In patients with AR, forward flow is improved by peripheral vasodilation. Typically, a normal ejection fraction is maintained by a large stroke volume. However, over time, increases in the left ventricular wall stress and afterload result.14 Eventually, as left ventricular dilation and hypertrophy progress, irreversible left ventricular dysfunction develops, and patients become symptomatic. Further impairment of systolic function occurs secondary to oxidative stress, collagen degradation, and matrix metalloproteinase activation.15 As a compensatory mechanism for poor cardiac output, sympathetic constriction of the peripheral vasculature occurs to maintain blood pressure, although this worsens regurgitation and cardiac output.