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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Demand for dialysis for patients with end-stage renal disease is growing, as is the comorbidity of dialysis patients. Accurate prediction of those destined to die quickly despite dialysis could be useful to patients, providers, and society in making decisions about starting dialysis. To determine whether age and comorbidity accurately predict death within 6 months of first dialysis for end-stage renal disease, a prospective cohort study of 822 patients starting dialysis at one of 11 Canadian centers was performed. Patient characteristics were recorded at first dialysis. Follow-up continued until death or study end (at least 6 months after enrollment). One hundred thirteen of 822 (13.7%) patients died within 6 months. Although an existing scoring system predicted prognosis, adverse scores greater than 9 were found in only 9.7% of those who died; only 52% of those who scored higher than 9 died within 6 months. No score cutoff point combined high true-positive and low false-positive rates for predicting early death. Age, severity of heart failure or peripheral vascular disease, arrhythmias, malnutrition, malignancy, or myeloma were independent prognostic factors identified in multivariate models. However, the best fit discriminant and logistic models were also unable to accurately predict death within 6 months. Clinicians were very accurate in assigning patients to prognostic groups up to a 50% risk of death by 6 months, above which they tended to overestimate risk. However, clinicians were only marginally better than the predictive models in determining whether a given high-risk patient would die. The inability of a scoring system or clinical intuition to accurately predict death soon after starting dialysis for end-stage renal disease suggests that limiting access to dialysis on the basis of likely short survival may be inappropriate in Canada.
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PMID:Prediction of early death in end-stage renal disease patients starting dialysis. 901 92

In senescence renal function is thought to decline markedly even in the absence of renal disease. It has also been proposed that the changes in renal function with age are not uniform and that confounding factors such as hypertension or atherosclerosis may play a role. We performed a comprehensive study to compare several aspects of renal function in four groups: (i) young healthy normotensive subjects (N = 24; 13 males; mean age 26 +/- 3 years); (ii) elderly healthy normotensive subjects (elderly NT; N = 29; 13 males; 68 +/- 7 years); (iii) elderly treated and untreated hypertensive patients (elderly HT; N = 25; 13 males; 70 +/- 6 years); and (iv) elderly patients with compensated mild to moderate heart failure (elderly HF; N = 14; 6 males; 69 +/- 6 years). Compared to young subjects mean GFR (C(In)) and ERPF (C(PAH)) were significantly lower in the elderly, despite similar mean plasma creatinine levels (young, 121 +/- 11, 650 +/- 85 ml/min/1.73 m2; elderly NT, 103 +/- 11, 486 +/- 102; elderly HT, 103 +/- 13, 427 +/- 55; elderly HF, 92 +/- 14, 377 +/- 103). Nevertheless, GFR was within the normal range in the majority of elderly NT and HT, but not in elderly HF. ERPF was significantly lower in elderly HT as compared with elderly NT, and still lower in elderly HF. Mean renovascular resistance and filtration fraction were significantly higher in the elderly, particularly in elderly HT and HF as compared with the young. Mean fractional excretion of Na+ was similar in all groups studied, but the lithium clearance was significantly lower in the elderly, suggesting a greater proximal and less distal sodium reabsorption in senescence. In the elderly, mean PTH concentration and urinary excretion of pyridoline cross-links were significantly higher and mean 25-(OH)D3, calcitriol and phosphate concentrations significantly lower; the correlation between PTH and GFR was significant (r = -0.432, P < 0.001). The results document that the decrease in renal hemodynamics with senescence is less marked than suggested by some studies using less stringent methodology and inclusion criteria. Comorbid conditions confound renal function in the elderly. Age-associated changes in renal hemodynamics are accompanied by significant alterations of renal hormones and of renal sodium handling.
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PMID:Renal function in the elderly: impact of hypertension and cardiac function. 908 86

Angiotensin-converting enzyme (ACE) inhibitors are widely used in the management of hypertension, heart failure, and nephropathy. It has been suggested that ACE inhibitors containing the sulfhydryl group (SH) have an additional effect on KATP channels. To prove this hypothesis, we studied the effects of the SH-containing ACE inhibitors, captopril and zofenopril, on KATP channel opening of bovine coronary arteries and guinea pig thoracic aortas. Bovine coronary arteries were precontracted with the thromboxane A2 analogue, U46619, and guinea pig thoracic aortas were precontracted with phenylephrine and then relaxed with either captopril or zofenopril (n = 8). Inhibition of KATP channel opening with glibenclamide moderately attenuated the zofenopril-induced relaxation of guinea pig thoracic aorta. However, in the bovine coronary arteries, the relaxing effect of both captopril and zofenopril remained uneffected by glibenclamide. In experiments with enalapril (a non SH-containing ACE inhibitor; n = 6) on guinea pig thoracic aortas, no effect on KATP channels could be seen. From our experiments, we conclude that the postulated opening of KATP channels by SH-group-containing ACE inhibitors contributes little to the vasodilation of guinea pig thoracic aortas caused by ACE inhibitors, and that SH groups have no influence upon KATP channels of bovine coronary arteries.
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PMID:KATP channel opening does not contribute significantly to the vasodilatory effect of SH-group-containing ACE inhibitors. 911 8

