Evaluation of left ventricular function in patients with aortic regurgitation using afterload stress.
Left ventricular function was assessed in 14 patients with chronic aortic regurgitation by afterload elevation with angiotensin. Seven of 14 patients maintained their resting ejection fraction with angiotensin (group A), while the remaining seven experienced a decline of greater than 0.10 in ejection fraction (group B). Six of seven group A patients showed an appropriate rise in left ventricular stroke work index in response to the angiotensin-induced rise in left ventricular end-diastolic pressure. In contrast, six of seven group B patients showed abnormal, flat, or declining stroke work indices. Included in the seven group B patients were two patients with left ventricular dysfunction secondary to coronary artery disease. The five other group B patients, who did not have coronary diseases, exhibited similar stress-induced ventricular dysfunction, despite the absence of any significant resting hemodynamic differences from patients in group A. These five stress-induced dysfunction patients were distinctive from patients who maintained their ejection fraction level in that the former all had regurgitant fractions of greater than 0.50, whereasl all gruop A patients had regurgitant fractions of less than 0.50. Similarly, these five stress-induced dysfunction patients had significantly larger left ventricular end-diastolic volumes than did the group A patients. These data suggest that patients with pronounced aortic regurgitation measured in terms of regurgitant fraction greater than 0.50 and left ventricular end-diastolic volume of greater than 160 cm3/m2 exhibit impaired ventricular function if appropriately stressed. As most of the patients with stress-induced dysfunction had a normal ejection fraction at rest, it may be that stress-induced dysfunction represents a stage before overt resting dysfunction and cardiac failure.
D000328:Adult; D000804:Angiotensin II / Q000494:pharmacology*; D001022:Aortic Valve Insufficiency / Q000503:physiopathology*; D002302:Cardiac Output; D005260:Female; D006352:Heart Ventricles / Q000503:physiopathology*; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D008297:Male; D008875:Middle Aged
D000804:Angiotensin II