![]() ![]() Is left ventricular ejection fraction (LVEF) normal?Ī normal-sized ventricle with hyperdynamic contractility suggests acute aortic regurgitation. ![]() Can all three cusps be visualized, or is the valve bicuspid?.The images are acquired in PLAX (parasternal long-axis view) and PSAX (parasternal short-axis view), with the valve zoomed. Marfan syndrome (may also cause aortic dissection)Įhlers-Danlos syndrome (may also cause aortic dissection)Įchocardiography in aortic regurgitation 2D Echocardiography Mechanically, wall stress (the load on individual muscle fibers) increases while the contractile function worsens.Ĭhronic aortic regurgitation also leads to increasing LVEDP and LAP, which in turn results in pulmonary hypertension and pulmonary edema. Contractile dysfunction further aggravates the regurgitation (the regurgitation volume increases). Thus, chronic aortic regurgitation gradually leads to impaired contractile function and the development of myocardial fibrosis. ![]() Ventricular dilatation and hypertrophy lead to myocardial remodeling and neurohormonal changes that further worsen the hemodynamic situation. Dilation and hypertrophy allow the ventricle to maintain cardiac output and prevent, or alleviate, the pressure increase in the left ventricle and left atrium.Ĭhronic aortic regurgitation leads to dilatation and hypertrophy of the left ventricle. Increasing diastolic volumes requires that the myocardium becomes hypertrophic. This initially results in greater diastolic volume and increased compliance. Unfortunately, adaptation implies that the left ventricle dilates, which induces irreversible cellular and extracellular processes that ultimately lead to heart failure. If aortic regurgitation develops gradually, then the ventricle will adapt to the volume overload. The most common causes of acute aortic regurgitation are aortic dissection, endocarditis and trauma.
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