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

To determine the possible association between anemia and clinical and echocardiographic cardiac disease, a cohort of 432 end-stage renal disease patients (261 on hemodialysis and 171 on peritoneal dialysis) who started dialysis therapy between 1982 and 1991 were followed prospectively for an average of 41 months. Baseline demographic, clinical, and echocardiographic assessments were performed, as well as monthly serial clinical and laboratory tests while the patients were on dialysis therapy. The mean (+/-SD) hemoglobin level during dialysis therapy was 8.8 +/- 1.5 g/dL. After adjusting for age, diabetes, and ischemic heart disease, as well as for blood pressure and serum albumin levels measured serially, each 1 g/dL decrease in mean hemoglobin was independently associated with the presence of left ventricular dilatation on repeat echocardiogram (odds ratio, 1.46; P = 0.018) and the development of de novo (relative risk [RR] = 1.28; P = 0.018) and recurrent (RR = 1.20; P = 0.046) cardiac failure. In addition, each 1 g/dL decrease in the mean hemoglobin level was independently associated with mortality while the patients were on dialysis therapy (RR = 1.14; P = 0.024). Anemia had no independent association with the development of ischemic heart disease while the patients were on dialysis therapy. Anemia, an easily reversible feature of end-stage renal disease, is an independent risk factor for clinical and echocardiographic cardiac disease, as well as mortality in end-stage renal disease patients.
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PMID:The impact of anemia on cardiomyopathy, morbidity, and and mortality in end-stage renal disease. 1255 21

A cohort of 432 ESRD (261 hemodialysis and 171 peritoneal dialysis) patients was followed prospectively for an average of 41 months. Baseline and annual demographic, clinical and echocardiographic assessments were performed, as well as serial clinical and laboratory tests measured monthly while on dialysis therapy. The average mean arterial blood pressure level during dialysis therapy was 101 +/- 11 mm Hg. After adjusting for age, diabetes and ischemic heart disease, as well as hemoglobin and serum albumin levels measured serially, each 10 mm Hg rise in mean arterial blood pressure was independently associated with: the presence of concentric LV hypertrophy (OR 1.48, P = 0.02), the change in LV mass index (beta = 5.4 g/m2, P = 0.027) and cavity volume (beta = 4.3 ml/m2, P = 0.048) on follow-up echocardiography, the development of de novo cardiac failure (RR 1.44, P = 0.007), and the development of de novo ischemic heart disease (RR 1.39, P = 0.05). The association with LV dilation was of borderline statistical significance (OR 1.48, P = 0.06). Mean arterial blood pressures greater than 106 mm Hg were associated with both echocardiographic and clinical endpoints. Paradoxically, low mean arterial blood pressure (RR 1.36 per 10 mm Hg fall, P = 0.009) was independently associated with mortality. The association of low blood pressure with mortality was a marker for having had cardiac failure prior to death. We conclude that even moderate hypertension worsens the echocardiographic and clinical outcome in ESRD patients, especially in those without previous clinical cardiac disease.
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PMID:Impact of hypertension on cardiomyopathy, morbidity and mortality in end-stage renal disease. 873 Nov 3

We report a prospective multi-centre study of the clinical course and hospital management of thoracic empyema in 119 patients (mean age 54.8). The commonest presenting symptom was malaise (75%), 55% were febrile; 31% were previously well with no predisposing condition. Initial treatments were antibiotics alone (5), needle aspirations (46), intercostal tube drainage (61), rib resection (3) and decortication (4). Overall, intercostal drainage was used in 77 patients (16 failed aspirations), surgical rib resection in 24 (1 failed aspirations, 20 failed drainage), and surgical decortication in 28 (6 failed aspirations, 17 failed drainage). Only 4 patients received intrapleural fibrinolytic agents. Aspiration and drainage were likely to fail if the empyema was > 40% of the hemithorax. Median time from treatment start to discharge was: aspirations, 26 days; drainage, 23 days; resection 11 days; decortication, 12 days. Overall 21 patients died (12 with empyema as the major cause); two had been surgically treated. Mortality correlated with age, diabetes, heart failure, and low serum albumin at admission. Infecting organisms, identified in 109 patients (92%) included anaerobes (37), Str. melleri (36), and Str. pneumoniae (28). Six months after discharge, all but six survivors had regained their previous health.
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PMID:The clinical course and management of thoracic empyema. 873 15

