Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0264733 (ventricular dilatation)
 2,163 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cardiovascular illness is an important contributor to the morbidity of kidney disease. The spectrum of cardiovascular disease (CVD) in patients with chronic renal insufficiency (CRI) includes left ventricular hypertrophy (LVH) and dilatation, ischemic heart disease, and peripheral vascular disease. Both "traditional" and "uremia-specific" factors contribute to the occurrence and progression of cardiac disease in renal patients. A growing body of recent evidence indicates that the processes contributing to CVD commence early in CRI, leading to concentric LVH, left ventricular dilatation, congestive heart failure, and ischemic heart disease. Many of the coexisting conditions that have been identified consistently as contributing to the burden of cardiovascular illness in renal populations can be modified through medical interventions. Specific therapies exist for hypertension, anemia, hyperparathyroidism, and dyslipidemia. Studies to date have demonstrated that treatment of many of these factors-such as anemia and hypertension during end-stage renal disease-appear to benefit the cardiovascular system. Earlier intervention may offer the best opportunity to reduce the burden of illness in all groups of CRI patients. Identification of patients at the onset of kidney disease and attention to the known traditional and "uremic" risk factors are emerging as promising strategies. Long-term interventional studies are needed to determine costs, benefits, and risks of such strategies.
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PMID:Cardiovascular disease in chronic renal insufficiency. 1111 55

Patients with chronic renal failure have, as compared with age-matched controls with normal renal function, a markedly higher cardiovascular mortality. The reason is probably accelerated atherosclerosis and left ventricular hypertrophy as a result of accumulation of "classical" cardiovascular risk factors and the presence of some risk factors relatively specific for "uraemia" (e.g. anaemia, hyperhydratation, dyslipidaemia). It is assumed that the reversibility of left ventricular hypertrophy is limited in chronic renal failure due to more marked myocardial fibrosis ("uraemic cardiomyopathy"). Its regression can be achieved by treatment of hypertension with inhibitors of angiotensin converting enzyme with a positive effect on cardiovascular mortality. Regression of left ventricular hypertrophy occurs also in some patients after renal transplantation. Treatment of anaemia reduces the risk of progressive left ventricular dilatation. The cardiovascular risk increases probably already a relatively slight decline of glomerular filtration which need not lead to a significant rise of serum creatinine. The cardiovascular risk obviously increases further with progression of chronic renal insufficiency. Patients with a reduced renal function and chronic renal insufficiency have lower target blood pressure and should have also lower target values e.g. of serum cholesterol. Therapeutic procedures in these patients should not be focused only on a slower progression of chronic renal insufficiency but also on reduction of their high cardiovascular risk.
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PMID:[Cardiovascular complications in patients with chronic renal insufficiency and chronic kidney failure]. 1290 73