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

Right ventricular dysfunction is a common clinical event after heart transplantation. The major cause is the failure of right ventricle (RV) to adapt to the pulmonary hypertension (PH) secondary to chronic heart failure. Nevertheless, this dysfunction is usually transient owing to the reversibility of PH, the nature of which is mainly passive. Therefore, it is particularly important to perform a preoperative hemodynamic study to identify those cases in which PH is a permanent component, a situation that excessively increases the risk of postoperative RV failure. Once this occurs, the treatment is complex. The available therapeutic measures include the use of vasodilators such as prostaglandin E1 and nitric oxide.
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PMID:[Special anesthesia care in heart transplantation. The management of right ventricular failure]. 877 18

Ambulatory pump-driven intravenous infusions are a novel and - compared with hospitalization-cost-effective procedure to bridge refractory heart failure patients to cardiac transplantation. In the present study 13 patients received chronic infusions with prostaglandin E1 alone or in conjunction with catecholamines and the acceptance of this bridging therapy was investigated over a period of seven weeks. Prostaglandin E1 was uptitrated from 2.5 ng/kg/min to a maximum of 40 ng/kg/min, according to individual tolerance. 50% of the maximum tolerated dose of prostaglandin E1 was used for chronic infusion with a further dose reduction if side effects occurred. Altogether 8 patients who completed the therapy were analysed; of the remaining 5 three patients had a heart transplant, one patient died and one patient did not comply with the protocol. The drugs were administered by an automatic portable pump, which was connected to a subcutaneous tunneled catheter. During hospitalization patients and their relatives were instructed how to prepare drug solutions and to handle the infusion system. Patients' perceptions were investigated by visual analog scale questionnaires (rating scale zero to ten) before, and at weekly intervals during bridging therapy. Initial acceptance was documented as belief in therapy (9.4 +/- 1.2 SD), absence of fear of handling the pump (8.9 +/- 1.2 SD) and confidence of receiving help of close relatives (8.7 +/- 1.8 SD). During the observation period there were no statistically significant differences compared with this favorable starting position and no significant disruption of life style occurred. Pain in the joints-a prostaglandin E1-associated side effect-increased significantly (p < 0.05) at week 5, but returned to baseline levels during the following two weeks. At study end patients confirmed that they would repeat the experience (7.6 +/- 1.4 SD) and advise other patients to undergo this form of therapy (8.2 +/- 1.9 SD). Thus, this pilot study suggests that ambulatory pump-driven intravenous infusion therapy comprising prostaglandin E1 and catecholamines is acceptable to patients as a bridge to heart transplantation and that there should be no major difficulties regarding compliance.
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PMID:Acceptance of a pump-driven infusion therapy with prostaglandin E1 as a bridge to heart transplantation. 884 Apr 97

Prostaglandin E1 (PGE1) is a physiologic vasodilator, which is broadly used in the therapy of peripheral arterial occlusive disease. In addition, the successful use of PGE1 in patients with severe heart failure has been described in several studies, where a decrease in pulmonary artery pressure and an increase in cardiac output were observed. In contrast to these positive effects, the development of lung edema was reported in individual cases after the infusion of PGE1 in patients with heart disease. We therefore conducted a double-blind study to evaluate the effect of PGE1 on extravascular lung water (EVLW) in patients with heart failure (NYHA III-IV) and borderline increased EVLW. Seven patients received an infusion of PGE1 (Prostavasin) at a dosage of 60 micrograms over 2 hours, while in 6 patients (control group) isotonic saline was given as placebo. EVLW was measured using a double indicator method at time points -15 h, -9 h before and at the start of the infusion, 1 h and 2 h during infusion, as well as +1 h, +4 h, +7 h, and +22 h after termination of the infusion. Infusion of PGE1 did not alter EVLW both in comparison to pre-study values (9.8 +/- 4.3 ml/kg bw preinfusion. 9.3 +/- 3.2 ml/kg bw after 1 hour and 9.4 +/- 3.5 ml/kg bw after 2 hours) or to the control group (6.5 +/- 3.3 ml/kg bw preinfusion, 7.1 +/- 2.7 ml/kg bw after 1 hour and 7.0 +/- 3.2 ml/kg bw after 2 hours). We conclude that there is no evidence that PGE1 might contribute to the development, or worsening of lung edema by inducing extravascular lung water accumulation and can, thus, be savely given to patients with even a severe degree of heart failure (NYHA III-IV).
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PMID:[Effect of prostaglandin E1 on extravascular lung water in patients with severe heart failure]. 896 94

