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

Renal hemodynamics and tubular solute and water handling were evaluated in normal subjects during water diuresis, before and after the acute administration of captopril, ibuprofen, or the combination of both drugs. The glomerular filtration increased after captopril administration but did not change after ibuprofen alone or in combination with captopril. Renal plasma flow increased with captopril alone and captopril plus ibuprofen but did not change after ibuprofen alone. Urine volume and Na excretion increased with captopril and decreased after ibuprofen; coadministration of ibuprofen attenuated the tubular effects produced by captopril alone. FELi, fractional delivery of solute to the distal nephron, and FELi-FENa, fractional distal reabsorption of solute, both significantly increased after captopril and decreased after ibuprofen but did not change with the combined regimen. (FELi-FENa)/FELi, fractional reabsorption of distally delivered Na, significantly decreased after captopril and increased after ibuprofen but remained unchanged after captopril plus ibuprofen. Thus captopril and ibuprofen have opposing effects on tubular Na and water handling, which are attenuated by the addition of the other drug. This interaction may have clinical relevance in patients with heart failure or hypertension, in whom captopril is used to enhance Na and water diuresis.
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PMID:Interaction of captopril and ibuprofen on glomerular and tubular function in humans. 220 Dec 4

The RAS is part of an extremely powerful feedback system for long-term control of arterial pressure and volume homeostasis as illustrated in Figure 4. Disturbances that tend to lower blood pressure such as heart failure, cirrhosis, and peripheral vasodilation, cause sodium and water retention until blood pressure returns to normal due in large part to the combined actions of ANGII and reduced renal perfusion pressure. In response to disturbances such as high sodium intake, suppression of ANGII greatly amplifies the effectiveness of the basic pressure natriuresis and diuresis mechanism, thereby preventing large increases in body fluid volumes and blood pressure. In circumstances in which the RAS is inappropriately activated, the sodium-water retaining effects of ANGII necessitate increased blood pressure to maintain sodium and water balance via pressure natriuresis. The sodium retaining actions of the RAS are mediated by intrarenal as well as extrarenal mechanisms. The intrarenal actions of ANGII include a direct effect on tubular sodium transport as well as a potent constrictor action on efferent arterioles which increases tubular reabsorption by altering peritubular capillary physical forces. The constrictor action of ANGII on efferent arterioles also plays an important role in stabilizing GFR and therefore in preventing fluctuations in excretion of metabolic waste products that depend upon a high GFR for excretion. ANGII is known to stimulate proximal reabsorption, but the effects on more distal tubular segments have not been completely elucidated. The primary extra-known to stimulate proximal reabsorption, but the effects on more distal tubular segments have not been completely elucidated. The primary extra-renal effect of ANGII which influences sodium excretion is stimulation of aldosterone secretion. Current evidence, however, suggests that the various intrarenal actions of ANGII are quantitatively more important in causing sodium retention than those mediated by changes in aldosterone secretion. However, the combined intrarenal and extrarenal actions of ANGII on sodium reabsorption provide the body with one of its most potent feedback systems for long-term regulation of body fluid volumes and arterial pressure.
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PMID:Role of the renin-angiotensin system in control of sodium excretion and arterial pressure. 222 Apr 9

The increased neuroendocrine activity in patients with congestive heart failure appears to be a generalized attempt to maintain blood pressure at the expense of reduced cardiac performance and salt and water retention. It is likely that baroreceptor dysfunction contributes to increased sympathetic nervous system activity in patients with congestive heart failure. The usual tonic inhibitory messages emanating from baro- and mechanoreceptors in the great vessels and heart fail to adjust sympathetic traffic from the brain to the periphery, leading to uninhibited sympathetic tone. Arginine vasopressin and plasma renin activity may be increased secondarily; however, plasma renin activity activation could also be induced by a low-salt diet and diuretic use. Preliminary baseline data indicate that patients with left ventricular dysfunction (ejection fraction less than or equal to 35%) but no or very mild symptoms of heart failure have increased plasma levels of norepinephrine, atrial natriuretic factor and arginine vasopressin, while plasma renin activity is normal, suggesting that neuroendocrine activity contributes to the pathogenesis of congestive heart failure. Neurohormones such as angiotensin II may alter gene expression, leading to changes in the shape and size of the cell. Remodeling of the heart and blood vessels is associated with both heart failure and hypertension. Angiotensin-converting enzyme inhibitors have been demonstrated to retard or reverse the remodeling process under certain experimental conditions. Studies are currently under way to test this possibility in patients.
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PMID:Neuroendocrine activity in congestive heart failure. 222 Jun 3