The aim of the investigation was microalbuminuria evaluation as an early symptom of renal involvement in systemic lupus erythematosus (SLE). Thirty patients aged 18 to 66 years (mean: 39,4 years) with mean duration of SLE of 6,3 years (range: 0,5 to 22 years) were examined. All of them fulfilled the preliminary criteria of the American Rheumatism Association for the classification of SLE. During the study none of patients had clinical or laboratory symptoms of nephropathy, hypertension, diabetes mellitus and heart failure. Microalbuminuria was measured by immunoturbidimetric method and the urine microalbumin concentration was expressed as the ratio microalbumin-creatinine concentration in 24 hour urine [equation: see text] Ratio I was 3,36 (+/- 2,76) in patients suffering from SLE comparing to I = 1,35 (+/- 0.89) in normal controls (p < 0.001). There was no correlation between increasing microalbuminuria and patients age and duration of disease. There was also no correlation between microalbuminuria and erythrocyte sedimentation rate or immunological activity parameters (i.e. antinuclear antibodies, anti dsDNA antibodies, levels of C3 and C4 components of complement).
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PMID:[Microalbuminuria in patients with systemic lupus erythematosus]. 912

A review of recent studies suggests that the use of angiotensin-converting enzyme (ACE) inhibitors may be preferred (usually along with a diuretic drug) as initial therapy in several subsets of hypertensive patients (i.e., those with diabetes and nephropathy or with diminished left ventricular function with or without symptoms of heart failure). Limited long-term data are available for the angiotensin II receptor antagonists. The use of nondihydropyridine calcium channel blocking agents (CCBs) appears to reduce reinfarction in patients with ischemic heart disease (however, mortality is not reduced). Long-acting formulas of CCBs appear to decrease congestive heart failure in patients with dilated, but not ischemic, cardiomyopathy and to decrease strokes and arrhythmias in hypertensive subjects. Short-acting agents (primarily those that increase heart rate) may increase coronary heart disease events in hypertensive patients. There is little evidence at present that CCBs offer a major advantage over other antihypertensive agents or that they should be recommended as initial therapy, except in special situations.
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PMID:Angiotensin-converting enzyme inhibitors, angiotensin II receptor antagonists and calcium channel blocking agents: a review of potential benefits and possible adverse reactions. 918 98

Cardiac abnormalities develop during chronic renal failure. The prevalence of ischemic heart disease, cardiac failure, and left ventricular disorders is high among patients initiating end-stage renal disease (ESRD) therapy, and appears to be getting higher. Age, gender, race, diabetes, and possibly geographic location are predictive of the presence of several cardiac conditions. Cardiac morbidity after the initiation of ESRD therapy is high, and cardiac causes are the most common reported cause of death. Cardiac abnormalities present on starting dialysis contribute to this morbidity and mortality. In epidemiological studies, higher cardiac death rates have also been associated with dialysis rather than transplantation as mode of ESRD therapy, peritoneal rather than hemodialysis, lower dose of dialysis, and unmodified cellulose rather than modified cellulose/synthetic hemodialysis membranes.
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PMID:Cardiac disease in chronic uremia: epidemiology. 923 24

Cardiac disease is common and is the major killer in end-stage renal disease (ESRD). Cardiac failure is a highly malignant condition in ESRD patients. Cardiac failure mediates most of the adverse prognostic impact of ischemic heart disease. Left ventricular (LV) abnormalities are already present at initiation of dialysis therapy in approximately 80% of patients. These abnormalities (ie, systolic dysfunction in approximately 15%, LV dilatation with preserved systolic function in 30%, concentric LV hypertrophy [LVH] in 40%) independently predict ischemic heart disease and cardiac failure, and are the largest baseline predictor of mortality after 2 years on dialysis therapy. The associations between classical risk factors (eg, hyperlipidemia, smoking, hypertension) and cardiac outcomes in ESRD are inconsistent. "Uremic" risk factors represent a nascent, but potentially important field. In our prospective 10-year study of 433 patients starting renal replacement therapy, we identified the following as major independent risk factors for cardiac disease: (1) hypertension (concentric LVH, LV dilatation, ischemic heart disease, cardiac failure, inverse relationship with mortality); (2) anemia (LV dilatation, cardiac failure, death); and (3) hypoalbuminemia (ischemic heart disease, cardiac failure, death). Transplantation dramatically improved LV abnormalities, suggesting that a uremic environment is cardiotoxic. Multiple risk factors act in concert to produce cardiac disease in ESRD; many of these are avoidable, suggesting that the enormous burden of disease can be reduced considerably.
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PMID:Cardiac disease in chronic uremia: clinical outcome and risk factors. 923 28