Prostaglandin E1 (PGE1, alprostadil) is a potent vasodilating agent that is frequently used to resolve cardiogenic pulmonary hypertension. To investigate the effect of PGE1 in refractory chronic heart failure in a double-blind trial, twenty patients (17 men, 3 women, 58 +/- 2 years, cardiac index < or = 2.5 l/min/m2, pulmonary capillary wedge pressure > or = 20 mmHg), who were in NYHA functional class IV on optimized treatment with ACE inhibitors and furosemide were infused with 30 ng/kg/min PGE1 or placebo through 48 hours. All patients received a concomitant therapy with standardized catecholamine infusions which were given 24 hours in advance and were continued throughout the study. There was no difference in baseline values between the randomized groups before PGE1 or placebo was added. PGE1 resulted in decrements in pulmonary artery pressure (from 37 +/- 4 to 30 +/- 4 mmHg; p < 0.01), pulmonary capillary wedge pressure (from 26 +/- 4 to 19 +/- 3 mmHg p < 0.001) systemic vascular resistance index (from 2048 +/- 213 to 1506 +/- 13 dyn.sec/cm5.m2, p < 0.05) and in increments in cardiac index and stroke volume index (from 2.2 +/- 0.1 to 2.8 +/- 0.2 l/min.m2; p < 0.05 and from 23 +/- 2 to 28 +/- 2 l/m2; p < 0.05, respectively). Moreover, creatinine clearance increased (p < 0.05). Placebo infusions did not result in any hemodynamic or renal effect. Between groups percentage hemodynamic changes differed with respect to pulmonary artery pressure (p < 0.01), cardiac index (p < 0.05), stroke volume index (p < 0.05) and pulmonary vascular resistance index (p < 0.05). It is concluded that intravenous infusions with PGE1 may add further substantial benefit to the hemodynamic state in refractory heart failure patients who are already stabilized on i.v. inotropic support with catecholamines.
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PMID:Effect of prostaglandin E1 infusion in severe chronic heart failure. 916 10

Prostaglandin E1 or prostacyclin were randomly infused in 18 patients with severe chronic heart failure who did not respond to oral treatment. Maximally tolerated dosages of both agents increased cardiac index; however, only prostacyclin decreased mean arterial pressure and increased plasma norepinephrine significantly. Twelve hours after 50% peak dose reduction, atrial natriuretic peptide levels, right atrial pressure, mean pulmonary artery pressure, and mean arterial pressure continued to decrease with prostaglandin E1, whereas the increase in cardiac index was sustained; in contrast, at 50% prostacyclin dose reduction, cardiac index decreased toward baseline, suggesting that, with reduced dosages for chronic infusions, desired hemodynamic changes seem to be sustained with prostaglandin E1 only.
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PMID:Prostaglandin E1 infusion compared with prostacyclin infusion in patients with refractory heart failure: effects on hemodynamics and neurohumoral variables. 928 80

Surgery is the treatment of choice for coarctation of the aorta in childhood. Coarctation presenting in the neonatal period carries a poorer functional and vital prognosis and it may be opposed to the paucisymptomatic forms observed in infants and children. Coarctation in the neonatal period presents with severe cardiac failure and is often associated with hypoplasia of the transverse aorta and/or other complex congenital malformation. Improved neonatal intensive care and the introduction of prostaglandin E1 have considerably reduced the immediate mortality by enabling surgery to be undertaken under the best possible haemodynamic conditions. However, early and late mortality in this group remain significantly higher due to associated cardiac lesions; in this context, the management varies with some groups carrying out surgery in one stage and others in two stages. Despite progress in neonatal surgery and operative techniques to increase the diameter of the transverse aorta, hypoplasia may persist and be a cause of restenosis or secondary hypertension. In this group of coarctations, the main problem is the timing of surgery in order to reduce the risks of restenosis and hypertension to a minimum. Restenosis is diagnosed by clinical examination. Doppler ultrasonography and eventually confirmed by magnetic resonance imaging (MRI). The risk factors for restenosis are young age at surgery, the type of procedure performed and the presence of extensive aortic hypoplasia. Recurrent, localised forms are accessible to percutaneous angioplasty when performed 6 months to 1 year after surgery; extensive restenosis and restenosis in older children should be referred for reoperation. Some subjects become hypertensive in the absence of residual obstruction and, in these cases, MRI should be requested to detect hypoplasia of the aortic arch. However, hypertension may be observed alone or only occur during exercise: late surgery and the length of follow-up seem to be associated with its occurrence. Aortic aneurysms occur after aortoplasty with a patch, a technique which has now be abandoned for this reason. Nevertheless, this risk is also associated with percutaneous angioplasty of restenosis, justifying systematic diagnostic MRI. In summary, coarctation of the aorta in children has a good overall prognosis at medium-term, the neonatal forms having considerably benefited from progress in the management of this condition in the intensive care unit and from advances in surgical technique. However, long-term cardiological follow-up remains necessary to detect the two potential complications: restenosis and hypertension.
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PMID:[Long-term results after surgery of coarctation of the aorta in neonates and children]. 958 57

