation and hypertrophy,
which can lead to secondary dilatation of the mitral valve annulus and left atrial
dilatation. The left ventricular hypertrophy in aortic regurgitation is conspicuous,
results from sarcomere replication in series, causes eccentric hypertrophy, and may
exceed in magnitude that observed with concentric aortic stenosis-induced hypertrophy.
This volume-induced eccentric hypertrophy in response to aortic regurgitation is
an attempt to maintain wall tension (and the ratio of wall thickness to left ventricular
cavity diameter) constant in accord with the law of Laplace.
Patients with chronic aortic regurgitation remain asymptomatic
for several decades. The pathophysiologic mechanisms underlying the development
of symptoms are outlined in Figure
50-21
. Symptoms generally occur only after the development of considerable
cardiomegaly and myocardial dysfunction. Dyspnea (especially exertional dyspnea),
orthopnea, and paroxysmal nocturnal dyspnea are usually the main symptoms. As with
the symptoms of aortic stenosis, which are multifactorial, dyspnea in patients with
aortic regurgitation is not exclusively secondary to passive mitral regurgitation
(see Fig. 50-21
). Fatigue,
especially on exertion, reflects inadequate effective forward flow. Angina is not
common but, when present, generally occurs at night (nocturnal angina) and is a manifestation
of decreased coronary flow secondary to decreased heart rate and blood pressure occurring
at night. Severe, acute symptoms (dyspnea, hypotension) develop in patients with
acute aortic regurgitation as a result of an inability of the left ventricle to accommodate
acute increases in volume.
The presence or absence of symptoms and an assessment of left
ventricular systolic function are important management and prognostic variables in
patients with aortic regurgitation ( Fig.
50-22
). In general, patients with severe aortic regurgitation who are
symptomatic should undergo aortic valve replacement. Moreover, symptomatic patients
with normal left ventricular systolic function (left ventricular ejection fraction
at rest greater than 60%, fractional shortening greater than 35%) have a lower
Figure 50-21
Pathophysiology of aortic regurgitation. Aortic regurgitation
results in an increased left ventricular (LV) volume, increased stroke volume, increased
aortic (Ao) systolic pressure, and decreased effective stroke volume. Increased
LV volume results in an increased LV mass, which may lead to LV dysfunction and failure.
Increased LV stroke volume increases systolic pressure and prolongation of left
ventricular ejection time (LVET). Increased LV systolic pressure results in a decrease
in diastolic time. Decreased diastolic time (myocardial perfusion time), diastolic
aortic pressure, and effective stroke volume reduce myocardial O2
supply.
Increased myocardial O2
consumption and decreased myocardial O2
supply produce myocardial ischemia, which further deteriorates LV function. ↑,
Increased; ↓, decreased). (Redrawn from Boudoulas H, Gravanis MB:
Valvular heart disease. In Gravis MB [ed]: Cardiovascular
Disorders: Pathogenesis and Pathophysiology. St Louis, CV Mosby, 1993.)
5-year mortality rate than do those with subnormal left ventricular systolic function
(left ventricular ejection fraction at rest less than 60%, fractional shortening
less than 30%).[142]
Asymptomatic patients are
a more challenging management dilemma. Asymptomatic patients with normal left ventricular
function are usually monitored and treated medically with cardiac glycosides, salt
restriction, diuretics, and afterload reduction. In the past, asymptomatic patients
with reduced left ventricular systolic function were also managed medically. However,
advances in surgical technique and advances in the perioperative management of these
patients may justify valve replacement. Such decisions have to balance the risks
of the procedure, the long-term morbidity and mortality associated with valve replacement,
and the natural history of asymptomatic aortic regurgitation with decreased left
ventricular systolic function.[142]
The principles underlying the perioperative medical management
of patients with aortic regurgitation are predicated on the principles outlined in
Figure 50-21
. These management
principles are directed at augmenting forward flow and include afterload reduction,
avoidance of bradycardia, and when appropriate, inotropic augmentation.
