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Background Cardiac retransplantation is a controversial procedure due to the disparity between donor heart demand and supply. Methods Of 7,290 patients undergoing primary cardiac transplantation between January 1990 and December 1999 at 42 institutions contributing to the Cardiac Transplant Research Database (CTRD), 106 patients later underwent a second and 1 patient a third cardiac transplant procedure. Results The actuarial freedom from retransplantation was 99.2% and 96.8% at 1 and 10 years, respectively. Reasons for retransplantation included early graft failure ( n = 34), acute cardiac rejection ( n = 15), coronary allograft vasculopathy (CAV, n = 39), non-specific graft failure ( n = 7), and miscellaneous ( n = 10). The only risk factor associated with retransplantation was younger age, reflecting the policy of preferential retransplantation of younger patients. Survival after retransplantation was inferior to that after primary transplantation (56% and 38% at 1 and 5 years, respectively). Risk factors associated with death after retransplantation included retransplantation for acute rejection ( p = 0.0005), retransplantation for early graft failure ( p = 0.03), and use of a female donor ( p = 0.005). Survival after retransplantation for acute rejection was poorest (32% and 8% at 1 and 5 years, respectively) followed by retransplantation for early graft failure (50% and 39% at 1 and 5 years, respectively). Survival after retransplantation for CAV has steadily improved with successive eras. Conclusions The results of retransplantation for acute rejection and early graft failure are poor enough to suggest that this option is not advisable. However, retransplantation for CAV is currently associated with satisfactory survival and should continue to be offered to selected patients.

Recently, portable C-arm systems have been developed for cardiac studies. While these systems have been used at a number of centers on a small scale for procedures in the operating room, emergency room, or intensive care unit, there are no published data on the performance of the system under more demanding circumstances. Theoretically, a reliable portable C-arm system could provide a low-cost alternative to a fixed system in centers with limited resources, such as in developing countries. To test whether a portable C-arm system could substitute for a permanent laboratory for cardiac catheterization and interventional procedures, we used a C-arm system as our sole catheterization laboratory for a period of 3 months. The system's performance was compared to a comparable time period using a fixed catheterization laboratory system. The portable system was used to perform 222 procedures (36 interventional and 186 diagnostic), as compared to 236 procedures (30 interventional and 206 diagnostic) with the fixed lab during a comparable time period the preceding year. Although the image quality of the portable system was not as good as with the fixed laboratory, all procedures were performed successfully, with no difference in fluoroscopic time, radiation exposure to the patient, procedure related complications, or clinical restenosis at 1 year. However, radiation exposure to staff was greater, possibly due to the lack of shielding in the temporary lab and the need for the technician to remain close to the unit to set up views. Our results suggest that a portable C-arm system, while subject to some limitations, can perform as a general catheterization laboratory for diagnostic and interventional procedures.

Background —Vessel dilator, a 37–amino acid peptide hormone synthesized in the heart, enhances urine flow 4- to 12-fold and sodium excretion 3- to 6-fold in healthy humans. The present investigation was designed to determine whether vessel dilator might have similar beneficial effects in persons with congestive heart failure (CHF). Methods and Results —Vessel dilator (100 ng/kg body weight per minute) given intravenously for 60 minutes to NYHA class III CHF subjects increased urine flow 2- to 13-fold, which was still increased ( P P P Conclusions —These results indicate that vessel dilator has significant beneficial diuretic, natriuretic, and hemodynamic properties in humans with congestive heart failure.

Objectives: The present investigation was designed to determine the best endogenous plasma marker of early congestive heart failure (CHF). Methods: Forty volunteers with mild CHF (New York Heart Association Class I, n = 12), moderate (Class II, n = 8), or severe (Class III and Class IV, each= n of 5) and 10 age-matched healthy individuals had the simultaneous evaluation of their respective plasma samples by the following radioimmunoassays: atrial natriuretic peptide, ANP; three N-terminal ANP prohormone assays, i.e., proANPs 1–30, 31–67, and 79–98 with the numbers referring to their amino acid (a.a.) sequences in their 126 a.a. prohormone; brain (BNP) and C-natriuretic peptides; N-terminal BNP prohormone; adrenomedullin; neuropeptide Y and endothelin. Results: ProANPs 31–67, 1–30 and 79–98 had 100% ( P = 0.01), 83% ( P = 0.09) and 50% ( P = 0.74) sensitivity in differentiating Class I CHF subjects from healthy subjects. The ANP, BNP, NT-proBNP, CNP, adrenomedullin, neuropeptide Y, and endothelin assays could not differentiate mild CHF subjects from healthy individuals. Logistic regression analysis revealed that only proANP 31–67 significantly ( P = 0.0001) discriminated between early CHF (5226±377 pg/ml) and healthy individuals (1595±157 pg/ml). The positive and negative predictive values of proANP 31–67 were excellent (100% for each). The peptides measured in these assays were found to be independent markers of CHF with respect to left ventricular ejection fraction. Conclusions: ProANPs 31–67 is the most sensitive marker in discriminating NYHA Class I CHF subjects from healthy individuals. The ANP, BNP, NT-proBNP, CNP, adrenomedullin, neuropeptide Y and endothelin radioimmunoassays cannot discern mild CHF. These peptides are independent of left ventricular ejection fraction.

