[Intracranial hemorrhage after sinus venous thrombosis during cochlear implantation : A case report]. / Intrakranielle Blutung nach Sinusvenenthrombose bei Cochleaimplantation : Ein Fallbericht.

Cochlear implantation is a safe surgical procedure with low complication rates. In particular, intracranial complications are rare. We present the case of a patient with difficult anatomical relations, which led to injury of the sigmoid sinus during cochlear implantation. Thrombosis and intracerebral hemorrhage followed. The diagnostic steps and treatment of these complications are explained in this case report.

Natriuretic peptides and the prevalence of congestive heart failure in patients with pacemakers.

AIM: The aim of the study was to investigate the diagnostic potential of natriuretic cardiac peptide measurement in the context of left ventricular dysfunction and comorbidities in a pacemaker population. MATERIAL AND METHODS: Ninety-five consecutive patients with pacemakers were included in the study. All patients underwent echocardiography and were asked to complete the Minnesota Living with Heart Failure Questionnaire (MLHFQ). Brain natriuretic peptide (BNP), N-terminal proatrial natriuretic peptide (N-ANP) and atrial natriuretic peptide levels in plasma were measured. RESULTS: Twenty-six percent of patients had reduced systolic left ventricular function; only 16 patients had a history of congestive heart failure. BNP was abnormally elevated in 64%, N-BNP in 72% and N-ANP in 96% of patients. Both BNP (r = 0.30; P < 0.01) and N-ANP (r = 0.39; P < 0.0005) correlated with MLHFQ. The strongest correlation was found between N-ANP and the ejection fraction (r = 0.6; P < 0.0001). Patients were stratified in a high-risk group and a low risk-group according to their N-ANP (N-ANP > 5000 fmol L(-1); n = 63 and N-ANP < 5000 fmol L(-1), n = 32) and BNP levels (BNP > 400 pg mL(-1); n = 17 and BNP < 400 pg mL(-1), n = 78). N-ANP was correlated with hypertension (P < 0.003) and atrial fibrillation (P < 0.03), and BNP with mitral insufficiency (P < 0.002). CONCLUSIONS: Cardiac natriuretic peptides are markedly elevated in the majority of patients with pacemakers. The prognostic significance of BNP and N-ANP in left ventricular dysfunction warrants close follow-up schedules.

Long-term effect of atenolol on ejection fraction, symptoms, and exercise variables in patients with advanced left ventricular dysfunction.

AIMS: We recently reported a beneficial clinical effect of atenolol, a beta(1) selective adrenergic antagonist, in 100 ambulatory heart failure patients with low left ventricular ejection fraction (LVEF,

Prognostic evaluation of neurohumoral plasma levels before and during beta-blocker therapy in advanced left ventricular dysfunction.

OBJECTIVES: The study assessed the relative predictive potency of neurohumoral factors in patients with advanced left ventricular (LV) dysfunction during neurohumoral blocking therapy. BACKGROUND: The course of heart failure is characterized by progressive LV deterioration associated with an increase in cardiac (natriuretic peptides) and predominantly extracardiac (norepinephrine, big endothelin [big ET]) hormone plasma levels. METHODS: Plasma hormones were measured at baseline and months 3, 6, 12 and 24 in 91 patients with heart failure (left ventricular ejection fraction [LVEF] <25%) receiving 40 mg enalapril/day and double-blind atenolol (50 to 100 mg/day) or placebo. After the double-blind study phase, patients were followed up to four years. Stepwise multivariate regression analyses were performed with 10 variables (age, etiology, LVEF, symptom class, atenolol/placebo, norepinephrine, big ET, log aminoterminal atrial natriuretic peptide, log aminoterminal B-type natriuretic peptide [N-BNP] and log B-type natriuretic peptide [BNP]). During the study, the last values prior to patient death were used, and in survivors the last hormone level, New York Heart Association class and LVEF at month 24 were used. RESULTS: Thirty-one patients died from a cardiovascular cause during follow-up. At baseline, log BNP plasma level (x2 = 13.9, p = 0.0002), treatment allocation (x2 = 9.5, p = 0.002) and LVEF (x2 = 5.6, p = 0.017) were independently related to mortality. During the study, log BNP plasma level (x2 = 21.3, p = 0.0001) remained the strongest predictive marker, with LVEF (x2 = 11.2, p = 0.0008) log N-BNP plasma level (x2 = 8.9, p = 0.0027) and treatment allocation (x2 = 6.4, p = 0.0109) providing additional independent information. CONCLUSIONS: In patients with advanced LV dysfunction receiving high-dose angiotensin-converting enzyme inhibitors and beta-blocker therapy BNP and N-BNP plasma levels are both independently related to mortality. This observation highlights the importance of these hormones and implies that they will likely emerge as a very useful blood test for detection of the progression of heart failure, even in the face of neurohumoral blocking therapy.

