The aortic valve separates the left ventricle from the aorta. In normal hearts, it is pliable, opens widely, and presents minimal resistance to flow. The normal aortic valve is a trileaflet structure that is composed of three equal‐sized bowl‐shaped tissues that are referred to as cusps (left coronary cusp, right coronary cusp, and noncoronary cusp). The aortic valve serves an essential hemodynamic function in isolating the left ventricle from the arterial circulation and can fail in two ways. The valve can fail to open properly during systole, which thus inhibits ejection of blood from the left ventricle (aortic stenosis). Alternatively, the valve can fail by becoming incompetent, thus enabling back flow into the ventricle during diastole (aortic regurgitation) [1].

The hemodynamic changes associated with aortic regurgitation (AR) differ depending on the time–course of the valve dysfunction. If AR develops rapidly (i.e., acute or subacute AR), the left ventricle (LV) is unable to handle the pressure and volume overload, causing a rapid increase in LV pressures during diastole, markedly elevated pressures at end diastole, and premature closure of the mitral valve. Systemic diastolic pressures may be low, but generally there is a minimal increase in pulse pressure; in very severe cases of acute AR, cardiac output may fall, leading to hypotension. LV function can be further impaired by decreased coronary blood flow resulting from the combination of decreased aortic diastolic pressure and elevated LV diastolic pressures.

In chronic AR, stroke volume increases to maintain effective forward flow. This causes dilation of the LV, leading in some patients to the development of a massively dilated LV termed cor bovinum (the largest left ventricles are seen in patients with chronic AR). The body’s adaptation to chronic AR results, at least in part, in the classic physical examination findings of a widened pulse pressure and low aortic diastolic pressure. If and when the regurgitant flow overwhelms the adaptive mechanisms, this leads to uncompensated chronic AR with signs and symptoms of heart failure.

Before the development of aortic valve replacement, severe AR had an ominous prognosis. The availability of surgical treatment has greatly reduced the mortality of this disease (currently there are few percutaneous options available for AR, but several transcatheter valves that could be used to treat AR are in the development stage). The important question now in treating patients with this disease is the timing of aortic valve replacement. An understanding of the hemodynamic changes associated with chronic AR can help in determining cardiac adaptation to the regurgitant flow, and also help determine the severity of AR in patients with moderate AR by angiography or echo but decreased ejection fraction.

Hemodynamic changes of chronic aortic regurgitation

Hemodynamic changes associated with chronic AR result from aorta to left ventricle blood flow during diastole, compensatory responses of the left ventricle to increased diastolic filling, and adaptations by the cardiovascular system to maintain systemic blood flow. In mild AR, increased ejection fraction and/or heart rate lead to an increase in cardiac output across the aortic valve, thus maintaining systemic blood flow. As the severity of AR increases, increases in LV stroke volume are necessary to maintain cardiac output and thus the left ventricle begins to remodel and dilate. This remodeling allows the maintenance of relatively normal filling pressures as left ventricular volumes increase. Left ventricular dilation progresses as the severity of AR worsens and patients with severe chronic AR, if untreated, often develop the largest end‐diastolic volumes associated with any heart disease (cor bovinum). LVEDP will increase if the progression of the valve incompetence exceeds the rate of left ventricular remodeling (e.g., acute AR), if the limits of left ventricular remodeling are reached, or if systemic vascular resistance increases to such a degree as to increase regurgitant flow above the ability of the left ventricle to adapt.

Aortic pressures

The two most common blood pressure manifestations associated with chronic AR are a wide systemic pulse pressure and a low aortic diastolic pressure. The wide pulse pressure results from an increased stroke volume (which is needed to deliver enough blood to the aorta to maintain systemic blood flow despite large regurgitant fractions) and decreased peripheral vascular resistance. The low diastolic pressure results from a relatively low resistance to aortic diastolic flow: both backward flow into the LV and forward flow into the periphery. As the competence of the aortic valve decreases, resistance to flow from aorta to LV decreases, regurgitation increases, and aortic diastolic blood pressure drops. A widened and elevated systemic arterial pressure without a dichrotic notch is sometimes observed.

There are other, more subtle changes in arterial pressure that are associated with AR. Peripheral arterial pressures are generally higher than aortic pressures because of amplification due to summation of pressure wave reflections. In AR, because of the accelerated velocity of ventricular ejection, peripheral amplification is more profound than normal. This phenomenon may also lead to the appearance of a bisferiens systolic aortic pressure waveform, in which the first peak is due to ventricular emptying and the second peak to reflections propagated back from the arterial circulation.

Left ventricular pressures

The LV hemodynamic findings associated with chronic AR depend on the extent of ventricular remodeling. In mild to moderate AR, filling from the aorta enables the left ventricle to increase stroke volume by increasing LV end‐diastolic volume (i.e., Starling’s law). As the AR becomes more severe, the LV dilates in order to handle increased volumes with minimal changes in ventricular diastolic pressures. Thus patients with longstanding, severe AR may have very large hearts with normal diastolic pressures. In some patients with AR and dilated left ventricles, myocardial function begins to decline for reasons that are poorly understood. The development of LV dysfunction leads to increased LV diastolic pressures and eventually to development of pulmonary congestion and symptoms of dyspnea.