Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We analyzed the effect of enalapril (0.1 mg/kg p.o. twice daily) on plasma electrolytes, urea, and creatinine in low cardiac output failure. In 14 male dogs implanted with chronic instrumentation, tachycardia was induced by ventricular pacing (265 impulses/min., 10-14 days). In 7 untreated dogs, pacing progressively lowered aortic flow by 44% and induced hyponatremia and elevations of plasma urea, creatinine, and potassium. Treatment with enalapril (n = 7) during pacing reduced the decrease in aortic flow by 33% and prevented changes in plasma urea, potassium, and sodium. We conclude that this is due to enalapril-induced retardation of heart failure progression.
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PMID:Converting enzyme inhibition by enalapril in experimental heart failure. 234 93

Because of inappropriate signals from the volume-regulation system and a reduction in renal blood flow, the kidney is not able to prevent sodium and water retention in chronic congestive heart failure (CHF). A brief summary of normal renal function and renal involvement in CHF is given and a study of renal function in patients with moderate or severe chronic CHF is presented. To evaluate the impact of cardiac output reduction on the regulation of the glomerular filtration rate (GFR) in heart failure, GFR (inulin clearance), renal plasma flow [p-aminohippurate (PAH) clearance], invasive haemodynamics, blood volume, plasma renin and plasma catecholamines were measured in 34 patients with chronic CHF. The patients were divided into 3 groups according to their cardiac index (CI): CI greater than 2.0 L/min/m2 (group A), CI 1.5 to 2.0 L/min/m2 (group B), and CI less than 1.5 L/min/m2 (group C). Differences in the relationship between GFR, renal plasma flow and filtration fraction for the 3 groups emerged. Despite an intergroup reduction in the renal fraction of cardiac output and renal blood flow, GFR was similar in groups A and B (62 and 67 ml/min/1.73 m2, respectively), and was accompanied by a compensatory increase in filtration fraction, from 24% in group A to 35% in group B. Group C had a much lower GFR (38 ml/min/1.73 m2), however, the filtration fraction (28%) was intermediate in value between those of groups A and B. The differences in GFR were reflected by blood urea nitrogen levels but not by serum creatinine levels. The occurrence of a non-compensatory filtration fraction response in the patients with the greatest impairment of CI and renal blood flow suggests that GFR becomes dependent on afferent arteriolar flow in the most severe heart failure, despite stimulation of haemodynamic and hormonal pathways, which would normally increase efferent arteriolar tone. It is thus suggested that GFR becomes flow dependent in patients in the most severe stage of chronic CHF.
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PMID:Role of the kidney in congestive heart failure. Relationship of cardiac index to kidney function. 235 70

The clinical background relating to edema in elderly inpatients was investigated, in terms of various items in elderly (aged greater than or equal to 65) cases with edema (n = 96) and without edema (controls, n = 95). Both groups were matched for sex, age, and underlying diseases. As compared with the control patients, the patients with edema had longer hospital stays with more disabled status, and showed less activity of daily living (ADL). The rates of bed-restricted patients, dementia patients, and patients with decubitus, muscle atrophy, or incontinence were found to be significantly higher in the patients with edema. The measurement of biochemical parameters revealed that the patients with edema had significantly lower levels of serum albumin, Na, Cl, creatinine, and uric acid, in contrast to higher levels of C-reactive protein. According to the classification of the assumed causes of edema, we divided the patients with edema into five groups; group 1 (n = 33): edema associated with immobilization, group 2 (n = 18): edema due to heart failure, group 3 (n = 15): edema on paretic limbs, group 4 (n = 6): edema due to hypoproteinemia, group 5 (n = 5): edema associated with liver cirrhosis. Both group 1 and group 4 patients had lower levels of hemoglobin and albumin, whereas group 3 patients had higher scores of ADL, higher blood pressure, and higher levels of hemoglobin and albumin. These results suggest that immobilization and restriction in bed, as well as malnutrition, were important factors in causing edema in elderly inpatients.
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PMID:[A controlled study on edema in elderly inpatients]. 238 89