Angiogenesis stimulation in explanted hearts from patients pre-treated with intravenous prostaglandin E(1).

BACKGROUND: Prostaglandin E(1) (PGE(1)) is a potent vasodilator and induces angiogenesis in animal tissues. Previous clinical studies demonstrated that PGE(1) improves hemodynamic parameters in patients with heart failure listed for heart transplantation (HTX). Therefore, we designed a retrospective immunohistochemistry study to investigate various markers of angiogenesis using hearts explanted from PGE(1)-treated patients with idiopathic dilated cardiomyopathy (IDCM). METHODS AND RESULTS: We investigated neovascularization in 18 hearts explanted from patients with IDCM: 9 patients received treatment with chronic infusions of PGE(1) for end-stage heart failure before HTX, whereas the remaining patients with IDCM did not receive PGE(1) and served as controls. We used immunoreactivity against CD34, von Willebrand factor (vWf), vascular endothelial growth factor (VEGF), and MIB-1 (Ki-67) to quantify angiogenesis, and used sirius red staining to determine the degree of fibrosis. Compared with the control group, PGE(1)-treated patients had significantly more CD34-, vWf- and MIB-1-positive cells in the sub-endocardium, myocardium and sub-epicardium (p < 0.01). The degree of fibrosis in the hearts of PGE(1)-treated patients was significantly lower than in control patients (p < 0.05), but we did not see any difference in the percentage of muscle mass. Finally, throughout the ventricles, we found significantly more VEGF-positive capillaries in the PGE(1) group (p < 0.0001). CONCLUSIONS: The data suggest that PGE(1) could be a potent inducer of angiogenesis and the angiogenic factor VEGF, and could cause reduced fibrosis in the failing human heart.

Effects of endothelin a receptor blockade on endothelial function in patients with chronic heart failure.

BACKGROUND: Chronic heart failure (CHF) is associated with impaired endothelium-dependent vasodilation and increased basal vascular tone due, in part, to elevated endothelin-1 plasma levels. In the present study, we investigated whether a reduction of vascular tone using an endothelin A receptor blocker attenuates the impairment of endothelium-dependent, flow-mediated vasodilation (FMD). METHODS AND RESULTS: Twenty-one patients with CHF randomly received either the endothelin A receptor blocker LU 135252 (30 mg/d, n=7; 300 mg/d, n=7) or a placebo (n=7). Using high-resolution ultrasound, FMD and endothelium-independent, nitroglycerin-induced dilation of the brachial artery were assessed at baseline in the 21 patients with CHF and in 11 controls and after 3 weeks treatment in the 21 patients with CHF. FMD at baseline was impaired in all 21 patients with CHF (3.2+/-2%) when compared with the 11 controls (9.7+/-4.9%; P=0.0005). In comparison with baseline, FMD significantly improved after 3 weeks of treatment with LU 135252 in all 14 patients receiving it (from 3.0+/-2.0% to 4.9+/-2.9%; P=0.04), but FMD remained unchanged with placebo. Subgroup analysis, according to different dosages, revealed a significant increase of FMD compared with baseline (from 2.4+/-1.5% to 5.5+/-2.4%; P=0.03) in the patients treated with the low-dose (30 mg/d), whereas a high dose of 300 mg/d failed to increase FMD significantly. Improvement in the high-dose group, however, may have been masked by reduced vasodilator capacity due to a significant increase in vessel size (from 4.8+/-0.4 to 5.1+/-0.7 mm; P=0.03). CONCLUSIONS: These results suggest that endothelin A receptor blockade improves FMD in CHF patients.

