Morphology of the heart and arteries in renal failure.
In patients with renal failure, cardiovascular complications are a major clinical problem; cardiac death is the main cause of death in these patients. Cardiac risk is increased by a factor of 20 in uremic patients, compared with matched segments of the general population. It has been known for a long time that atherosclerosis, particularly plaque in the epicardiac coronary conduit arteries, are more frequent in patients with chronic renal failure. Recently, however, clinical studies showed that myocardial infarction is responsible for only 30% to 50% of all cardiac deaths. In contrast, 30% to 40% of patients with renal failure and ischemic heart disease show patent coronary arteries on coronary angiogram. Thus, it is very likely that in uremic patients myocardial ischemia tolerance is markedly reduced even in the absence of classical atherosclerosis (i.e., relevant stenosis of coronary arteries). This finding in uremic patients can be at least partially explained by structural and metabolic abnormalities of the myocardium, and in part by alterations of the extracardiac vasculature. The present paper focuses on structural changes of the heart and the vasculature, in particular on atherosclerosis of cardiac and extracardiac arteries, and its potential repercussions for cardiovascular function. In 1827 Richard Bright already pointed to the common presence of left ventricular hypertrophy (LVH) and thickening of the aorta in patients with end-stage renal failure (ESRF). At present, cardiovascular complications account for 45% of all deaths in uremic patients [1]. The recent report of Herzog, Ma, and Colins [2] documented a 59.3% 1-year mortality rate in dialyzed patients who survived myocardial infarction (i.e., mortality was significantly higher than in the general population). It is widely acknowledged that several specific structural and nonstructural alterations of the heart and the extracardiac vasculature are present in patients with renal failure, which presumably contribute to the markedly increased cardiovascular risk in these patients [3].
Tyralla
Karin
K
Department of Pathology, University of Erlangen, Erlangen, Germany.
Amann
Kerstin
K
D001158:Arteries / Q000473:pathology*; D001161:Arteriosclerosis / Q000401:mortality* / Q000473:pathology; D006801:Humans; D007676:Kidney Failure, Chronic / Q000401:mortality*; D009203:Myocardial Infarction / Q000401:mortality* / Q000473:pathology; D009206:Myocardium / Q000473:pathology*; D012307:Risk Factors; D014511:Uremia / Q000401:mortality