A cohort of 432 ESRD (261 hemodialysis and 171 peritoneal dialysis) patients was followed up prospectively for an average of 41 months. Baseline and annual demographic, clinical, and echocardiographic assessments were performed, as well as serial clinical and laboratory tests measured monthly while patients were on dialysis therapy. Among hemodialysis patients, after adjustment was made for age, diabetes, and ischemic heart disease, as well as hemoglobin and blood pressure levels measured serially, a 10-g/L fall in mean serum albumin level was independently associated with the the development of de novo (relative risk [RR], 2.22; P = 0.001) and recurrent cardiac failure (RR, 3.84; P = 0.003), de novo (RR, 5.29; P = 0.001) and recurrent ischemic heart disease (RR, 4.24; P = 0.005), cardiac mortality (RR, 5.60; P = 0.001), and overall mortality (RR, 4.33; P < 0.001). Among peritoneal dialysis patients, a 10-g/L fall in mean serum albumin level was independently associated with the progression of left ventricular dilation as seen on follow-up echocardiography (beta, 13.4 mL/m2; P = 0.014), the development of de novo cardiac failure (RR, 4.16; P = 0.003), and overall mortality (RR, 2.06; P < 0.001). Hypoalbuminemia, a major adverse prognostic factor in dialysis patients, is strongly associated with cardiac disease.
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PMID:Hypoalbuminemia, cardiac morbidity, and mortality in end-stage renal disease. 873 8

Heart failure in hypertensive patients is known to be dependent not only on the absolute value of blood pressure but also on other factors, hence the prognosis varies. In this study, the effect of renal dysfunction on the development of heart failure in hypertensive patients was assessed. Fifty-five patients who were admitted in hypertensive heart failure (HHF) were compared with 55 hypertensive patients who had never been in heart failure (HT), in their renal function, assessed by serum creatinine and urea levels. The haemoglobin (Hb) and serum albumin (Alb) levels were also measured. The two groups were matched for age, sex, level of blood pressure and body mass index. The duration of hypertension was similar in both groups. Mean serum creatinine was higher in the HHF group: 4.50 +/- 0.90 vs. 0.97 +/- 0.06 mg/100ml (P < 0.001). Also the Hb and Alb levels were lower in the HHF than the HT group: 11.63 +/- 0.40 vs. 13.2 +/- 0.21 g/100 ml (P < 0.001) and 3.7 +/- 0.1 vs. 4.40 +/- 0.09 g/100 ml (P < 0.001), respectively. The proportion with abnormal renal function (creatinine > 1.5 mg%) was also significantly higher in HHF: 28/55 vs. 8/54, chi 2 = 16.3 (P < 0.001). When adjustment was made for low serum albumin, Hb and fundal changes by multivariate analysis, serum creatinine was significantly higher in the HHF group: F = 4.294 (P < 0.05). Low serum albumin was also independent of haemoglobin and creatinine: F = 19.52 (P < 0.001), but Hb was not significantly different after adjustment for Alb and creatinine. This study suggests that renal dysfunction is independently associated with the development of heart failure in HT patients.
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PMID:Heart failure in Nigerian hypertensive patients: the role of renal dysfunction. 878 84

Gall-bladder wall thickening is commonly seen in patients with cirrhosis, but its exact causes have not been well established. We evaluated clinical, biochemical and haemodynamic data of patients with cirrhosis with respect to the presence of thickening of the gall-bladder wall. After excluding patients who presented with gallstones, acute or chronic cholecystitis, heart failure, a serum creatinine level greater than 2 mg/dL and/or a serum alanine aminotransferase level greater than 400 U/L, 77 patients with cirrhosis (75 male, two female; mean age 58 +/- 8 years) were enrolled in the study. Clinical, biochemical, ultrasound and haemodynamic data were obtained in every patient. Forty-one (53%) of 77 patients with cirrhosis had gall-bladder wall thickening (> 4 mm). Compared with patients with a normal gall-bladder wall, patients with gall-bladder wall thickening had significantly lower serum albumin levels (3.6 +/- 0.6 vs 2.9 +/- 0.7 gm/dL, respectively; P < 0.05), a longer prothrombin time (13 +/- 6 vs 16 +/- 6 s, respectively; P < 0.05), more patients with Child-Pugh class C (6 vs 37%, respectively; P < 0.05) and more patients with ascites (8 vs 50%, respectively; P < 0.05). In addition, compared with patients with a normal gall-bladder wall, those patients with gall-bladder wall thickening had a higher hepatic venous pressure gradient (13.9 +/- 4.5 vs 17.1 +/- 4.1 mmHg, respectively; P < 0.01) and a lower systemic vascular resistance (SVR; 1144 +/- 332 vs 1010 +/- 318 dyn.s/cm5, respectively; P < 0.05). Using a multivariate analysis, the presence of ascites and SVR lower than 900 dyn.s/cm5 were independently correlated with the presence of gall-bladder wall thickening, while a hepatic vein pressure gradient greater than 10 mmHg had only a marginally significant association. The presence of ascites, decreased SVR and portal hypertension are related to the occurrence of gall-bladder wall thickening in patients with cirrhosis, indicating that the development of gall-bladder wall thickening may be multifactorial.
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PMID:Gall-bladder wall thickening in patients with liver cirrhosis. 919 2