Effect of beta 1 blockade with atenolol on progression of heart failure in patients pretreated with high-dose enalapril.

BACKGROUND: The survival benefit of beta-blocker treatment in patients with heart failure has been established in recent trials. Yet, the impact of beta-blockers added on high dose angiotensin converting enzyme inhibitors has not been reported. AIMS: To investigate the effect of atenolol, a hydrophilic, selective beta1-adrenergic antagonist, added on enalapril 40 mg/day in patients with advanced left ventricular dysfunction in a double-blind placebo-controlled trial. METHODS: One hundred and nineteen patients with class II or III heart failure, left ventricular ejection fraction < or = 25% and treatment with 40 mg enalapril daily were given an initial challenge dose of atenolol 12. 5 mg. One hundred patients (54 with idiopathic, 28 with ischemic, 18 with other dilated cardiomyopathy) tolerated challenge and were randomized to atenolol (maintenance dose 89+/-11 mg/day, range 50-100 mg/day) or placebo. The primary endpoint was combined worsening heart failure or death within 2 years, the secondary endpoint was hospitalization for cardiac events. RESULTS: After 395+/-266 days interim analysis revealed a significant difference between the atenolol and placebo group (log rank P<0.01) and the trial was concluded. Twenty-seven patients had developed worsening heart failure (8 in the atenolol group vs. 19 in the placebo group) and 13 patients had died (5 in the atenolol vs. 8 in the placebo group). Overall there were 23 hospitalizations for cardiac events (6 in the atenolol group vs. 21 in the placebo group, P=0.07); 17 hospitalizations were due to worsening heart failure (5 in the atenolol group, 12 in the placebo-group, P=0.05) and 10 due to arrhythmias (1 in the atenolol group vs. 9 in the placebo group, P<0.01) CONCLUSIONS: The data suggest that in patients with advanced left ventricular dysfunction, beta-blockers can provide substantial benefits supplementary to that already achieved with high dose enalapril treatment.

Experience with beta-blocker therapy in patients with advanced heart failure evaluated for HTx.

BACKGROUND: The aim of this study was to review our experience with beta-blocker therapy on top of high-dose angiotensin-converting enzyme inhibitors (ACE-I) in patients with advanced heart failure evaluated for heart transplantation, and to question the value of intended heart transplantation for patients receiving this therapy. METHODS: Three hundred eighteen patients (New York Heart Association (NYHA) function class III 34%, class IV 66%, average left ventricular ejection fraction (LVEF) 16%, and average cardiac index 2.2 l/min per m(2) at time of referral) were treated with digitalis, loop diuretics, maximally uptitrated ACE-I, beta-blockers (if tolerated), and intravenous support (if needed). After 3 months, patients were retrospectively stratified into those receiving beta-blockers plus ACE-I (Group A, n = 126), ACE-I (Group B, n = 135), and ACE-I plus intravenous support (Group C, n = 57). Endpoint 1 of the study was combined urgent heart transplantation, mechanical assist device implantation, and pretransplant death during a follow-up of 12 to 48 (mean 19 +/- 11) months. Endpoint 2 was posttransplant mortality up to 48 (mean 14 +/- 8) months. RESULTS: In the pretransplantation period the survival rate was 58% and the mortality rate was 20%. Between Groups A and B there was a significant difference in mortality (9% vs 27%, p = 0.001) due to a lower sudden-death rate in Group A (6% vs 17%, p < 0.01). While between Groups A and C all event rates of Endpoint 1 differed significantly, between Group C and Group B total mortality (30% vs 27%) was similar. However, in Group C urgent heart transplantation (HTx) was more often performed than in Group B (54% vs 11%, p < 0.0001). Seventy of 318 patients (22%) underwent heart transplantation (16% urgent, 6% elective). Posttransplant actuarial survival of the entire transplanted cohort (n = 70, 12 deaths) was significantly lower (log rank p < 0.01) than event-free survival in Group A (n = 126, 18 events), significantly higher (log rank p < 0. 0001) than event-free survival in Group C (n = 57, 34 events), and similar to that in Group B (n = 135, 52 events). CONCLUSION: This experience suggests that it may be particularly useful to add a beta-blocker to ACE-I therapy in patients referred for heart transplantation. In patients who tolerate this treatment, heart transplantation does not seem to provide additional survival benefit in the short term (2 years).