There remains controversy over the effects of angiotensin-converting enzyme inhibitors on renal function in patients with heart failure. Accordingly, we investigated the effects of long-term captopril therapy on renal function in 14 patients with congestive heart failure in a double-blind fashion. Creatinine clearance declined (from 61 +/- 21 to 56 +/- 21 ml/min; p less than 0.01), and both serum urea and creatinine rose. Glomerular filtration rate estimated radioisotopically also fell (from 53 +/- 19 to 48 +/- 18 ml/min), although this was not statistically significant. Effective renal plasma flow estimated radioisotopically increased (from 241 +/- 72 to 287 +/- 100 ml/min; p less than 0.05). Thus, filtration fraction--the ratio of glomerular filtration rate to effective renal plasma flow--fell. Because blood pressure also fell, the rise in renal plasma flow indicates a fall in calculated renal vascular resistance. Whole body sodium and chlorine, measured by total body in vivo neutron activation analysis, were unchanged, indicating no long-term natriuresis, despite evidence of clinical improvement. While converting enzyme inhibition causes symptomatic improvement in cardiac failure, there is a concomitant loss of compensatory direct effects of angiotensin II within the kidney, and hence usually some decline in renal function.
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PMID:Captopril in heart failure: a double-blind study of the effects on renal function. 242 7

Cardiac decompensation occurred in three patients of the placebo group, but not in the perindopril group. The effectiveness of perindopril in heart failure was demonstrated by the improvement observed in exercise test and severity score and by the decrease of cardiothoracic ratio. Changes in SAP, and serum creatinine levels, in particular, showed that the drug was well tolerated.
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PMID:[Contribution of perindopril to the treatment of chronic congestive cardiac insufficiency. Multicenter pilot double blind study versus placebo]. 250 16

Pre-dialysis plasma oxalate concentration was measured in a cross-sectional study of 75 patients receiving maintenance haemodialysis. The aims of this study were to enable formulation of hypotheses regarding the determinants of plasma oxalate concentration and to allow preliminary examination of the possibility that hyperoxalaemia confers an increased risk of cardiac and vascular disease even in the absence of primary hyperoxaluria. Plasma oxalate concentration ranged between 7 and 76 mumol/l, mean (SD) 34.6 (18.1) mumol/l (normal range less than 0.8-2.0 mumol/l). Significant correlations were found between plasma oxalate concentration and plasma creatinine, duration of dialysis, current dose of ascorbic acid, and serum phosphate, and each of these variables retained significance on multiple linear regression. Oxalate clearance across a 1 m2 hollow-fibre Cuprophan dialyser, at 500 ml/min dialysate flow and blood flow between 175 and 225 ml/min, was measured 1 h after commencement of dialysis (n = 19). Mean (SD) clearance was 96.5 (27.0) ml/min. No significant association was found between self-reported maximum walking distance or the occurrence of symptoms of cardiac failure and plasma oxalate concentration. No relationship was found between plasma oxalate concentration and electrocardiographic conduction disturbances (n = 8) 'major' ST/T wave changes (n = 22), 'minor' ST/T wave changes (n = 49). Plasma oxalate was significantly greater in patients with radiologically detectable calcification of medium-sized arteries than in those without calcification, but duration of dialysis was also significantly longer in these patients. Routine haemodialysis results in marked hyperoxalaemia, which may be exacerbated by ascorbate supplementation. Oxalate clearance is similar to that of other small molecules such as creatinine and phosphate.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma oxalate concentration, oxalate clearance and cardiac function in patients receiving haemodialysis. 251 11

In order to determine the relationships between allograft function and the recipient's plasma concentrations of atrial natriuretic factor (ANF), plasma ANF was measured by radioimmunoassay for 14 days after cadaveric renal transplantation in 9 patients aged 19-64 years. All received immunosuppression with prednisolone, azathioprine, and cyclosporine. No patient was in heart failure. During the study period, six grafts functioned, and three were nonfunctioning--two due to rejection and one to acute tubular necrosis. Plasma ANF concentration at the time of transplantation was 48 +/- 16 pmol/L (mean +/- SEM) range 15-145 pmol/L. In the six patients with functioning grafts, ANF declined in parallel with the fall in serum creatinine (658 +/- 35 to 210 +/- 34 mumol/L). In the three with nonfunctioning grafts, serum creatinine and plasma ANF concentration both increased. There was overall a significant linear relation between serum creatinine and plasma ANF (r = 0.527, P less than 0.001). The changes in plasma ANF after renal transplantation bore no relationship to changes in body weight or blood pressure. However, plasma ANF concentration was related to allograft fractional sodium excretion (r = 0.687, p less than 0.001). We conclude that elevated plasma ANF concentrations in end-stage renal disease are restored to normal by successful renal transplantation, implying that renal function is a determinant of plasma ANF concentration. Circulating plasma ANF may also have a direct effect on allograft sodium excretion.
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PMID:Plasma atrial natriuretic factor and graft function in renal transplant recipients. 253 Jun 66