Background Despite therapy with diuretics, ACE inhibitors and digoxin morbidity and mortality in heart failure remain high and might respond favorably to an additional vasodilator. Methods and Results Male patients (n=450) with chronic heart failure (cardiac dysfunction and impaired exercise performance) on optimal current therapy (97% enalapril, 89% diuretics) were randomly assigned to double-blind treatment with felodipine extended release (5 mg BID) or placebo for 3 to 39 months (average, 18 months). Felodipine significantly reduced blood pressure and, at 3 months, increased ejection fraction (2.1% versus −0.1% units in the placebo group, P =.001) and reduced plasma atrial natriuretic peptide levels (−2.9 versus 26.9 pg/mL in the placebo group, P =.01) but did not improve exercise tolerance, quality of life, or the need for hospitalization. During long-term follow-up, the favorable effects on ejection fraction and atrial peptide did not persist, but felodipine prevented worsening exercise tolerance and quality of life. In the felodipine and placebo groups, mortality (13.8% versus 12.8%, respectively) and hospitalization (43% versus 42%) rates were similar, and a higher incidence of peripheral edema was the only apparent side effect of felodipine therapy. Conclusions Felodipine exerts a well-tolerated additional sustained vasodilator effect in patients with heart failure treated with enalapril, but the only possible long-term benefit was a trend for better exercise tolerance and less depression of quality of life in the second year of treatment. The drug appears to be safe but not clearly efficacious in patients with heart failure.

Background and Methods. To define better the efficacy of vasodilator therapy in the treatment of chronic congestive heart failure, we compared the effects of hydralazine and isosorbide dinitrate with those of enalapril in 804 men receiving digoxin and diuretic therapy for heart failure. The patients were randomly assigned in a double-blind manner to receive 20 mg of enalapril daily or 300 mg of hydralazine plus 160 mg of isosorbide dinitrate daily. The latter regimen was identical to that used with a similar patient population in the effective-treatment arm of our previous Vasodilator—Heart Failure Trial. Results. Mortality after two years was significantly lower in the enalapril arm (18 percent) than in the hydralazine—isosorbide dinitrate arm (25 percent) (P = 0.016; reduction in mortality, 28.0 percent), and overall mortality tended to be lower (P = 0.08). The lower mortality in the enalapril arm was attributable to a reduction in the incidence of sudden death, and this beneficial effect was m...

Background Prior studies on chronic systolic heart failure (HF) have demonstrated that body mass index (BMI) is inversely associated with mortality, the so-called obesity paradox. The aim of this study was to determine whether BMI influences the mortality risk in acute decompensated HF, a subject not previously studied. Methods The Acute Decompensated Heart Failure National Registry was analyzed for acute HF hospitalizations in 263 hospitals in the United States from October 2001 through December 2004. Patients with documented height and weight were divided into BMI (measured in kilograms per square meter) quartiles. Inhospital mortality by BMI quartile for all the patients and for those with reduced (n = 43255) and preserved (n = 37901) systolic function was assessed. Results Body mass index quartiles in the 108927 hospitalizations were QI (16.0-23.6 kg/m 2 ), QII (23.7-27.7 kg/m 2 ), QIII (27.8-33.3 kg/m 2 ), and QIV (33.4-60.0 kg/m 2 ). Patients in the higher BMI quartiles were younger, had more diabetes, and had a higher left ventricular ejection fraction. Inhospital mortality rates decreased in a near-linear fashion across successively higher BMI quartiles. After adjustments for age, sex, blood urea nitrogen, blood pressure, creatinine, sodium, heart rate, and dyspnea at rest, BMI quartile still predicted mortality risk. For every 5-U increase in BMI, the odds of risk-adjusted mortality was 10% lower (95% CI 0.88-0.93, P Conclusions In this cohort of hospitalized patients with HF, higher BMI was associated with lower inhospital mortality risk. The relationship between BMI and adverse outcomes in HF appears to be complex and deserving of further study.