Intravenous therapy for advanced heart failure.

Because of the standard use of oral neurohumoral antagonists, the role of intravenous agents for advanced heart failure patients has changed profoundly. Their current use as medical therapy is restricted to two indications: first, as short-term infusion (hours to days) in advanced heart failure patients who decompensate into a symptomatic New York Heart Association class IV condition and who are admitted for rapid hemodynamic support with intravenous vasodilators or inotropes; in these patients after hemodynamic and clinical stabilization, optimization of conventional heart failure therapy has to be reconsidered; second, as long-term application in heart transplantation candidates who are in a similar desperate condition although already receiving maximal oral heart failure therapy.

Prognostic value of hemodynamic vs big endothelin measurements during long-term IV therapy in advanced heart failure patients.

STUDY OBJECTIVE: To compare hemodynamics and plasma big endothelin levels in patients awaiting heart transplantation who are receiving continuous IV therapy, and to establish their respective potency for predicting future cardiac events. DESIGN: A randomized, prospective trial of ambulatory continuous treatment with IV prostaglandin E(1) (PGE(1)) vs dobutamine. A subanalysis was conducted of all patients who completed 4 weeks of follow-up in regard to treatment effects on hemodynamics and big endothelin plasma levels. PATIENTS: Thirty-two listed heart transplant candidates who were refractory to oral treatment, 21 patients who were receiving PGE(1), and 11 patients receiving dobutamine. MEASUREMENTS AND RESULTS: Hemodynamics and plasma big endothelin levels were measured at baseline and after 4 weeks. The cardiac index increased significantly (PGE(1) group, 1.7 +/- 0.4 vs 2.5 +/- 0.6 L/min/m(2); dobutamine group, 1.8 +/- 0.3 vs 2.3 +/- 0.6 L/min/m(2); p < 0.05), whereas the systemic vascular resistance index (SVRI) decreased significantly only in the PGE(1) group (3,352 +/- 954 vs 2,178 +/- 519 dyne. s. cm(-5)/m(2); p < 0. 05). The plasma big endothelin level decreased significantly (PGE(1) group, 7.6 +/- 3.1 vs 4.7 +/- 2.6 fmol/mL; dobutamine group, 6.5 +/- 3.7 vs 5.0 +/- 2.6 fmol/mL; p < 0.01 for the time effect). Plasma big endothelin (beta = 0.393; chi(2) = 10.8; p = 0.001) and SVRI (beta = 0.003; chi(2) = 6.9; p < 0.01), both measured after 4 weeks of continuous treatment, were the only independent predictors of future outcome. CONCLUSION: Continuous treatment over 4 weeks with either PGE(1) or dobutamine in patients awaiting heart transplantation yields an improved hemodynamic state accompanied by a reduction of increased big endothelin levels. Plasma big endothelin measured after 4 weeks of continuous therapy provides prognostic information about future outcome.

Optimising management of patients with advanced heart failure: the importance of preventing progression.

