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)

Benazepril (BP), an angiotensin convertive enzyme inhibitor, was administered orally once daily for 4 weeks to 31 dogs with mild to moderate (NYHA functional classes II and III) congestive heart failure caused from mitral insufficiency (MI). There were no significant changes in clinical signs, electrocardiogram findings, radiographical observations and plasma biochemical results in 11 dogs treated with placebo for 4 weeks. In 31 dogs treated with BP, appetite increased, and mean scores of heart failure signs, such as activity, exercise tolerance, cough and respiratory effort, were significantly improved. No dog displays signs suggesting systemic hypotension. One dog died suddenly on the 26th day of treatment with BP. This dog had good vigor and appetite till the evening before the death, and cough and exercise tolerance had been gradually improving. The heart rate and ECG parameters of BP treated dogs did not change significantly, but length of long axis of the heart decreased. In plasma biochemical tests, plasma urea nitrogen (UN) levels did not change significantly, and plasma creatinine (CRE) levels increased slightly within the normal ranges during BP trial. Two dogs had higher plasma UN levels with slightly higher plasma CRE levels, but had normal general condition and other biochemical results. Plasma ACE activity decreased to 57.3% of pre-treatment level at 4 weeks after BP treatment. It is concluded that BP monotherapy was efficacious at least in dogs with relatively low grade congestive heart failure caused by MI.
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PMID:Efficacy of monotherapy with benazepril, an angiotensin converting enzyme inhibitor, in dogs with naturally acquired chronic mitral insufficiency. 927 44

The application of intermittent renal replacement therapies in critically ill patients with both acute renal failure and heart failure is often associated with circulatory instability and refractory hypotension. We have evaluated the efficacy and safety of a continuous technique (continuous veno-venous hemofiltration-CVVH) in 7 patients (1 male, 6 females, mean age 77 +/- 4 years) referred to our intermediate care unit for oliguria, acute renal failure and NYHA functional class IV, CVVH was performed by a peristaltic pump with blood flow at 200 ml/min, controlled ultrafiltration production rate (25 ml/min), minute to minute microprocessor controlled fluid balance system, biocompatible filters, low-dose prostacyclin for the extracorporeal circuit maintenance. Non invasive evaluation of cardiac function was performed by Doppler echocardiography. A total of 673 hours of CVVH were performed, with a mean extracorporeal circuit duration of 96 +/- 26 hours/patient (range 15-134). Daily urea clearance was 32 +/- 21. A mean body weight decrease of 10% was obtained (body weight before-CVVH 64.5 +/- 6 kg vs end-CVVH 58.5 +/- 5 kg, p < 0.01, paired data Student's test) without any hemodynamic worsening; metabolic control was adequate (urea before-CVVH 251 +/- 73 mg% vs end-CVVH 117 +/- 18 mg%, p < 0.01). Hospital survival was 42% (3/7 patients). In patients with acute renal failure and severe heart failure, CVVH allows an easy control of both fluid balance and acid-base equilibrium, along with the maintenance of acceptable hemodynamic stability.
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PMID:[Continuous veno-venous hemofiltration in acute renal insufficiency and heart failure]. 931 10

