HEART DISEASE Time course of regression of left ventricular hypertrophy after aortic valve replacement

To assess the time course and extent of regression of myocardial hypertrophy after removal of the inciting hemodynamic stress, 21 patients with either aortic stenosis or aortic insufficiency were studied preoperatively, after an intermediate period (1.6 + 0.5 years), and late (8.1 + 2.9 years) after aortic valve replacement, and results were compared with those in 11 control patients. After aortic valve replacement there was significant hemodynamic improvement, with a fall in the left ventricular end-diastolic volume index (164 + 73 to 105 + 35 ml/m2, p < .01), a fall in left heart filling pressure (19 + 9 to 12 + 5 mm Hg, p < .01), and maintenance of the cardiac index (3.3 + 0.8 to 3.5 ± 0.8 liters/min/m2, NS) and left ventricular ejection fraction (60 ± 13% to 64 ± 10%, NS). By the late study the cardiac index (4.0 ± 0.6 liters/min/m2, p < .01) and left ventricular ejection fraction (66 ± 15%, p < .05) had further increased and were significantly greater than before surgery. For the group as a whole, the left ventricular muscle mass index fell 31% after surgery by the time of the intermediate postoperative study (174 ± 38 vs 120 ± 29 g/m2, p < .01), and a further 13% from the intermediate to the late study (105 ± 32 g/m2, p < .05). At the preoperative study left ventricular muscle mass index was greatest in those patients with aortic insufficiency (191 ± 36 g/m2), and greater in those with aortic stenosis (158 ± 33 g/m2) than in control subjects (85 ± 9 g/m2, p < .05). At the intermediate postoperative study left ventricular muscle mass index remained significantly higher in both those with preoperative aortic insufficiency (128 ± 29 g/m2) and those with stenosis (114 ± 27 g/m2) than in the control subjects (p < .01). By the time of the late postoperative study there were no longer any significant differences in left ventricular muscle mass index. Thus, the regression of myocardial hypertrophy is a process that occurs over many years after correction of the primary hemodynamic abnormality. As this process of myocardial remodeling occurs, continued improvement in cardiac function may occur, and the improvement occurring between the intermediate and late postoperative studies at a slight but constant afterload excess (inherent in the relative stenosis of the aortic prosthesis) suggests that the hypertrophied myocardium is operating at a reduced level compared with normal myocardium. Circulation 77, No. 6, 1345-1355, 1988. LEFT VENTRICULAR pressure and volume overloads in response to aortic valve stenosis and aortic valve insufficiency lead to a marked hypertrophic response of the myocardium, likely as an adaptative response to normalize the increased wall stress accompanying these states.' While this allows for maintenance From the Medical Policlinic, Division of Cardiology, University Hospital, Zurich. Supported by a grant from the Swiss National Science Foundation, and by grant RR-0001032 from the General Clinical Research Centers Program of the Division of Research Resources, NIH. Address for correspondence: Hans P. Krayenbuehl, M.D., Chief, Division of Cardiology, Medical Policlinic, University Hospital, Raemistrasse 100, 8091 Zurich, Switzerland. Received June 12, 1987; revision accepted Feb. 11, 1988. A preliminary report was presented at the Annual Scientific Sessions of the American Heart Association in Dallas, November, 1986. *Current address: Division of Cardiology, Albert Einstein College of Medicine, Bronx, NY. of cardiac performance, it may lead to progressive myocardial failure.2 Aortic valve replacement has produced a dramatic change in the "natural" history of these disorders. There has been reported improvement in survival,3 New York Heart Association class,4,5 and resting hemodynamics.4-'1 This improvement occurs even though the prosthetic valve itself constitutes a relative and persistent, although not progressive, stenotic obstruction to left ventricular ejection.,2 ` The extent to which the myocardium itself may recover or deteriorate as a result of the initial hemodynamic insult in the years after such successful surgery and the regression of the attendant hypertrophy have not been defined. In this study, we investigated the time course of regression of myocardial hypertrophy in 21 patients Vol. 77, No. 6, June 1988 1345 by gest on N ovem er 8, 2017 http://ciajournals.org/ D ow nladed from