title: Significance of coronary circulation in hypertensive heart disease for development and prevention of heart failure.
abstract: Coronary hemodynamics (coronary blood flow, coronary reserve, myocardial oxygen consumption) were analyzed in both experimental and clinical essential hypertension. Significant reduced coronary reserve was found in hypertensive patients with left ventricular hypertrophy. Extracoronary reasons for these phenomena were ruled out. Considerable thickening of the coronary resistance vessels (medial hypertrophy) in hypertensive hypertrophy associated with a marked increase in the wall thickness/radius ratio was considered sufficient to explain the impairment of coronary flow. After long-term pharmacotherapy there was normalization of both medial hypertrophy and coronary reserve. This small-vessel abnormality correlates well with clinical findings in hypertensive heart disease (angina and electrocardiographic changes despite normal coronary arteriogram). Moreover, this structural adaptation of the small vessels may carry the inherent risk of an impaired oxygen supply to the hypertrophied myocardium. Thus, late cardiac failure of the hypertrophied heart in hypertension may be attributed, in part, to this microcirculation disorder. Conversely, reversal of left ventricular hypertrophy and of hypertrophy of vascular smooth muscle by specific pharmacotherapy can be considered a possible approach to the rational prevention of cardiac failure in hypertensive patients. For future investigations, controlled clinical trials are needed to confirm these findings with regard to prevention of heart failure, and pharmacotherapeutic studies are necessary to define the optimal drug regimen for reversal of vascular smooth muscle hypertrophy.
authors: Department of Medicine, University of Duesseldorf, Federal Republic of West Germany.
authors: B E
authors: BE
authors: Strauer
mesh_terms: D000328:Adult; D000818:Animals; D002303:Cardiac Output, Low / Q000209:etiology* / Q000517:prevention & control; D006332:Cardiomegaly / Q000209:etiology / Q000503:physiopathology* / Q000517:prevention & control; D003326:Coronary Circulation / Q000187:drug effects / Q000502:physiology*; D003327:Coronary Disease / Q000150:complications / Q000503:physiopathology*; D003331:Coronary Vessels / Q000503:physiopathology; D015736:Felodipine / Q000627:therapeutic use; D006801:Humans; D006830:Hydralazine / Q000627:therapeutic use; D006973:Hypertension / Q000150:complications / Q000503:physiopathology* / Q000517:prevention & control; D008790:Metoprolol / Q000627:therapeutic use; D009543:Nifedipine / Q000627:therapeutic use; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D014655:Vascular Resistance / Q000187:drug effects / Q000502:physiology
chemical_list: D006830:Hydralazine; D008790:Metoprolol; D009543:Nifedipine; D015736:Felodipine