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

We investigated the hemodynamic effects of a single infusion of PGE1 (60 micrograms infused over a period of 2 h--this is the single dose used in courses of treatment for peripheral occlusive arterial disease) in patients with chronic heart failure NYHA class II-III. The ejection fraction of these patients was < 55%, their average age was 58.4 years (standard deviation 10 years), and their condition was stable. Nineteen of the patients had coronary heart disease and one patient had myocarditis. The hemodynamic data were obtained invasively by catheterization of the right and left heart. Blood pressure and pulse rate were measured manually. Intravenous infusion of 60 micrograms PGE1 over a period of 2 hours did not significantly alter contractility or hemodynamics. Dp/dtmax, dp/dtmax/p, and dp/dt DP40, which are parameters of left ventricular contractility, determined with the aid of a catheter-tip manometer, did not differ significantly over time from those in the placebo control group. Similarly, the other data furnished no evidence that administration of PGE1 had any hemodynamic or myocardial effects. Hence, it is reasonable to state that it is safe to administer PGE1 to patients with peripheral occlusive arterial disease.
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PMID:[Hemodynamic effects of a single intravenous administration of prostaglandin E1 in a patient sample with chronic NYHA-stage II/III heart failure]. 981 50

Transposition of great vessels (TGV) is the most frequent neonatal cyanotic malformative cardiopathy. The Authors report their experience in surgical anatomical correction of transposition of the great arteries in 55 patients, 44 male and 11 female. Minimum age was 2 days, maximum 6 months. TGV was simple in 38 cases and associated with ventricular defect in 12 cases, with double outlet right ventricle in 3 cases, and with complex cardiopathy in 2 cases. There have been 11 deaths. The cause of death was: cardiac failure in 3 patients, myocardial infarct in 4 patients, respiratory insufficiency in 2 patients, and sepsis in 2 patients. There was one death by myocardial infarction and 1 asymptomatic ostial left coronary stenosis during follow-up (from 1 to 104 months). There were neither anastomotic pulmonary stenosis nor aortic valve incompetence. The authors review the literature on functional and anatomic correction of TGV and underline the importance of precocious anatomic together with early diagnosis, percutaneous atrioseptostomy and pharmacologic (PGE1) therapy in determining further reduction of mortality and to improve late outcome.
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PMID:[Physiopathologic findings and surgical treatment in transposition of great vessels: our experience]. 1033 35

Excessive neurohumoral activity remains a major burden to the circulation of patients with advanced heart failure. Prostaglandin E1 (PGE1), a balanced i.v. vasodilator, was shown to elicit favorable hemodynamic and clinical effects in this cohort. A prospective randomized parallel group trial was performed to evaluate acute, intermediate and chronic changes in hemodynamic, neurohumoral and renal variables in response to PGE1, dobutamine and placebo. Thirty patients with class III and IV heart failure and low cardiac index (mean 1.9 l/min/m2) two hours after oral drugs including high dose enalapril were included. A 7-day-infusion of PGE1 (16.5 +/- 5 ng/kg/min, range 10 to 20 ng/kg/min, group A n = 10), dobutamine (4.5 +/- 1 micrograms/kg/min, range 2.5 to 5 micrograms/kg/min, group B n = 10) or placebo (saline, group C n = 10) was administered via a central venous access line after stepwise titration until intolerable side effects developed with PGE1 or a 20% increase in cardiac index occurred with dobutamine, which was continued on this dose throughout while PGE1 was maintained on 50% peak dose. Hemodynamic data were collected at baseline, at peak dosages, after 12 hours and after 7 days. Of neurohumoral variables plasma norepinephrine, big endothelin (Big ET) and atrial natriuretic peptide (ANP) were simultaneously evaluated using RIA methods. Renal plasma flow (by paraaminohippurate clearance) and glomerular filtration rate (by iothalamate clearance) was measured prior to and during the infusions (after 12 hours and after 7 days). At peak dose and at 12 hours significant drops from baseline of mean pulmonary artery pressure, pulmonary capillary wedge pressure and systemic vascular resistance were observed which were accompanied by a rise in cardiac output with both PGE1 and dobutamine. These changes were maintained through 7 days when pulmonary vascular resistance levels also fell with both active drugs. Blood pressure did not change throughout, but PGE1 increased heart rate slightly at 12 hrs. Both PGE1 and dobutamine enhanced renal plasma flow after 7 days, but only PGE1 decreased glomerular filtration fraction significantly. Glomerular filtration rate did not change with either drug. PGE1 decreased ANP levels at 12 hrs, and dobutamine increased big ET levels at peak, but decreased big ET at 7 days. Norepinephrine levels were unaffected throughout. Except a slight decrease in right atrial pressure after 7 days placebo did not change any measured variable significantly. Taken together, these data suggest that treatment with PGE1 is as efficacious as low-dose dobutamine in improving cardiac performance and renal perfusion in advanced heart failure. Of importance, no deleterious neurohumoral counterregulation was observed with PGE1.
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PMID:Effects of prostaglandin E1, dobutamine and placebo on hemodynamic, renal and neurohumoral variables in patients with advanced heart failure. 1050 54


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