The effects of acute severe aortic regurgitation on the left ventricle were investigated in conscious, chronically instrumented dogs. Left ventricular dimensions and volumes were measured from biplane cineradiographs of beads positioned near the endocardium. Data were collected before and after the production of aortic regurgitation by a catheter technique. The aortic regurgitation resulted in increases in mean aortic pulse pressure from 44 to 73 mmHg (P smaller than 0.001), heart rate from 87 to 122 beats/min (P smaller than 0.02), and left ventricular end-diastolic pressure from 11 to 25 mmHg (P smaller than 0.05). Mean end-diastolic volume rose from 61 to 69 cc (P smaller than 0.001), while end-systolic volume remained unchanged at 37 cc. The end-diastolic dilatation following regurgitation was asymmetrical in that the increase in size was due principally to an increase in the septal-lateral axis. The acute volume load of aortic regurgitation was accomplished by an increase in end-diastolic volume, i.e., the Frank-Starling mechanism. The tachycardia probably reflects augmented cardiac sympathetic activity, but the constant end-systolic volume at a similar mean systolic pressure suggests that the net contractile state was unchanged.
A case report of pseudoaneurysm of left sinus of Valsalva invaded into the left ventricle with severe aortic regurgitation
