Current Topics in Heart Failure: Experimental and Clinical by Prof. Dr. R. Jacob (auth.), Prof. Dr. Rainer W. Gülch, Prof.

By Prof. Dr. R. Jacob (auth.), Prof. Dr. Rainer W. Gülch, Prof. Dr. Gerolf Kissling (eds.)

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Extra resources for Current Topics in Heart Failure: Experimental and Clinical Aspects

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The findings of this study led us to conclude that ventricular systolic pressure was responsible for myocyte growth and LVH, which was found in each model of arterial hypertension. Given that right ventricular weight was unchanged in all models, we further concluded that elevations in coronary perfusion pressure did not cause myocyte hypertrophy in the right ventricle, despite previous inferences drawn from studies of myocardial protein synthesis in the isolated heart (19). Finally, it was clear that elevations in either left ventricular systolic or coronary perfusion pressures were not responsible for the abnormal fibrous tissue response unless there was an associated activation of the RAA system.

Brilla CG, Janicki JS, Weber KT (1990) Kardioprotektive Effekte von Lisinopril bei arterieller Hypertonie. Z Kardiol79 (suppl1):130 8. Capasso JM, Robinson TF, Anversa P (1989) Alterations in collagen cross-linking impair myocardial contractility in the mouse heart. Circ Res 65:1657-1664 9. Capasso JM, Palackal T, Olivetti G, Anversa P (1990) Left ventricular failure induced by longterm hypertension in rats. Circ Res 66:1400-1412 10. Clozel J-P, Kuhn H, Hefti F (1989) Effects of chronic ACE inhibition on cardiac hypertrophy and coronary vascular reserve in spontaneously hypertensive rats with developed hypertension.

Perhaps, it is the growth of nonmyocyte cells, rather than myocyte hypertrophy that accounts for pathologic LVH in the patient with cardiovascular disease. Nonmyocyte cells include endothelial and vascular smooth muscle cells, cardiac fibroblasts, macrophages, and mast cells. Their growth, or the consequences of their growth, can adversely alter myocardial structure. , hypertrophy) can lead to intimal and medial thickening of in- * This work was supported in part by NIH grant R01-31701 and Deutsche F orschungsgemeinschaft Br-1029-2.

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