Clinical scenario of acute aortic regurgitation is quite different from familiar finding in chronic aortic regurgitation. Due to the atypical findings, it may be difficult to diagnose acute aortic regurgitation. All the same, it is not a stable condition like chronic aortic regurgitation. Acute regurgitation can rapidly progress to heart failure and early mortality if left untreated.
Important causes of acute aortic regurgitation are infective endocarditis, aortic dissection, and rarely trauma . Rare causes reported are necrotizing granulomatous inflammation of the aortic valve in rheumatoid arthritis  and avulsion of aortic valve commissure [3,4] and spontaneous rupture of a fibrous strand in fenestrated aortic valve .
Pathophysiology of acute aortic regurgitation is characterized by the sudden volume overloading of the left ventricle which is unprepared and has a normal size. In chronic AR, left ventricle dilates progressively when AR progresses as the left ventricle gets time to accommodate the additional volume load. In acute AR there is a rapid increase in left ventricular diastolic pressure which approaches the aortic diastolic pressure. This causes mitral valve preclosure in diastole. Premature closure of the mitral valve prevents transmission of elevated left ventricular diastolic pressure to the pulmonary veins and hence pulmonary edema. But when the left ventricular diastolic pressure rises further, this protection is lost and the mitral valve opens in late diastole causing diastolic mitral regurgitation . Mitral regurgitation can extend to the isovolumic contraction period and early systole when the left ventricular diastolic pressure is very high. Left atrium serves as a reservoir to decompress the left ventricle in acute AR. But this compensatory mechanism can also fails soon when AR progresses, leading to pulmonary edema.
Premature closure of mitral valve in acute AR is demonstrated on M-Mode echocardiography. Premature mitral valve closure was graded as + when it occurred before the QRS, but after the P wave. When it occurred before the P wave, it was graded as ++ . These have been called as grade I and grade II by other authors . Grade II premature closure of mitral valve can occur up to 200 ms before the QRS while grade I is up to 50 ms before the QRS.
The classical decrescendo early diastolic murmur and peripheral signs of chronic aortic regurgitation are not features of acute AR. An early diastolic murmur if it is heard, is usually softer and shorter in acute AR. A soft to-and-fro murmur may be heard in acute AR. Murmur can be absent and the heart sounds quite soft or absent sometimes, leading to a silent precordium . Auscultatory timing of heart sounds are difficult because of their softness and shortening of diastole, often shorter than systole. Systole becomes longer because of prolonged systolic ejection time as the left ventricle has volume and pressure overload. Mitral valve closes prematurely opens late because of prolonged systole. It has been suggested that those with grade II premature closure of mitral valve should undergo early aortic valve replacement.
Aortic regurgitation in Stanford type A aortic dissection has several mechanisms and they have implications for repair . Five potential mechanisms are: (1) Incomplete closure of leaflets due to tethering by a dilated sinotubular junction (2) Leaflet prolapse due to disruption of attachment by dissection flap (3) Prolapse of dissection flap through the valve leaflets preventing leaflet coaptation (4) Bicuspid aortic valve and associated leaflet prolapse unrelated to the dissection process (5) Degenerative leaflet thickening leading to abnormal leaflet coaptation. First three can be considered for repair without replacement of the valve.
Hamirani YS, Dietl CA, Voyles W, Peralta M, Begay D, Raizada V. Acute aortic regurgitation. Circulation. 2012 Aug 28;126(9):1121-6.