We describe a 64-year-old male with severe hemophilia A (factor VIII-dependent), acute myocardial infarction (MI) and congestive heart failure (CHF) who underwent successful multi-vessel percutaneous coronary intervention (PCI). The patient was administered factor VIII transfusion to maintain activity levels between 60-80%. Anticoagulation during the PCI procedure was maintained with the direct thrombin inhibitor, bivalirudin. There were no procedural complications and the patient was discharged home the following day. These results suggest that bivalirudin may be used effectively in patients at very high risk of bleeding with enhanced procedural safety.

E evidence and clinical trials have shown the beneficial effects of -adrenergic blockers (BBs) in patients with heart failure (HF). A large database supports the contention that BB therapy improves survival, reduces the rate of hospitalization, delays the progression of HF, and improves cardiac function. However, there is little information regarding how elderly patients with HF tolerate and respond to BBs. To test the hypothesis that BB therapy can be safely administered to, and improves cardiac function in elderly patients with HF, we analyzed, according to age, patients who were randomized to receive the BB bucindolol or placebo in the Beta-Blocker Evaluation of Survival Trial (BEST).

We report a case of elevated B-type natriuretic peptide (BNP) without volume overload in a left ventricular assist device patient with a subdural hematoma and cerebral salt wasting syndrome suggesting a noncardiac etiology for BNP elevation.

For nearly 30 years clinicians have assumed that diuretic therapy, per se, even in the absence of clinical hypokalemia, can cause false-positive exercise ST-segment responses. The precept has stubbornly persisted in the literature and in the day-to-day interpretation of exercise tests in clinical settings. The assumption probably originated with very early studies of patients on diuretics, in which other causes of false-positive tests were not excluded. This study was undertaken to show that diuretic therapy alone is not sufficient to cause ST depression. Twenty healthy male volunteers, aged 18 to 35, with normal history and physical examinations, echocardiograms, electrocardiograms, serum electrolytes, renal function tests and exercise tests, took 50 mg of hydrochlorothiazide daily for four weeks. Exercise tests, serum electrolytes, and renal function tests were repeated at Weeks 2 and 4. The administration of the diuretic resulted in a statistically significant reduction in serum potassium (from 4.37 +/- 0.37 to 3.96 +/- 0.28, and 3.94 +/- 0.31 mEq/l at 2 and 4 weeks, respectively). There were no abnormal ST-segment shifts on any of the exercise tests. It is concluded that exercise-induced ST-segment shifts in otherwise healthy young male normokalemic subjects who are taking diuretics should not be ascribed to a false-positive response to diuretics.

In cardiac transplantation, extremely potent immunosuppressive agents are used, which leave the host vulnerable to a variety of infections and malignancies. Among the malignancies, lymphoproliferative disorders are the most common. 1 Most cases of posttransplant lymphoproliferative disorders have been described in patients who have undergone several months of immunosuppression. 2,3 This report describes our experience with patients who developed lymphoproliferative disorder within 3 months of heart transplantation.

To evaluate the incidence, clinical characteristics and course of right ventricular infarction, 96 patients with an established diagnosis of acute myocardial infarction were evaluated during a 10 month study period. Of the 44 patients with acute inferior wall myocardial infarction, 16 had bedside evidence of right ventricular dysfunction. All had a positive Kussmaul's sign, and 12 had either a right ventricular third or fourth heart sound. Inspiratory elevation of right atrial and right ventricular end-diastolic pressures was documented in nine patients. Ventricular fibrillation developed in one patient and advanced atrioventricular block in three. All 16 patients survived and were alive 3 months after infarction. The hospital course and 3 month survival rate were not different from those of the usual patient with inferior wall infarction. Approximately one third of the patients with inferior wall myocardial infarction have bedside evidence of right ventricular infarction, which usually does not alter short-term prognosis.

Myocardial ischemia due to coronary atherosclerosis is the usual cause of exercise-induced S-T segment changes. A number of drugs, electrolyte alterations, and hemodynamic factors may accentuate or mask these changes. The clinician should keep this in mind during the electrocardiographic interpretation of exercise tests.