A total of 111 elderly patients from the cardiac surgery intensive care unit (ICU) with acute renal failure (ARF) were studied during a period of 7 years (1988-1994). Forty-two patients being operated for coronary bypass (CBP) (31 M, 11 F), 26 patients for valve replacement (VR) (18 M, 8 F), 20 patients for a combined operation of coronary bypass and valve replacement (CBP+VR) (14 M, 6 F) and 23 patients for resection of aneurysm of the abdominal aorta (ROAOAA) (11 M, 12 F). Average age of the patients was 70 +/- 4 yr (65-80). Their blood pressure on the first day of continuous renal replacement therapy (CRRT) was 75 +/- 19 mmHg (50-95) and was maintained at about 95 +/- 15 mmHg (70-120) by using vasopressor drugs. From the results of this study a survival of 38% was registered within the CBP group, 65% within the VR group, 45% within the CBP+VR group and 91% within the ROAOAA group. The overall survival in all of the patients was 58%. It was a high mortality (62%) within CBP group compared to that of 35%, 55% and 9% within the VR, CBP+VR and ROAOAA groups, respectively. This is because more patients with predisposing preoperative risk factors, e.g., hypertension (33%) and Diabetes (17%) etc were found in the CBP group, in addition to their post operative complications of which bleeding necessitating reoperations was encountered in 31%. Multiple organ failure (MOF) was a common major problem of which respiratory failure needing artificial ventilation was encountered in about 90% of the patients. The overall mortality was 42% in which the major cause of death was MOF/circulatory failure. Heart failure was the second cause of death. Other secondary complications, e.g., liver failure (n = 6) and atrial fibrillation (n = 11) etc. might have added to the high mortality in this study. The effect of CRRT on uremic control was measured by following-up of the daily levels of the serum urea and creatinine and a steady-state uremic control was achieved. We conclude that CRRT can be considered as a reliable artificial renal support for ARF in ICU elderly patients.
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PMID:Acute renal failure and outcome of continuous arteriovenous hemodialysis (CAVHD) and continuous hemofiltration (CAVH) in elderly patients following cardiovascular surgery. 942 39

Author investigated the safety of combined ACE inhibitor (captopril) and spironolacton therapy on 237 pts with severe heart failure (NYHA III-IV.) treated with digitalis and loop diuretic during on average 65.4 months follow-up period. Incidence of clinically significant increase in serum urea, creatinine and potassium level was evaluated and compared with those of in group treated 47 pts with the same standard therapy captopril, digitalis, furosemide, without spironolacton. There was no significant difference between the incidence of azotemia and hyperkalemia in the two groups. The author emphasizes on the base of their results the safety of combined captopril and low dose spironolactone therapy in heart failure.
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PMID:[Effect of combined captopril-spironolactone therapy of cardiac insufficiency on kidney function and serum electrolyte values]. 945 4

We identified 174 cases of chronic severe renal failure (blood creatinine > 650 mumol/l) and/or blood urea > 35 mmol/l) in a retrospective study of patients admitted to hospital between January 1989 and June 1996. Of these patients, 110 were men and 64 were women. The mean age was 36 +/- 15 years. Fifty three patients had a history of hypertension before admission, 3 patients had diabetes and 3 had gout. The most frequent clinical signs were dyspnea (55.2% of all patients), fatigue (78.2%), vomiting (63.2%) and edema (66.1%). The prevalence of hypertension was 64.9%. Glomerulonephritis was found in 42.5% of patients, chronic interstitial nephritis in 16.1%, polycystic kidney disease in 2 cases, congenital renal hypoplasia in 4 cases and unclassified kidney disease in 14.4% of cases. End-stage renal failure was complicated by heart failure in 40.2% of patients, pericarditis in 31.6%, hemorrhage of the gastrointestinal tract in 15% and infections in 22.4%. 47.7% of the patients died following admission.
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PMID:[Epidemiology of severe chronic renal insufficiency in Burkina Faso]. 950 95

The CASSIS study was a double-blind multicentric controlled Czech and Slovak study focused on treatment of chronic heart failure with the ACE inhibitor spirapril; it was conducted for 12 weeks. The present work analyzes the second year of the extended open part of the study when all patients (n = 168) were treated with 3 mg or 6 mg spirapril. A small proportion of the patients was treated with 12 mg spirapril. The objective of the study was to test the long-term effectiveness and tolerance of spirapril. The general mortality was analyzed throughout the whole two-year period. The results revealed an unchanging total mortality, analyzed after three-month intervals, during the whole two-year period. Also the functional improvement of the patients according to NYHA which occurred after the first three months of treatment was preserved during the second year. Spirapril proved to be a well tolerated ACE-inhibitor. The authors did not observe angioneurotic oedema in any of the patients. Hypotension and cough were recorded in 0.6% of the patients. The incidence of undesirable laboratory effects was also low and the majority was due to the basic disease. Creatinine did not rise significantly and a rise of urea was observed only in a small number of patients. Liver functions and haemogram did not change during treatment. The results of the second year of erxtension indicate that spirapril is a very effective and safe ACE-inhibitor which will extend in a significant way therapeutic means in patients with chronic heart failure.
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PMID:[Therapy of heart failure with spirapril--the open phase of the CASSIS study. Analysis of the 2nd year extension of the CASSIS study]. 960 64