The safety of 738 high-risk patients treated with enalapril under various clinical programs was evaluated. High risk was defined as the presence of a collagen vascular disease; a renal disease, including renovascular hypertension; or either hypertension or refractory cardiac failure with serum creatinine greater than or equal to 1.7 mg/dl at baseline. Essential hypertension was the primary diagnosis in most of these patients. Treatment with enalapril in these patients usually continued without interruption for the length of the particular protocol. The incidence of adverse reactions resulting in discontinuation of treatment was comparable to that observed with other standard antihypertensive therapies in patients with milder forms of disease. No enalapril-related neutropenia, proteinuria, dysgeusia or ageusia were reported in these high-risk patients. The incidence of discontinuation due to rash was less than 0.5%. Resolution and/or improvement of captopril-related adverse effects was observed in many patients crossed over to treatment with enalapril. In patients with collagen vascular diseases and those with severe impairment of renal function (serum creatinine greater than or equal to 3.0 mg/dl), the incidence of discontinuation due to adverse experiences or death as well as the profile of reported adverse experiences was similar to those for the total group of high-risk patients. The data suggest that enalapril is efficacious and well tolerated by the high-risk patients.
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PMID:High-risk patients treated with enalapril maleate: safety considerations. 253 44

This report reviews the tolerability profile of enalapril, an angiotensin-converting enzyme (ACE) inhibitor, in the treatment of patients with congestive heart failure. Data have been collected from 546 patients treated with enalapril for up to 9 months in clinical trials other than the Cooperative North Scandinavian Enalapril Survival Study. Results in patients treated with enalapril (n = 193) or placebo (n = 195) in double-blind, controlled clinical trials show that the incidences of death, serious adverse experiences, and adverse experiences requiring discontinuation of double-blind therapy, as well as the overall incidence of such experiences, were similar in the 2 groups. However, certain adverse experiences that are related to the mechanism of action of ACE inhibitors were seen more often after enalapril than after placebo treatment. Dizziness and hypotension were the most frequent adverse experiences reported in patients with heart failure treated with enalapril. The most frequent laboratory adverse experiences were increases in blood urea nitrogen and serum creatinine levels. hyperkalemia was also seen in patients receiving enalapril. It is possible to identify patients at risk of these experiences before initiating treatment with enalapril and to take certain measures (such as withholding or reducing the dose of diuretic drugs and discontinuing potassium supplements or potassium-sparing diuretic drugs) to reduce the likelihood that hypotension, increases in blood urea nitrogen and serum creatinine levels, or hyperkalemia will occur. Angioedema, a recognized adverse effect of ACE inhibitors, was not seen in the clinical trials reviewed here. Cough , another recognized adverse effect of these agents, was seen infrequently and rarely resulted in the discontinuation of enalapril.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Tolerability of enalapril in congestive heart failure. 253 64

1. The population pharmacokinetics of lisinopril were investigated using data collected from two multicentre trials of lisinopril in the treatment of hypertension in elderly patients (n = 40) and patients with renal disease (n = 20). 2. Lisinopril was started at doses of 2.5-5 mg daily and increased at 2-4 weekly intervals as required for control of blood pressure. Steady-state concentration-time profiles were measured after at least 2 weeks at a constant dose. 3. All concentration-time data were analysed simultaneously using the program NONMEM and the influence of clinical factors on clearance/F and volume of distribution/F was tested. 4. Clearance was significantly influenced by creatinine concentration, age, weight and cardiac failure. No clinical features tested were found to influence volume of distribution. 5. The influence of renal function and cardiac failure on lisinopril clearance has been confirmed using a population pharmacokinetic analysis technique.
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PMID:Lisinopril population pharmacokinetics in elderly and renal disease patients with hypertension. 253 50


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