Cardiovascular changes in chronic renal failure--pathogenesis and therapy.
Cardial death caused by ischemia, which is not necessarily connected with coronary arterial changes, represents the main death cause in chronic renal failure patients. The present overview article compiles the latest findings on structural and functional changes of the heart and vessels in uremia, which have a potential effect on the ischemia tolerance of the myocardium and thus help to explain the high cardiovascular mortality in chronic renal failure. The cardiovascular structural changes comprise: 1. A left ventricular myocardium hypertrophy, 2. an interstitial myocardium fibrosis and 3. changes in the myocardial microcirculation like, above all, a rarefaction of the intramyocardial capillaries with increase in the intercapillary oxygen diffusion passage and a vascular wall thickening of intramyocardial arteries. In addition, characteristic metabolic changes, like for instance a decrease of phosphates rich in energy, which contribute likewise to a heightened ischemia sensitivity of the myocardium. At the same time an involvement of extra-myocardial vascular changes is also probable in the development of the prognostically unfavorable myocardium hypertrophy in chronic renal failure. These extracardial vascular changes consist, above all, of a wall thickening of the aorta, of the peripheral arteries and veins with reduction of the share of elastic fiber, of an increase in the extracellular matrix and of a diffuse media calcification and lead to an increase in vascular stiffness and to reduction of aortal compliance.
Amann
K
K
Institute for Pathology, University Erlangen-Nürnberg, Germany. kerstin.amann@patho.imed.uni-erlangen.de
Tyralla
K
K
D000818:Animals; D001161:Arteriosclerosis / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D001808:Blood Vessels / Q000473:pathology; D002318:Cardiovascular Diseases / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control; D003331:Coronary Vessels / Q000473:pathology / Q000503:physiopathology; D005355:Fibrosis; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D007676:Kidney Failure, Chronic / Q000150:complications / Q000473:pathology* / Q000628:therapy; D017202:Myocardial Ischemia / Q000209:etiology / Q000503:physiopathology; D009206:Myocardium / Q000473:pathology