The differential diagnosis of ascites often leads to confusion and an inability to exclude its multitude of causes in many patients. In this review, we outline the clinical features and laboratory investigations that usually elucidate the cause of ascites for the clinician in a simple and logical manner. Roughly 80-85% of cases of ascites are related to underlying chronic liver disease, but cardiac failure, tuberculosis, malignancy-related ascites and other less common causes should always be considered. Careful evaluation of the patient, including a clinical history, physical examination and diagnostic paracentesis should routinely be performed to determine the cause of ascites. Fluid should be sent for cell count and albumin along with simultaneous determination of serum albumin to determine the serum: ascites albumin gradient. This gradient allows classification of the cause of ascites into portal hypertension-related and nonrelated with a diagnostic accuracy of > or = 97%. The causes of ascites are individually discussed in relationship to their clinical features and to the laboratory investigations that are relevant in each situation.
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PMID:Differential diagnosis of ascites. 930 24

Despite considerable differences in technique and blood purification characteristics, hemodialysis and peritoneal dialysis have been thought to have similar patient outcomes. An inception cohort of 433 end-stage renal disease patients was followed prospectively for a mean of 41 mo. The outcomes of hemodialysis (HD) and peritoneal dialysis (PD) patients were compared using intention to treat analysis based on the mode of therapy at 3 mo. After adjustment for PD patients less likely to have chronic hypertension and more likely to have diabetes, ischemic heart disease, and cardiac failure at baseline (P < 0.05), a biphasic mortality pattern was observed. For the first 2 yr, there was no statistically significant difference in mortality. After 2 yr, mortality was greater among PD patients with an adjusted PD/HD hazard ratio of 1.57 (95% confidence interval [CI], 0.97 to 2.53). Both the occurrence (adjusted hazards ratio 6.87 [95% CI, 2.01 to 23.5]) and the direction (toward PD, adjusted hazards ratio 6.25 [95% CI, 1.54 to 25]) of a therapy switch were subsequently associated with mortality after 2 yr. Progressive clinical and echocardiographic cardiac disease were not responsible for this late mortality. Lower mean serum albumin levels in PD patients in the first 2 yr of therapy (3.5 +/- 0.5 versus 3.9 +/- 0.5 g/dl, P < 0.0001) accounted for a large proportion of the increase in subsequent mortality. Hemodialysis has a late survival advantage over peritoneal dialysis; antecedent hypoalbuminemia is a major marker of the increased late mortality in PD patients.
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PMID:Mode of dialysis therapy and mortality in end-stage renal disease. 952 3

Digitoxin is frequently used in Norway in the treatment of cardiac failure. Digitalis glycosides may give rise to a number of side effects difficult to separate from disease in the elderly. Six patients aged 77-93 years, treated with digitoxin 0.05 mg/day, were hospitalized due to digitalis intoxication. Mean digitoxin half-life was 25.2 days. This is significantly more than reported in other studies on younger patients. The symptoms of digitoxin intoxication disappeared on discontinuation of medication. The slow elimination of digitoxin may be related to reduced serum albumin concentration. When digitoxin is used in the treatment of heart failure in the very elderly patients, one should be aware of the possibility of digitoxin intoxication, even at a low dose.
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PMID:[Prolonged half-life of digitoxin in the elderly]. 1007 32

Protein-losing enteropathy is frequently overlooked in patients suffering from congestive heart failure. Although textbooks often quote heart failure as one of the causes of protein-losing enteropathy, this association has not been clearly documented in the literature. Furthermore, conventional diagnostic techniques for protein-losing enteropathy are both cumbersome and time-consuming. We report the first case of protein-losing enteropathy of a 79 year-old lady who suffered from dilated cardiomyopathy. The profound hypoalbuminemia could not be explained by urinary loss or impaired hepatic synthesis. Protein-losing enteropathy was confirmed by means of Technetium-99m- (99mTc) labelled human serum albumin scintigraphy which showed diffuse activity in the entire colon. The use of this simple and non-invasive diagnostic technique in protein-losing enteropathy is discussed.
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PMID:Protein-losing enteropathy in congestive heart failure: diagnosis by means of a simple method. 1043 Mar 51


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