This document discusses the pathophysiology of aortic regurgitation. In chronic aortic regurgitation, the left ventricle undergoes compensatory mechanisms to maintain cardiac output, including increasing end diastolic volume, chamber compliance, and total stroke volume. This results in eccentric left ventricular hypertrophy. Over time, increased afterload leads to concentric hypertrophy as well. In some patients, the compensatory mechanisms eventually fail, resulting in left ventricular systolic dysfunction and heart failure symptoms. Early afterload reduction therapy can potentially reverse the compensatory changes and reduce regurgitation severity.