In end stage congestive heart failure activation of a series of compensatory mechanisms increase renal vascular resistance and impair renal function. Prostaglandin E1 is increasingly used in the treatment of severe heart failure for its vasodilating actions. In various experimental settings prostaglandin E analogues are known to improve renal function by modulating renal filtration pressure and redistribution of renal blood flow. However, prostaglandin E1 decreases systemic blood pressure and thus, also renal perfusion pressure, a fact by which renal function might be further compromized in heart failure patients. The aim of the study was to evaluate the effects of prostaglandin E1 on excretory renal function in patients with end stage heart failure and to prove the hypothesis, that the well known local actions of prostaglandins on renal microcirculation might outweigh the negative impact of an expected decrease in perfusion pressure. 25 patients with terminal congestive heart failure were investigated. 13 patients received prostaglandin E1 at a dose of 13.5 +/- 1.9 ng/kg/min in combination with constant rates of dopamine and dobutamine (group A), 12 patients received prostaglandin E1 at a dose of 10.3 +/- 1.7 ng/kg/min without catecholamines (group B). There was no significant difference in prostaglandin dosages between groups. Kidney function was assessed by measuring plasma creatinine and urea nitrogen, urinary output, creatinine clearance, osmotic and free water clearance at baseline and after 72 h of infusion therapy. Hemodynamic parameters were measured by using a balloon tipped pulmonary arterial catheter. Hemodynamic measurements during infusion showed a significant improvement in all patients. At the same time as expected mean arterial pressure decreased in both groups (p < 0.001). Nevertheless, in both groups a significant increase of creatinine clearance during infusion was observed (in group A from 45 ml/min to 78 ml/min., p < 0.05, in group B from 59 ml/min to 105 ml/min., p < 0.001). Creatinine clearance in group B (without catecholamines) reached higher levels than group A (p < 0.05). Urinary volumes did not change during infusion therapy, whereas free water clearance significantly decreased, as an indication of an improvement of renal concentrations ability. We conclude, that in patients with end stage heart failure continuous infusion of prostaglandin E1 improves excretory kidney function. These findings suggest that the local effects of prostaglandin E1 on renal microcirculation can counterregulate the negative impact of prostaglandins on renal perfusion pressure.
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PMID:[Improved kidney function with intravenous prostaglandin E1 in patients with terminal heart failure]. 974 60

An increased pulmonary vascular resistance (PVR) or an increased transpulmonary gradient (TPG) is a risk factor for increased 3-day and 3-month mortality after heart transplantation (HTx). The reversibility of increased PVR or TPG under pharmacologic testing is supposed to indicate a decreased probability of right ventricular failure/death after transplantation. We tested the response of an increased PVR (> 2.5 Wood units, WU) and/or of an increased TPG (> 15 mm Hg) in 29 right heart catheterizations (thermodilution catheter) of 23 patients (54 +/- 8 years, mean NYHA-class 3.1 +/- 0.6, ischemic n = 8, dilated cardiomyopathy n = 15). Increasing doses of prostaglandin I2 (PGI2, mean maximum dose 13.5 +/- 6.4 ng/kg/min) were applied stepwise over at least 10 min at the maximum dose level. We analyzed any dependence of the reversibility of PVR and TPG under prostaglandin I2 on hemodynamic values, echocardiographic parameters, demographic data, and laboratory findings. A decrease of PVR to a range usually accepted as no contraindication for HTx (< or = 4 WU) was found in each patient without symptomatic systemic hypotension during application of PGI2 (baseline value: 4.7 +/- 1.3 WU, during PGI2: 2.3 +/- 0.6 WU). An unresponsive, fixed increased PVR or TPG was not observed using PGI2. In 62% of investigations, both PVR and TPG decreased below 2.5 WU and 15 mmHg, respectively. The extent of reversibility of PVR and TPG was individually different and did not depend on the mean pulmonary artery pressure, mean capillary wedge pressure, cardiac output, mean systemic artery pressure or echocardiographic parameters (EDD, FS, ES-distance), sodium, urea or bilirubin levels, medication, age of the patients or the duration of the disease. The baseline PVR correlated inversely with its percentile value during PGI2 (r = -0.76, p < 0.05). In advanced heart failure, PGI2 decreases PVR in ranges of lower risk concerning orthotopic HTx, without causing an intolerable systemic hypotension. The individual extent of reversibility of PVR and TPG under PGI2 is not influenced by basic hemodynamic parameters or the patient's demographic profile.
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PMID:[Pharmacological testing of the reversibility of increased pulmonary vascular resistance before heart transplantation with prostaglandin I2 (prostacyclin)]. 1020 34

