Ischemia and fibrosis: the risk mechanisms of hypertensive heart disease

Abstract

Mechanisms underlying risk associated with hypertensive heart disease (HHD) and left ventricular hypertrophy (LVH) are discussed in this report and provide a rationale for understanding this very common and important cause of death from hypertension and its complications. Emphasized are impaired coronary hemodynamics, endothelial dysfunction, and ventricular fibrosis from increased collagen deposition intramurally and perivascularly. Each is exacerbated by aging and, perhaps, also by increased dietary salt intake. These functional and structural changes promote further endothelial dysfunction, altered coronary hemodynamics, and diastolic as well as systolic ventricular contractile function in HHD. The clinical endpoints of HHD include angina pectoris (with or without atherosclerosis of the epicardial coronary arteries), myocardial infarction, cardiac failure, lethal dysrhythmias, and sudden death. The major concept to be derived from these alterations is that not all that is clinically recognized as LVH is true myocytic hypertrophy and structural remodeling. Other major co-morbid changes occur that serve to increase cardiovascular risk including impaired coronary hemodynamics, endothelial dysfunction, and ventricular fibrosis.

Cardiac and renal effects induced by different exercise workloads in renovascular hypertensive rats

“…This is consistent with the eccentric hypertrophy induced by exercise training, which can lead to proportional growth of myocyte width and length (39). A variety of hemodynamic mechanisms that may account for hypertensive vascular disease include coronary arteriolar compression by the hypertrophied and stiffer left ventricle, increased arteriolar wall thickness/lumen ratio, and increased left ventricle chamber diameters, reflecting not only myocyte hypertrophy but also collagen deposition (40). The present data showed that Ex 0% prevented cardiac concentric hypertrophy, increased cardiomyocyte diameter, and decreased the cardiac vasculature wall thickness/lumen ratio in 2K1C rats.…”

Killing Many Birds With Two Stones: Hypoxia and Fibrosis Can Generate Ectopic Beats in a Human Ventricular Model

“…In addition, changes in coronary arterial flow involve ventricular wall compression, luminal obstruction, the increased wall thickening of the hypertensive arteriole and reduced ventricular wall vascularity (Frohlich, 2001 ). These pathophysiological changes are frequently associated with ischemic heart disease and the combination with the fibrotic substrate increases the risk of sudden cardiac death (Frohlich, 2000 ).…”