To compare the acute and sustained effect of intravenous isosorbide dinitrate to intravenous nitroglycerin in patients with acute myocardial infarction and elevated pulmonary artery wedge pressure, 111 patients were randomized and studied within 96 hours of admission to the coronary care unit. All patients had a pulmonary artery wedge pressure greater than or equal to 10 mm Hg and received either isosorbide dinitrate (74 patients) or nitroglycerin (37 patients) for 24 to 48 hours. Blood pressure, heart rate, pulmonary artery wedge pressure, cardiac output, medication dose in micrograms per minute and retitration episodes were compared at baseline and at 6, 12, 18 and 24 hours. Both drugs significantly (p less than 0.05) lowered pulmonary artery wedge pressure and blood pressure and increased cardiac output. Isosorbide dinitrate required fewer retitration episodes and less increases in dosage than nitroglycerin at 24 hours. In the patient with acute myocardial infarction complicated by high pulmonary artery wedge pressure who requires intravenous nitrates for 24 hours, isosorbide dinitrate may offer the benefit of a more stable hemodynamic effect.

A patient with rheumatoid disease initially had the physical findings of isolated tricuspid stenosis. Postmortem examination demonstrated adhesive pericarditis with localized hemopericardium which compressed the atrioventricular groove in the area of the tricuspid valve. Historical, physical, electrocardiographic, and cardiac catheterization features which suggested the diagnosis are discussed.

Thirteen patients underwent right cardiac catheterization during the first 24 hours after the onset of symptoms of acute myocardial infarction. All had normal (less than 12 mm Hg) pulmonary arterial diastolic pressure or normal mean pulmonary wedge pressure (7.6 +/- 0.6 mm Hg). The patients did isometric forearm contraction to a measured level of 100 mm Hg. All patients had elevation of systemic systolic blood pressure, with a mean rise of 14.2 +/- 2.9 mm Hg; heart rate rose by 12 +/- 2 beats per minute. When compared to a control group, patients with acute myocardial infarction had a significant (P less than 0.005) elevation of 5.4 +/- 1.3 mm Hg in the pulmonary arterial diastolic or pulmonary wedge pressure. This may be a result of either increased left ventricular stiffness or decreased myocardial functional reserve. In the setting of acute myocardial infarction, patients with normal left ventricular filling pressures have abnormal ventricular performance. Isometric effort is poorly tolerated and should be avoided.

Eight hundred twelve men with presumed acute myocardial infarction and left ventricular filling pressure of at least 12 mm Hg participated in a randomized double-blind placebo-controlled trial to assess the efficacy of a 48-hour infusion of sodium nitroprusside. The mortality rates at 21 days (10.4 per cent in the placebo group and 11.5 per cent in the nitroprusside group) and at 13 weeks (19.0 per cent and 17.0 per cent, respectively) were not significantly affected by treatment. The efficacy of nitroprusside was related to the time of treatment: the drug had a deleterious effect in patients whose infusions were started within nine hours of the onset of pain (mortality at 13 weeks, 24.2 per cent vs. 12.7 per cent; P = 0.025) and a beneficial effect in those whose infusions were begun later (mortality at 13 weeks, 14.4 per cent vs. 22.3 per cent; P = 0.04). Nitroprusside should probably not be used routinely in patients with high left ventricular filling pressures after acute myocardial infarction. However, the results in the patients given late treatment suggest that those with persistent pump failure might receive sustained benefit from short-term nitroprusside therapy.

To determine the cardiovascular effects and safety of dental anesthesia and dental interventions in patients within three weeks of uncomplicated acute myocardial infarction, 40 patients were studied. Twenty patients, group 1, underwent injectable local dental anesthesia with 2% lidocaine and 1:100 000 epinephrine. Group 2, 20 patients, underwent vigorous dental prophylaxis (13 patients) or dental extraction (seven patients) after local anesthesia. Heart rate, blood pressure, electrocardiograms, and symptoms were monitored before, during, and after the dental intervention. There were no significant hemodynamic changes or complications related to dental anesthesia or the dental procedures. One patient experienced an asymptomatic, uncomplicated, self-limited, eight-beat run of ventricular tachycardia two hours after dental extraction. Limited dental anesthesia and dental interventions were well tolerated by these patients with recent myocardial infarction.