Within the past decade an entire family of membrane proteins--aquaporins--which function as transmembrane water channels has been identified; they occur throughout the plant, animal, and bacterial kingdoms. Several family members permit glycerol and urea permeability. Most aquaporins are inhibited by mercury. Constitutively expressed aquaporin 1 is the major permeability channel of the proximal tubule, descending thin limb of the loop of Henle, and it is also found in vasa recta. Aquaporin 2 is expressed in the principal cells of the collecting duct where it shuttles between intracellular vesicles and the apical membrane in response to vasopressin. Aquaporin 2 mutations cause nephrogenic diabetes insipidus; increased aquaporin 2 activity is implicated in the pathophysiology of heart failure, cirrhosis, and nephrotic syndrome. Aquaporins 3 and 4 provide basolateral membrane water channels in the collecting duct. These 4 channels and 6 others are also found elsewhere throughout the body. The physiological importance of several of the channels remains unknown. Aquaporin 1 inhibitors might induce useful diuresis, but humans who lack aquaporin 1 have no significant clinical disease. Inhibition of aquaporin 2 activity by vasopressin receptor antagonists may be useful in heart failure, cirrhosis, nephrotic syndrome, and the syndrome of inappropriate antidiuretic hormone (ADH) release.
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PMID:Aquaporin mediated water flux as a target for diuretic development. 1059 41

Disorders of the serum sodium concentration (hypo- and hypernatremia) are amongst the most frequent electrolyte disorders in clinical medicine. They are attributable to disturbance of to water metabolism. Hyponatremia is almost always a condition of water excess while hypernatremia is due water deficiency. Physiological normonatremia (normal plasma osmolality) is maintained by an integrated system involving regulated water intake via thirst and control of water excretion via antidiuretic hormone secretion. Therefore hypo- and hypernatremia should be analyzed in terms of dysregulated ADH secretion, fluid intake and renal water excretion. Hyponatremia is usually a disorder of vasopressin excess, due to 'non-osmotic' vasopressin release. The latter may occur in two different settings: (I) SIADH, (II) baroreceptor mediated vasopressin secretion (cardiac failure, liver cirrhosis). This entities are easy to distinguish in clinical practice. SIADH is associated with striking lower plasma concentrations of urate, creatinine and urea. In SIADH the blood pressure is normal and there is no edema. In contrast in the hyponatremia of liver cirrhosis and heart failure the plasma measurements indicated are usually slightly elevated, the blood pressure is low and there is edema. The typical patient with hypernatremia is old and has no thirst sensation. Hypo- or hypernatremia may cause major neurologic symptoms. These symptoms are more related to the rate of change in the serum sodium concentration than to the absolute level of a hypo- or hypernatremia reached. The traditional treatment for hyponatremia used to be water restriction. However V2-Vasopressin-Antagonists may provide a better treatment modality in the future. Hypernatremia is treated by slow rehydratation.
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PMID:[Hyponatremia--with comments on hypernatremia]. 1089 27


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