FIBROSIS, MYOCYTE DEGENERATION AND HEART-FAILURE IN CHRONIC EXPERIMENTAL AORTIC REGURGITATION

Myocardial fibrosis and myocyte degeneration have been reported in pat ients with chronic aortic regurgitation (AR), and may be related to th e pathophysiology of congestive heart failure (CHF) in this disease. T o define the relationship between myocardial histopathologic variation s and CHF in chronic AR, we performed gross and microscopic evaluation s of postmortem tissue from a rabbit model of chronic AR manifesting l eft ventricular (LV) responses to AR similar to those in humans. Moder ate-to-severe chronic AR (echocardiographic regurgitant fraction = 52 +/- 13%) was induced by closed-chest aortic valve perforation in II Ne w Zealand White rabbits; 5 control rabbits were sham operated. Six of the 11 AR rabbits died 1.5 +/- 0.8 years (range 0.6-2.8 years) after A R induction; all 6 had gross and histologic anatomic evidence of CHF a t necropsy. The remaining 5 AR rabbits survived until sacrifice at 2.9 +/- 0.1 years of AR; none had pathologic evidence of CHF. Cardiac hyp ertrophy and the extent of LV fibrosis and myocyte necrosis all were g reatest among the 6 AR CHF rabbits. No inflammatory response was appar ent in any animal. Moderate-to-severe chronic experimental AR frequent ly results in CHF which is strongly associated with myocardial fibrosi s and necrosis, without evidence of inflammation. These histopathologi c variations may be pathophysiologically related to CHF development.