Clinical Pearls & Morning Reports
Published December 12, 2018
Severe aortic regurgitation is associated with a large forward stroke volume, which causes an increase in systolic blood pressure. It is also associated with rapid runoff of blood from the aorta backward into the left ventricle, which results in a relative decrease in diastolic blood pressure. Collectively, these hemodynamic changes produce a wide pulse pressure, which is defined as a diastolic blood pressure that is less than 50% of the systolic blood pressure. Read the Latest NEJM Case Records of the Massachusetts General Hospital here.
Q: What findings in the peripheral circulation are typical of aortic regurgitation?
A: The large stroke volume and rapid runoff that are associated with severe aortic regurgitation can be manifested by pronounced arterial pulsations. The carotid pulse may be described as “bounding,” often with visible pulsation, or “collapsing” (Corrigan’s pulse). The peripheral pulses often feel unusually brisk (water hammer pulses), and there may be alternating blanching and reddening of the nail beds that is synchronized with the cardiac cycle (Quincke’s pulse).
Q: What valvular abnormalities other than aortic regurgitation may cause an isolated diastolic murmur?
A: Other causes of isolated diastolic murmurs include mitral stenosis, tricuspid stenosis, and pulmonary regurgitation.
A: Severe aortic regurgitation can be either acute or chronic. Acute severe aortic regurgitation is usually due to infectious endocarditis or type A aortic dissection. Causes of chronic aortic regurgitation include abnormalities of the aortic valve, the aorta, or both. Valvular causes include bicuspid aortic-valve disease (with prolapse of the conjoined leaflet), which accounts for approximately one fourth of all cases of clinically significant aortic regurgitation. Calcific changes of the aortic valve can cause aortic regurgitation. Clinically significant aortic regurgitation can arise as a late consequence of endocarditis. Finally, aortic regurgitation can arise in rheumatic heart disease; rheumatic aortic-valve disease rarely occurs in the absence of marked rheumatic mitral-valve disease. Dilatation of the aortic root, ascending aorta, or both accounts for approximately one fourth of all cases of clinically significant aortic regurgitation. The aortic-valve cusps are suspended from the sinotubular junction (where the aortic root meets the ascending aorta), and therefore, dilatation of either the aortic root or the ascending aorta can widen the diameter of the sinotubular junction, causing incomplete valve closure and a central jet of aortic regurgitation. Conditions that affect both the aortic valve and the aorta and can cause secondary aortic regurgitation include Takayasu’s arteritis, giant-cell arteritis, Behçet’s disease, and syphilis.
A: Chronic aortic regurgitation progresses slowly, over a period of years to decades. Consequently, the left ventricle is able to accommodate the increased volume through a combination of eccentric hypertrophy and progressive dilatation. Even with a moderate degree of dilatation of the left ventricular cavity, left ventricular systolic function is preserved and the patient remains asymptomatic. Eventually, the left ventricular cavity grows large enough that the left ventricle is no longer able to compensate, and then systolic function declines, cardiac output decreases, left atrial pressure increases, and heart failure develops on the left side. In turn, chronic heart failure on the left side leads to heart failure on the right side.