High-dose firosemide is considered effective in primary renal sodium retention but is not generally recommended in congestive heart failure. In order to evaluate efficacy and safety of high-dose furosemide (greater than 500 mg/day), the authors studied 20 patients (pts) resistant to therapy (including furosemide less than 500 mg/day) selected from 161 pts admitted for chronic heart failure. All refractory pts (15 men and 5 women, mean age sixty +/- 12 years) were in NYHA class IV and showed hyponatremia (130 +/- 5 mEq/L) and impaired renal function (BUN 31 +/- 14 mg/dL, serum creatinine 1.3 +/- 0.3 mg/dL and BUN/creatinine ratio 23 +/- 7). In addition to digitalis, dopamine, angiotensin-converting enzyme inhibitors, or vasodilators, IV high-dose furosemide (775 +/- 419 mg/day, 500-2000) was given for ten +/- five days under daily clinical and laboratory monitoring. Three pts died of low-output syndrome while 16 pts were upgraded to NYHA class III and 1 pt to class II; a mean weight reduction of 7.3 +/- 2.9 kg in ten + five days (0.80 +/- 0.4 kg/day) and a mean diuresis increase of 88 +/- 57% occurred. The maximal dose of furosemide did not correlate with serum creatinine but did correlate with BUN/creatinine ratio (r = 0.78, p less than .001). Pts were discharged on with chronic heart failure, and 43% in the subgroup in NYHA class IV with hyponatremia. High dose furosemide was effective for rapid removal of excess water and salt in "furosemide-resistant" congestive heart failure. The relationship between renal impairment and maximal furosemide doses seems to confirm the role of renal pharmacokinetics in the appearance of furosemide resistance.
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PMID:Effect of high-dose furosemide in refractory congestive heart failure. 222 64

Ibopamine is a novel oral dopamine analogue with vasodilatory, positive inotropic and diuretic effects. In a double-blind, randomized study, the drug was investigated in 12 patients (mean age 49 +/- 10 years, 8 male, 4 female) with mild or moderate heart failure (NYHA classes II:8 patients, III:4 patients). Effects of single oral doses of 200 mg ibopamine, of 40 mg furosemide and of 200 mg ibopamine + 40 mg furosemide were compared in each patient at 3-day intervals. 1 h after administration, systolic and diastolic blood pressure increased from 120 +/- 11 to 124 +/- 9 and from 76 +/- 5 to 81 +/- 6 mm Hg in the ibopamine group. During 4 h after drug ingestion, urinary flow was significantly raised from 124 +/- 81 to 228 +/- 166 ml/2 h in the ibopamine group (p less than 0.05), while the administration of furosemide (with or without ibopamine) resulted in several folds increases of urinary flow. After ibopamine, the 2-h creatinine clearance rose from 123 +/- 73 to 131 +/- 85 ml/min (not significant). Sodium and potassium excretion remained essentially unchanged by ibopamine, while effects of furosemide were several folds of those of ibopamine. Plasma renin activity was lowered to 65% by ibopamine (p less than 0.01). No additive effects of ibopamine in the presence of furosemide were observed for all parameters tested. These results indicate that ibopamine has smaller renal effects than furosemide with regard to water diuresis and kaliuresis. These effects of ibopamine could reflect direct changes of renal function or secondary effects of neurohumoral origin. Ibopamine does not produce undesirable renal side effects, but affects the neurohumoral status favourably. This drug, thus, could be useful as an adjuvant therapy in mild heart failure.
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PMID:Extracardial effects of oral ibopamine versus furosemide in patients with mild or moderate heart failure. A double-blind, randomized trial. 227 57

All patients with supraventricular tachycardia during the first 12 months of life who presented between 1977 and 1988 were identified by a retrospective survey of records in this hospital and by a questionnaire sent to paediatricians in the Northern region. Twenty two of 29 patients (76%) were in heart failure and seven (24%) had cardiogenic shock. Seven patients (24%) were free of symptoms. All had narrow QRS tachycardia at 215-315 beats/minute (mean (SD) 292 (21)). Initial treatment included digoxin (effective in seven of 14 patients, with overdose in three), verapamil (effective in three of three but fatal in one), cardioversion (effective in all 10 who were treated in this way), iced water applied to the face (effective in all 16 patients on 53 of 59 occasions, 90%). Initial treatment in local hospitals was less effective and associated with more complications than that given in the regional referral centre. Digoxin is often ineffective, return to sinus rhythm is delayed, and overdosing is common. Cardioversion is effective but tachycardia often recurs. Iced water is safe and effective, and should become the treatment of choice for termination of supraventricular tachycardia in neonates and young infants.
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PMID:Supraventricular tachycardia in infants: response to initial treatment. 230 75