Heart disease is a common cause of morbidity in end-stage renal disease (ESRD) patients. The management of heart disease in these patients requires a multidimensional approach to the management of heart failure, coronary disease, and arrhythmias, and to risk factors such as hypertension, anemia, secondary hyperparathyroidism, and electrolyte/acid-base disturbances. Coronary artery disease management includes use of antianginal drugs and revascularization of coronary arteries with angioplasty +/- stent placement or coronary artery bypass grafting. The long-term outcomes of these procedures need to be assessed and improved. Hypertension occupies a major role in the pathogenesis of heart disease in ESRD, and early and adequate control of hypertension is likely to have a major impact on the progression of cardiac disease. This entails the achievement of optimal volume status, combined with the appropriate use of antihypertensive agents such as calcium channel blockers, beta-blockers, angiotensin-converting enzyme (ACE) inhibitors, vasodilators, alpha-blockers, and central sympatholytic drugs. In ESRD patients, specific dialysis-related complications such as intradialytic hypotension and pericardial effusion may have additional effects on cardiac function and require attention. The choice of dialysate composition and membrane may influence clinical outcomes with specific effects on cardiac performance.
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PMID:Cardiac disease in chronic uremia: management. 923 29

Little is known about the epidemiology of cardiac disease in diabetic end-stage renal disease. We therefore prospectively followed a cohort of 433 patients who survived 6 months after the inception of dialysis therapy for an average of 41 months. Clinical and echocardiographic data were collected yearly. At baseline, diabetic patients (n = 116) had more echocardiographic concentric left ventricular hypertrophy (50 vs 38%, p = 0.04), clinically diagnosed ischaemic heart disease (32 vs 18%, p = 0.003) and cardiac failure (48 vs 24%, p < 0.00001) than non-diabetic patients (n = 317). After adjusting for age and sex, diabetic patients had similar rates of progression of echocardiographic disorders, and de novo cardiac failure, but higher rates of de novo clinically diagnosed ischaemic heart disease (RR 3.2, p = 0.0002), overall mortality (RR 2.3, p < 0.0001) and cardiovascular mortality (RR 2.6, p < 0.0001) than non-diabetic patients. Mortality was higher in diabetic patients following admission for clinically diagnosed ischaemic heart disease (RR 1.7, p = 0.05) and cardiac failure (RR 2.2, p = 0.0003). Among diabetic patients older age, left ventricular hypertrophy, smoking, clinically diagnosed ischaemic heart disease, cardiac failure and hypoalbuminaemia were independently associated with mortality. The excessive cardiac morbidity and mortality of diabetic patients seem to be mediated via ischaemic disease, rather than progression of cardiomyopathy while on dialysis therapy. Potentially remediable risk factors include smoking, left ventricular hypertrophy, and hypoalbuminaemia.
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PMID:Cardiac disease in diabetic end-stage renal disease. 938 23

While the bulk of the existing data are in diabetic renal disease, there are some animal and clinical studies that compare the effects of angiotensin I (AT-1) receptor antagonists to angiotensin converting enzyme (ACE) inhibitors in renal disease of nondiabetic origin. Based on these data, preservation of renal function and morphology occurs with AT-1 receptor antagonists in animal models where renal injury is hemodynamically mediated such as in the remnant kidney. Conversely, in non-hemodynamically mediated renal injury such as in puromycin nephrosis, AT-1 receptor antagonists have not consistently protected against declines in glomerular filtration rate or development of interstitial fibrosis. This may, however, be related to dosage, since high doses of AT-1 receptor antagonists show some protection against progression in these models. It is too early, however, to make judgments regarding the clinical impact of the AT-1 receptor antagonists on progression of nondiabetic renal disease. The result of the ELITE trial support the concept that progression of renal dysfunction associated with heart failure is ameliorated to a similar extent between ACE inhibitors and the AT-1 receptor antagonist, losartan. The AT-1 receptor antagonist group also had fewer side effects including the absence of cough as well as a lower, albeit not statistically significant, incidence of hyperkalemia. Thus, the emerging database supports the concept that AT-1 receptor antagonists have an efficacy similar to ACE inhibitors for preserving renal function and morphology in hemodynamically mediated renal injury. It is unclear, however, whether this drug class will reduce immunologically-mediated renal injury.
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PMID:Angiotensin II receptor blockade and progression of nondiabetic-mediated renal disease. 940 25


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