Fibrosis and ischemia: The real risks in hypertensive heart disease

The increased cardiovascular morbidity and mortality in hypertension are re lated to the target organs (ie, heart, brain, kidneys) involvement from vas cular disease. Left ventricular hypertrophy (LVH), the major expression of cardiac involvement, is both a structural and functional adaptation to the afterload imposed by the vascular disease. Without this adaptation, cardiac failure would result much earlier in the natural history of hypertensive h eart disease (HHD). However, LVH imposes an independent risk that is even g reater than the risk associated with the height of systolic or diastolic pr essure. The mechanisms that explain this risk have not been defined precise ly, several have been postulated. Among these are the following: 1) coronar y hemodynamic alterations associated with HHD (ie, increased coronary vascu lar and minimal vascular resistance, reduced coronary blood how and flow re serve, and increased blood viscosity); 2) enhanced predisposition for letha l cardiac arrhythmias, cardiac failure, and accelerated atherosclerosis of the coronary arteries (with exacerbation of the ischemia); and 3) collagen deposition and ventricular fibrosis. From the earliest controlled therapeut ic trials, deaths from stroke and coronary heart disease were significantly reduced. However, more recent data have indicated that the prevalence of c ardiac failure (CHF) continues to rise progressively. The nature of the CHF is no longer primarily from systolic dysfunction, but is now chiefly from diastolic dysfunction. Diastolic dysfunction occurs primarily in the elderl y hypertensive patient or in the patient with ischemic heart disease, both of which are associated with increased collagen deposition. Indeed, these e ffects 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 occur ring in hospitalized patients over 65 years of age. In this report, both ex perimental and clinical evidence demonstrating that increased ventricular f ibrosis occurs in the spontaneously hypertensive rats and in hypertensive p atients are provided, and that treatment with the newer antihypertensive ag ents reduce ventricular hydroxyproline (ie. collagen) content while. at the same time, improve coronary hemodynamics. (C) 2001 American Journal of Hyp ertension, Ltd.