A 51-year-old male remained immersed in sea water (6 degrees C) for 40 min. Brought ashore, the ECG showed asystole. Advanced life support was immediately commenced. On arrival in hospital his rectal temperature was 27 degrees C, but continued to fall to 24 degrees C. The ECG remained isoelectric. Cardiopulmonary resuscitation was continued until extracorporeal circulation was established 190 min after rescue. Upon rewarming ventricular fibrillation occurred which was converted to sinus rhythm with a bolus of lignocaine followed by D.C. conversion at 31.5 degrees C. When rewarming was complete after 60 min, signs of severe heart failure became evident. Sternotomy and pericardiotomy were performed to exclude cardiac tamponade. After 60 min of re-perfusion the patient was be weaned from bypass supported by a high-dose vasopressor infusion and nitroglycerine. He was discharged after 13 days with no evidence of any permanent organ damage. Given the advantage of providing circulatory support, extracorporeal circulation may be useful when rewarming hypothermic victims with cardiac arrest.
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PMID:Accidental hypothermia with cardiac arrest: complete recovery after prolonged resuscitation and rewarming by extracorporeal circulation. 221 65

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

Iron catalysis is involved in the generation of the highly cytotoxic hydroxyl radical and in the chain reactions of subsequent lipid peroxidation that lead to irreversible membrane damage. Assuming that ischemically stored heart transplants may incur free radical injury at the time of reoxygenation, we assessed the effects of the iron chelator deferoxamine in 70 isolated isovolumic buffer-perfused rat hearts subjected to the following protocol: cardioplegic arrest; cold (2 degrees C) storage for 5 hours; global ischemia at 15 degrees C for 1 hour, intended to simulate the implantation procedure; and normothermic reperfusion for 1 additional hour. During poststorage ischemic arrest, the following techniques of myocardial protection were evaluated: hypothermia alone; high-pressure (60 cm H2O) cardioplegia given at 0, 30, and 55 minutes of arrest; low-pressure (30 cm H2O) cardioplegia given at 0 and 55 minutes of arrest; and low-pressure (30 cm H2O) cardioplegia only given at 55 minutes of arrest. Treated hearts had deferoxamine (6 mumol) added to the cardioplegic solution used throughout the experimental time course. Further, in the treated group subjected to the protocol of single cardioplegic delivery at end ischemia, deferoxamine was given both in the cardioplegic reperfusate and in the Krebs buffer over the 15 initial minutes of reflow. Based on comparisons of postreperfusion ventricular pressure development, maximal rate of rise of ventricular pressure, left ventricular compliance, and coronary flow, the best myocardial protection was afforded by deferoxamine given as an additive to single-dose cardioplegic solution at the end of arrest and to the reperfusate during the initial phase of reoxygenation. As the drug has no inotropic effect, its protective action is most likely related to a decrease in catalytic iron available for free radical production and lipid peroxidation. These results support the hypothesis that oxidative damage may contribute to donor heart failure and demonstrate that this form of damage can be efficiently acted upon by iron chelation. The clinical relevance of these data stems from the fact that deferoxamine is available for human use and might become an effective means of improving donor heart preservation in the setting of clinical heart transplantation.
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PMID:A promising approach for improving the recovery of heart transplants. Prevention of free radical injury through iron chelation by deferoxamine. 236 51

In order to evaluate the incidence and the prognostic value of hyponatremia (hypoNa) in patients (pts) with severe chronic heart failure (SCHF), the authors studied 161 consecutive pts (113M, 48F ages sixty-seven +/- ten) with SCHF in NYHA class III-IV. The cause of SCHF was ischemic in 64 pts, hypertensive in 39, valvular in 14, alcohol-related in 3, and idiopathic in 41. Pretreatment hypoNa (less than 135 mmol/L) was found in 64/161 pts (40%) (Group I); Na+ was less than 125 in 10 pts, 125-130 in 19, and 131-135 mmol/L in 35; 42/64 pts (66%) of Group I were in NYHA class IV at admission. In the pts with pretreatment Na+ less than 125 mmol/L, hypoNa was persistent and refractory to high-dose furosemide (less than 500 mg/day) and water restriction. Cardiovascular mortality of Group I pts was 69% within twenty-four months (34 pts died of low-output syndrom and 10 suddenly). All pts with Na+ less than 130 mmol/L died within six months. The 20 pts who normalized Na+ are alive, and in NYHA class II-III (follow-up: twenty-six +/- fifteen, six to sixty months). Pts without hypoNa were 97/161 (Group II), and 58/97 (60%) are alive (follow-up: thirty +/- eighteen, five to fifty-eight months), whereas 39 pts died (27 suddenly, 9 of low-output syndrome, and 3 of extracardiac disease) within twenty-four months. The mortality rate of Group II was significantly lower (40% vs 69%, p less than 0.001) compared with Group I. The two groups were similar for age, sex, and cause and duration of SCHF.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prognostic value of hyponatremia in patients with severe chronic heart failure. 238 44


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