Heart failure is a highly complex, progressive and deadly disease. When incorrectly treated, it results in irreversible structural damage to the myocardium and resists any conventional treatment. This stage has been arbitrarily termed refractory heart failure. However, with timely and sufficiently applied neurohumoral antagonists, progression can be prevented, or at least delayed. In contrast, as soon as heart failure has become moderate or severe due to advanced left ventricular dysfunction, polypharmacy is the rule. Physicians should make every effort to maintain or reconsider optimal neurohumoral antagonist therapy in such patients, even if symptomatic improvement from these agents may be slow. Proper use of diuretics is essential not only for symptom relief but also to achieve full benefit from angiotensin converting enzyme inhibitors and beta-blockers. Digitalis may be particularly indicated in severe heart failure, irrespective of rhythm. Adjunctive regimens can be helpful in specific patients, but evidence of their salutary effects to prolong life is lacking. In the decompensated state, tailoring intravenous therapy to haemodynamic goals followed by (re-)institution of optimal oral therapy is an option. Only if these strategies fail is heart transplantation justified. While waiting for a donor, patients have been bridged with various intravenous agents, most often inotropes, but symptom relief is associated with risk of increased mortality due to these drugs. New hope emerges from drugs interfering with endothelin and the cytokines, and from research into increasing contractility with calcium sensitising agents. Even though these developments follow established routes, they may enable a more effective approach to prevent worsening heart failure in every single patient.

ACE inhibitor dosage at the time of listing predicts survival.

BACKGROUND: To be listed for heart transplantation (HTx), optimization of the dosage of angiotensin converting enzyme (ACE) -inhibitors is recommended worldwide even though this issue has not been thoroughly investigated in the pre-transplantation cohort. OBJECTIVE: The aim of this database study was to analyze the prognostic impact of a pre-defined high vs a low ACE inhibitor dose range at the time of listing for elective HTx in addition to various previously established prognostic factors. METHODS: Medical records from 237 patients (84% male, mean age 54 years) admitted between January 1995 and January 1998 from 25 different centers in Austria were reviewed. Forty-seven percent were taking > or =75 mg captopril, > or =20 mg enalapril, > or =20 mg lisinopril or > or =5 mg ramipril daily ("high-dose" group) and 53% received smaller doses ("low-dose" group). RESULTS: No significant differences between groups were detected at baseline except that patients with higher ACE inhibitor doses were more likely to take nitrates, beta-blockers and amiodarone, received higher furosemide doses and had higher serum gamma-glutamyl transferase levels. Follow-up was 328 days (248 SD) with 16% deaths in the "high-dose" group vs 288 days (270 SD) with 25% deaths in the "low-dose" group. Kaplan-Meier survival curves demonstrated a significant difference over time between the two treatment groups (P = 0.03). Furthermore, dichotomized ACE inhibitor treatment at the time of listing was the strongest independent single predictor of mortality (P = 0.01) with only blood pressure (P = 0.02), alanine transaminase (P = 0.02) and left ventricular end diastolic diameter (P = 0.02) providing additional prognostic information. To explain these findings several factors have to be considered a) greater benefit with higher ACE inhibitor doses b) sicker patients receiving lower ACE inhibitor doses and c) more experienced heart failure care of the "high-dose" group. CONCLUSIONS: Heart transplantation candidates who, for whatever reason, receive ACE-inhibitors below the recommended dosages, are at increased mortality risk and thus merit greater scrutiny.

Effects of prostaglandin E1, dobutamine and placebo on hemodynamic, renal and neurohumoral variables in patients with advanced heart failure.

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.

Moderate-intensity exercise training with elements of step aerobics in patients with severe chronic heart failure.

