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Titolo:
Fibrosis and ischemia: The real risks in hypertensive heart disease
Autore:
Frohlich, ED;
Indirizzi:
Alton Ochsner Med Fdn & Ochsner Clin, New Orleans, LA 70121 USA Alton Ochsner Med Fdn & Ochsner Clin New Orleans LA USA 70121 A 70121 USA
Titolo Testata:
AMERICAN JOURNAL OF HYPERTENSION
fascicolo: 6, volume: 14, anno: 2001,
parte:, 2 supplemento:, S
pagine: 194S - 199S
SICI:
0895-7061(200106)14:6<194S:FAITRR>2.0.ZU;2-N
Fonte:
ISI
Lingua:
ENG
Soggetto:
LEFT-VENTRICULAR HYPERTROPHY; ANGIOTENSIN-CONVERTING ENZYME; CORONARY RESISTANCE VESSELS; ANGINA-PECTORIS; ARTERIAL-HYPERTENSION; MYOCARDIAL FIBROSIS; BLOOD-FLOW; ENDOTHELIAL DYSFUNCTION; L-ARGININE; RATS;
Keywords:
left ventricular hypertrophy; coronary flow reserve; hydroxyproline; angiotensin converting enzyme inhibition; angiotensin II; type II receptor antagonism; calcium antagonists;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
64
Recensione:
Indirizzi per estratti:
Indirizzo: Frohlich, ED Alton Ochsner Med Fdn & Ochsner Clin, 1516 Jefferson Highway,New Orleans,LA 70121 USA Alton Ochsner Med Fdn & Ochsner Clin 1516 Jefferson Highway New Orleans LA USA 70121
Citazione:
E.D. Frohlich, "Fibrosis and ischemia: The real risks in hypertensive heart disease", AM J HYPERT, 14(6), 2001, pp. 194S-199S

Abstract

The increased cardiovascular morbidity and mortality in hypertension are related to the target organs (ie, heart, brain, kidneys) involvement from vascular disease. Left ventricular hypertrophy (LVH), the major expression ofcardiac involvement, is both a structural and functional adaptation to theafterload imposed by the vascular disease. Without this adaptation, cardiac failure would result much earlier in the natural history of hypertensive heart disease (HHD). However, LVH imposes an independent risk that is even greater than the risk associated with the height of systolic or diastolic pressure. The mechanisms that explain this risk have not been defined precisely, several have been postulated. Among these are the following: 1) coronary hemodynamic alterations associated with HHD (ie, increased coronary vascular and minimal vascular resistance, reduced coronary blood how and flow reserve, and increased blood viscosity); 2) enhanced predisposition for lethal cardiac arrhythmias, cardiac failure, and accelerated atherosclerosis ofthe coronary arteries (with exacerbation of the ischemia); and 3) collagendeposition and ventricular fibrosis. From the earliest controlled therapeutic trials, deaths from stroke and coronary heart disease were significantly reduced. However, more recent data have indicated that the prevalence of cardiac failure (CHF) continues to rise progressively. The nature of the CHF is no longer primarily from systolic dysfunction, but is now chiefly fromdiastolic dysfunction. Diastolic dysfunction occurs primarily in the elderly hypertensive patient or in the patient with ischemic heart disease, bothof which are associated with increased collagen deposition. Indeed, these effects continue to be suggested by the data from the Framingham Heart Study as well as NHANES-III that indicate CHF is the most common diagnosis occurring in hospitalized patients over 65 years of age. In this report, both experimental and clinical evidence demonstrating that increased ventricular fibrosis occurs in the spontaneously hypertensive rats and in hypertensive patients are provided, and that treatment with the newer antihypertensive agents reduce ventricular hydroxyproline (ie. collagen) content while. at the same time, improve coronary hemodynamics. (C) 2001 American Journal of Hypertension, Ltd.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 11/07/20 alle ore 12:54:16