Myocardial structure and function in patients with aortic valve disease and their relation to postoperative results

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Left ventricular angiographic studies were performed before and 6 months after aortic valve replacement with a Björk-Shiley prosthesis in 21 patients, 5 with aortic stenosis, 8 with mixed aortic valve lesions and 8 with aortic insufficiency. The degree of myocardial fibrosis and myocardial ultrastructural changes were evaluated from transmural needle biopsy specimens obtained from the left ventricular anterior free wall at operation. Twelve patients without heart disease served as control subjects for angiographic data. Patients with aortic valve disease had a significantly higher left ventricular mass before operation than control subjects and a lower ejection fraction and mean normalized systolic ejection rate. After operation left ventricular mass decreased considerably but did not reach normal level. Ejection fraction and mean normalized systolic ejection rate became normal in all patients with aortic valve disease. The percent fibrosis determined with morphometry was significantly higher in the subendocardium than in the subepicardium of pressure-overloaded hearts (predominant stenosis) (19 versus 13 percent) but equal in both layers of volume-overloaded hearts (predominant regurgitation) (19 versus 18 percent). Electron microscopy revealed significant intracell alterations of the nucleus, sarcomeres, mitochondria and cytoplasmic reticulum. When all patients, regardless of type of aortic valve lesion, were considered, there was no significant correlation before operation between percent fibrosis and ejection fraction ( r 0.10) or mean normalized systolic ejection rate ( r 0.02) but a significant inverse relation between left ventricular mass and ejection fraction ( r 0.54) as well as mean normalized systolic ejection rate ( r 0.49). These data suggest that (1) Depressed left ventricular function in aortic valve disease is associated with ultrastructural degenerative cell changes, but complete recovery of cardiac function after aortic valve replacement is not prevented by these changes. (2) Interstitial myocardial fibrosis is not a primary determinant of depressed cardiac function in aortic valve disease.