Aortic regurgitation

Abstract

Left ventricular (LV) systolic function is an important determinant of long-term prognosis in patients with chronic aortic regurgitation (AR). Impaired LV systolic function identifies a group of patients who are at risk of developing postoperative congestive heart failure and death after aortic valve replacement (AVR). Hence, asymptomatic patients with definite evidence of impaired LV function should undergo operation without waiting for the development of symptoms or more severe LV dysfunction. Among asymptomatic patients with normal LV systolic function (normal ejection fraction), prognosis is excellent, and fewer than 5% per year require surgery because of symptom development or LV dysfunction. Patients likely to require surgery can be identified on the basis of age, severity of LV dilatation, and progressive increase in LV dimensions or decrease in resting ejection fraction during the course of serial follow-up studies. Afterload-reducing therapy in asymptomatic patients with severe AR and normal LV function has beneficial hemodynamic effects; chronic therapy may reduce the likelihood of symptoms or LV systolic dysfunction. Aortic valve replacement should be performed once significant symptoms develop. In the absence of important symptoms, the operation should also be performed in patients with AR who manifest consistent and reproducible evidence of either LV contractile dysfunction at rest or extreme LV dilatation. Noninvasive imaging should play a major role in evaluation. An important clinical decision--such as recommending AVR in the asymptomatic patient--should not be based on a single echocardiographic or radionuclide angiographic measurement. When these data consistently indicate impaired contractile function at rest or extreme LV dilatation on repeat measurement, however, operation is indicated in the asymptomatic patient. This strategy should reduce the likelihood of irreversible LV dysfunction in these patients and enhance long-term postoperative survival.

Fenofibrate reduces cardiac remodeling and improves cardiac function in a rat model of severe left ventricle volume overload

“…It is encountered mostly in subjects suffering from chronic heart valve diseases such as mitral (MR) or aortic valve regurgitation (AR). Untreated AR causes severe LV dilatation and hypertrophy (LVH) as well as slowly progressive systolic dysfunction and evolution towards heart failure (Bonow 2000;Bonow et al 1991). Chronic left ventricular (LV) volume overload diseases such as AR are well tolerated for many years before heart failure occurs.…”

Gene profiling of left ventricle eccentric hypertrophy in aortic regurgitation in rats: rationale for targeting the β-adrenergic and renin-angiotensin systems

“…heart hypertrophy; gene expression; renin-angiotensin system; adrenergic system SEVERE AORTIC VALVE REGURGITATION (AR) is associated with a long asymptomatic period during which the left ventricle (LV) progressively dilates and hypertrophies in response to a chronic volume overload. This process is accompanied by a decrease in LV function, occurrence of symptoms, and eventually heart failure (4,7). No drug has yet been clearly shown in humans to be effective to slow LV dilation, hypertrophy, and loss of systolic function or to have any impact on morbidity or mortality in chronic AR (5,15).…”

A β1-adrenergic receptor CaM kinase II-dependent pathway mediates cardiac myocyte fetal gene induction

“…myosin; adenosine 3Ј,5Ј-cyclic monophosphate ␤-ADRENERGIC SIGNALING plays an important antithetical role in the natural history of dilated cardiomyopathies (DCMs) exerting favorable compensatory effects on cardiac function and promoting the development and progression of the DCM phenotype (4,6,11,13). Activation of ␤-adrenergic receptors (␤ 1 -AR and ␤ 2 -AR) during periods of cardiac stress initially results in increases in heart rate and contractility, effectively improving cardiac output, but then ultimately harms the failing heart (5,8) by mechanisms that include alterations in gene expression (19).…”