OBJECTIVE: To evaluate whether a specific program of moderate-intensity step aerobics training may be sufficient to improve the exercise tolerance of patients with severe chronic heart failure. PATIENTS: Twenty-six patients (22 men, 4 women; mean +/- SD age, 54 +/- 9yrs) with a history of severe chronic heart failure (left ventricular ejection fraction of 18% +/- 8%). STUDY DESIGN: Prospective, randomized, controlled trial. Patients were randomized into exercise and control groups. All patients underwent a clinical examination and a ramp pattern cycle exercise test before and after the observation period. The exercise group underwent a moderate-intensity (50% of peak oxygen uptake) 12-week training program, progressing to 100 minutes per week of step aerobics and 50 minutes per week of cycling. The control group did not perform a training program. MAIN OUTCOME MEASURES: Peak oxygen uptake, peak workload, percent of predicted power ability. RESULTS: Significant increases in peak oxygen uptake (15 +/- 3.4 to 18.5 +/- 2.9mL/kg/min; p = .001), peak workload (77 +/- 26 to 99 +/- 31 watts; p = .000), and percent of predicted power ability (43% +/- 10% to 56% +/- 13%; p = .000) were observed in the exercise group. No significant changes in baseline parameters occurred in the control group. There were no critical changes in heart rate or blood pressure in either group. CONCLUSION: Moderate-intensity step aerobics training significantly increases peak oxygen uptake and peak workloads in patients with severe chronic heart failure.

Bridging to heart transplantation: prostaglandin E1 versus prostacyclin versus dobutamine.

BACKGROUND: Prostaglandin E1 (PGE1) and prostacyclin have potent pulmonary and systemic vasodilating properties. This prospective, randomized trial compared PGE1 vs prostacyclin vs. low-dose dobutamine in patients with low-output heart failure awaiting heart transplantation (HTx) who were refractory to oral treatment. METHODS: Patients in advanced heart failure in New York Heart Association (NYHA) Class IV, with a cardiac index < or = 2.5 L/minute/m2 and a pulmonary capillary wedge pressure > or = 20 mmHg, who were listed for HTx were studied. In an inpatient study phase of 12 hours duration, therapy was aimed to increase cardiac output by 20% or more, when compared to baseline values, and to achieve a reduction of pulmonary vascular resistance below 550 dyn.s/cm-5m-2. During a long-term outpatient phase, the drugs were continuously infused to bridge these patients to HTx using three combined negative endpoints (worsening heart failure, serious adverse events, death) for analysis. RESULTS: Sixty-eight patients were enrolled, 30 patients on PGE1, 8 patients on prostacyclin, and 30 patients on dobutamine. During the inpatient study phase, maximum doses were 22 +/- 1.8 ng/kg/minute for PGE1, 7 +/- 1 ng/kg/minute for prostacyclin and 5 +/- 0.4 micrograms/kg/minute for dobutamine. During the inpatient study phase 21 patients failed, 4/30 (13%) patients on PGE1, 4/8 patients on prostacyclin (50%), and 13/30 (43%) on dobutamine (p < 0.05). Long-term continuous intravenous drug infusion in outpatients was begun in 26 patients on PGE1, in 4 patients on prostacyclin, and in 17 patients on dobutamine. Infusion therapy lasted for 88 +/- 14 days in the PGE1 group with 31 +/- 22 days in the prostacyclin group, and 30 +/- 8 days in the dobutamine group (NS). During the outpatient phase 23 patients reached a negative endpoint with 16 patients developing worsening heart failure, 5 severe adverse events and 2 deaths. Seven out of 26 (27%) failed on PGE1, 4/4 (100%) failed on prostacyclin, and 12/17 (71%) failed on dobutamine (p < 0.05, log rank test). Because prostacyclin treatment was ineffective in the first 8 patients, this trial arm was stopped prematurely. CONCLUSIONS: The findings from this prospective open pilot trial suggest that continuous PGE1 infusions at individualized dosages can be useful in certain patients as a pharmacologic bridging procedure with reduced risk to develop worsening heart failure before HTx compared to prostacyclin and dobutamine. Further comparative studies are warranted to investigate the effects of PGE1 among other bridging agents.