[Complex hemodynamic analysis of left ventricular systole in hypertrophic cardiopathy--clinical implications].

Hypertrophic cardiomyopathy is characterized by hemodynamic disturbances concerning left ventricular systole and diastole. Both of them are probably connected with abnormal structure of myocardium. The aim of the study was to assess left ventricular sufficiency, LV contractility and answer the question: if there is relationship between hemodynamic disturbances and clinical state. Estimation of verapamil influence on evaluated parameters was performed in the second part of the study. 20 patients (13 M, 7 F) aged 16-59 years (mean age 33, 25 yrs) with various type of hypertrophic cardiomyopathy were studied. Catheterization of the right and left heart and coronarography were performed in each patient. The first pressure derivative (d/P/dt) was recorded simultaneously with left ventricular pressure recording. Left ventricular angiography was performed in RAO 30 degrees and LAO 60 degrees projections. Analysis of the angiographic image of the whole heart cycle every 40 ms was performed to evaluate the changes in the left ventricular volume and LV wall thickness. Relationships between left ventricular pressure and volume were defined using computer PDP 11/24. To define verapamil influence, 6 patients received 10 mg of the drug intravenously, 14 patients received verapamil directly into left coronary artery 0.02 mg/kg of 0.5 mg/min. Control blood pressure measurements were performed after 5 and 10 minutes, and ventriculography after 15 min. Obtained results were compared with the control group consisted of 10 patients with normal hemodynamic data. Left ventricular contractility was estimated using V max and power/volume relationship (stress/volume). Both indices showed decreased left ventricular muscle contractility in hypertrophic cardiomyopathy. Verapamil had no significant effect on left ventricular contractility in our patients. Ejection period was studied using few indices. Ejection volume and net work (strokework) of the left ventricle were found to be decreased significantly, what means decreased mechanical preformance. The most significant were differences concerning mechanical performance which did not change after verapamil administration whereas circumferential fibre shortening velocity (VCF) was found to be decreased. If was probably related to increased afterload which could be caused by ventricular kinetics change. Midsystolic stress and the afterload index, significantly lower in cardiomyopathic patients. Preload was similar in both groups. Ejection indices of decreased afterload and normal preload proved decreased contractility. If above changes were primary, hypertrophy might be the compensating mechanism of decreased myocardial sufficiency in patients with hypertrophic cardiomyopathy. Which proved Hiroto's and Furabayashi's. The lack of negative effect verapamil on LV contractility in the group of our patients was very interesting, and could be partially related to beneficial effects in diastole.(ABSTRACT TRUNCATED AT 400 WORDS)