In 24 patients with aortic insufficiency undergoing aortic valve replacement, a clinical and hemodynamic study was performed pre-operatively. Left ventricular biopsies were obtained perioperatively for morphometric study. No significant relations were found when morphometric data were compared to functional class, cardiothoracic radio and ECG findings. The percentage of interstitial fibrosis was not correlated with any of the measured hemodynamic parameters. Myocardial cell diameter was weakly correlated with left ventricular systolic function parameters. A decrease in the percentage of contractile material was strongly correlated with an impaired left ventricular function, assessed pre-operatively. During clinical follow-up, patients were divided into two groups: Group A (17 patients) included patients who were in class I or II of NYHA after surgery. Group B (seven patients) included patients who died or were in functional class III or IV. As compared with Group A, Group B patients had a significantly lower ejection fraction; their myocardial cell diameter was larger and the percentage of myofibrils, and the content of contractile material were significantly lower. This suggests that, in aortic regurgitation, left ventricular dysfunction is correlated with contractile material loss and not with interstitial fibrosis, and that morphometric changes are good predictors of follow-up after surgery.
Left ventricular myocardial biopsies were performed during surgery in 11 patients with pure and isolated mitral stenosis. Patients had undergone a preoperative angiocardiographic study of left ventricular function. Biopsy specimens were examined with the light and electron microscope. Myocyte cell diameter was normal (20 +/- 1.6 mu). Lesions existed which were probably degenerative, including anarchy and irregularities of sarcomeres, Nemaline Myopathy-type Z line changes and alterations of intercalated discs. A moderate fibrosis was found in the interstitial spaces with very few histiocytes. The coincidence planimetry study of the interstitial spaces showed a 37 +/- 5.5% increase compared to a control group with no fibrosis (23 +/- 1.5%, p less than 0.01). The angiocardiographic indices of left ventricular function were all decreased. Only four subjects had normal left ventricular function (EF greater than or equal to 55%). Nevertheless, it was not possible to establish a significant correlation between the extent of fibrosis and the decrease of left ventricular function. Although left ventricular fibrosis could be one of the factors responsible for decreased myocardial function, it is not sufficient to explain the changes of left ventricular function which are rather frequently observed in mitral stenosis.
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