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)

End-stage renal disease (ESRD) patients have a high cardiovascular mortality rate. Precise estimates of the prevalence, risk factors and prognosis of different manifestations of cardiac disease are unavailable. In this study a prospective cohort of 433 ESRD patients was followed from the start of ESRD therapy for a mean of 41 months. Baseline clinical assessment and echocardiography were performed on all patients. The major outcome measure was death while on dialysis therapy. Clinical manifestations of cardiovascular disease were highly prevalent at the start of ESRD therapy: 14% had coronary artery disease, 19% angina pectoris, 31% cardiac failure, 7% dysrhythmia and 8% peripheral vascular disease. On echocardiography 15% had systolic dysfunction, 32% left ventricular dilatation and 74% left ventricular hypertrophy. The overall median survival time was 50 months. Age, diabetes mellitus, cardiac failure, peripheral vascular disease and systolic dysfunction independently predicted death in all time frames. Coronary artery disease was associated with a worse prognosis in patients with cardiac failure at baseline. High left ventricular cavity volume and mass index were independently associated with death after two years. The independent associations of the different echocardiographic abnormalities were: systolic dysfunction-older age and coronary artery disease; left ventricular dilatation-male gender, anemia, hypocalcemia and hyperphosphatemia; left ventricular hypertrophy-older age, female gender, wide arterial pulse pressure, low blood urea and hypoalbuminemia. We conclude that clinical and echocardiographic cardiovascular disease are already present in a very high proportion of patients starting ESRD therapy and are independent mortality factors.
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PMID:Clinical and echocardiographic disease in patients starting end-stage renal disease therapy. 773 Nov 45

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

Cardiovascular diseases (CVDs) are the leading cause of mortality and hypertension contributes substantially to the incidence of stroke, coronary artery disease, heart failure, atrial fibrillation and peripheral vascular disease. The origin of hypertension is clearly multifactorial, and a complex and multifaceted approach is necessary to decrease its incidence. The most recognizable factors involved in reducing the incidence of hypertension are prevention, early diagnosis and treatment; however, the importance of the foetal environment and early postnatal development has recently been considered. In clinical practice, these factors are still frequently overlooked, probably because of a lack of knowledge about the underlying mechanisms and effective treatment or prevention. Pathophysiological mechanisms underlying the prenatal programming of CVDs were investigated in the study by Shah et al. published recently in Clinical Science (2017) 131(17), 2303-2317. The study explored cardiac susceptibility of adult male and female rat offspring to ischaemic myocardial injury due to prenatal exposure to hypoxia. The results demonstrated significant changes in global cardiac function and left ventricular dilatation following myocardial infarction in rat offspring prenatally exposed to hypoxia. The effects were gender specific and occurred only in males, whereas females were protected. These findings are important from several perspectives. First, they point to the fact that an inadequate foetal environment can increase susceptibility to death from myocardial infarction. Second, during their reproductive life, females are better protected from cardiovascular insult than males, but it is not known if they lose this advantage after menopause, and can be equally at risk as males.
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PMID:Sex-specific cardiovascular susceptibility to ischaemic myocardial injury following exposure to prenatal hypoxia. 2917 Mar 60