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Störk T, Möckel M, Danne O, et al. Left ventricular hypertrophy and diastolic dysfunction: their relation to coronary heart disease. Cardiovasc Drugs Ther. 1995;9:533-7doi: 10.1007/BF00877866.
Störk, T., Möckel, M., Danne, O., Völler, H., Eichstädt, H., & Frei, U. (1995). Left ventricular hypertrophy and diastolic dysfunction: their relation to coronary heart disease. Cardiovascular drugs and therapy, 9533-7. https://doi.org/10.1007/BF00877866
Störk, T, et al. "Left ventricular hypertrophy and diastolic dysfunction: their relation to coronary heart disease." Cardiovascular drugs and therapy vol. 9 (1995): 533-7. doi: https://doi.org/10.1007/BF00877866
Störk T, Möckel M, Danne O, Völler H, Eichstädt H, Frei U. Left ventricular hypertrophy and diastolic dysfunction: their relation to coronary heart disease. Cardiovasc Drugs Ther. 1995 Aug;9:533-7. doi: 10.1007/BF00877866. PMID: 8562471.
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Cardiovasc Drugs Ther. 1995 Aug;9:533-7. doi: 10.1007/BF00877866.

Left ventricular hypertrophy and diastolic dysfunction: their relation to coronary heart disease.

Cardiovascular drugs and therapy

T Störk, M Möckel, O Danne, H Völler, H Eichstädt, U Frei

Affiliations

  1. Department of Internal Medicine, Nephrology and Intensive Care Medicine, University Hospital Virchow Klinikum, Berlin, Germany.

PMID: 8562471 DOI: 10.1007/BF00877866

Abstract

Diastolic dysfunction is an early sign in the temporal sequence of ischemic events in coronary heart disease. The ischemic cascade, beginning with an oxygen demand supply imbalance and metabolic alterations, identifies diastolic disorders of the left ventricle (LV) as an early phenomenon, sometimes before systolic dysfunction, electrocardiographic changes, or chest pain occur. Although the physiology of diastolic function is complex, the factors contributing to diastolic disturbances can be differentiated into intrinsic and extrinsic LV abnormalities. Intrinsic mechanisms include (a) impaired LV relaxation, (b) the complex of LV hypertrophy, and (c) increased LV asynchrony. Myocardial hypertrophy leads to an increase of the myocardial mass/volume ratio, and the degree of hypertrophy is the main determinant of chamber stiffness. The main, if not unique, determinant of myocardial diastolic tissue distensibility is the structure and concentration of the collagen. Consequently, tissue stiffness is increased in coronary disease by reparative interstitial fibrosis or scar following myocardial infarction. In myocardial hypertrophy the LV collagen concentration is elevated due to reactive fibrosis. An increase in regional asynchrony of LV contraction and relaxation is a result of regional ischemia as well as of LV hypertrophy and tissue fibrosis. Factors extrinsic to the LV causing diastolic disorders include (a) increased central blood volume, which will increase left ventricular pressure without altering the LV pressure-volume relation, and (b) ventricular interaction mediated by pericardial restraint, which may cause a parallel upward shift of the diastolic LV pressure-volume relation. Improved insight into the mechanisms of LV relaxation and filling characteristics help in the treatment of LV diastolic dysfunction.

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