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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 = 43,255) and preserved (n = 37,901) systolic function was assessed., Results: Body mass index quartiles in the 108,927 hospitalizations were QI (16.0-23.6 kg/m2), QII (23.7-27.7 kg/m2), QIII (27.8-33.3 kg/m2), and QIV (33.4-60.0 kg/m2). 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 < .0001)., 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.

Objective: We sought to examine the prevalence of heart failure in elderly PD versus non-PD patients using a national sample of Medicare beneficiaries in the United States., Scope: The prevalence of heart failure in elderly PD patients was 2.27 times that of non-PD patients (19.4% versus 8.7%, 95% CI = 1.43-3.60, p 0.0005), and remained twice as high after excluding patients with stroke and possible vascular parkinsonism., Conclusions: In this cross-sectional study of a national Medicare database, heart failure occurred twice as frequently in elderly PD patients as in non-PD patients. Prospective studies are warranted to verify these findings.

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.

Background: Previous studies of allograft rejection have focused on early episodes and risk factors from pretransplant variables., Methods: This multiinstitutional study compared early (< 1 year) and late (> 1 year) rejection episodes and risk factors for recurrent rejection from variables both before and after transplantation among 1251 patients who underwent primary heart transplantation and available follow-up of greater than 1 year., Results: There were a total of 1882 rejection episodes over a mean follow-up of 26 +/- 0.3 months. The hazard function (instantaneous risk per patient per month) peaked at 1 month followed by a low constant risk of rejection after 12 months. By multivariable analysis, the most dominant risk factors for recurrent rejection during the first posttransplantation year were a shorter time interval since transplantation and a shorter time since a previous rejection episode. Other factors included young age, female gender, female donor, positive cytomegalovirus serology, prior infections, and OKT3 induction. In contrast, after the first year, the dominant risk factors for rejection were a greater number of rejections during the first year and the presence of prior cytomegalovirus infections., Conclusions: These data show a striking time dependency for rejection episodes among heart transplant recipients. Factors that increase risk for rejection in the first year differ from risk factors for rejection in subsequent years. These data suggest that it may be possible to tailor rejection surveillance protocols and immunosuppression intensity, according to specific patient and time-related risk factors.

To assess whether heart transplantation (Htx) alters the marked elevation of circulating atrial natriuretic peptides usually found in patients with congestive heart failure (CHF), 14 subjects (nine with compensated and five with decompensated CHF), each with an ejection fraction < or = 28%, were evaluated. Immediately before and hourly for the first 12 hours after Htx, then daily for 21 days and every 1 to 4 weeks for 6 months, the circulating concentrations of the N-terminus (pro atrial natriuretic factor [ANF] 1-98), midportion of the N-terminus (pro ANF 31-67), and C-terminus (that is, ANF) of the 126 amino acid prohormone were measured. Increased (p < 0.001) levels of these peptides were found in superior vena cava, right atrial, and peripheral venous samples 1 hour after Htx in all subjects except one. The atrial natriuretic peptide levels correlated only with right atrial pressure (p < 0.01) in the first 24 hours. Circulating concentrations of these peptides returned to those of healthy adults between 5 and 12 days after Htx in 11 out of 14 Htx recipients. Thus successful Htx can restore the elevated circulating concentrations of atrial natriuretic peptides to those of healthy adults.

Background: Patients with heart failure have a high prevalence of serious arrhythmias and sudden cardiac-death., Methods and Results: Male patients aged 18-75 years with chronic heart failure were randomized to enalapril or hydralazine-isosorbide dinitrate. Short-term (4-hour to 8-hour) Holter tape recordings were performed before randomization, at 3 months, at 1 year, and yearly thereafter. Of 804 patients randomized to therapy, 715 had Holters at baseline. Couplets were noted in 56% versus 60% and ventricular tachycardia (VT) (three or more consecutive ventricular premature beats) in 27% versus 29% of patients randomized to enalapril versus hydralazine-isosorbide dinitrate, respectively. The presence of VT at 3 months, 1 year, and 2 years predicted significantly higher mortality during the subsequent year (p < 0.0001, p < 0.001, and p < 0.037, respectively). In the enalapril group, VT prevalence decreased by 27% at 1 year (p < 0.02). A decrease in prevalence of VT was not seen in the hydralazine-isosorbide dinitrate group. New VT was seen in 11% of enalapril patients versus 24% of hydralazine-isosorbide dinitrate patients at 1 year (p < 0.002). When compared with hydralazine-isosorbide dinitrate at 1 and 2 years, there was a 52% and 49% reduction, respectively, in sudden deaths in the enalapril group. Thus, at 1 and 2 years, the decrease in sudden deaths in the enalapril group coincided with the decrease in VT prevalence and the decrease in new VT emergence., Conclusions: In patients with heart failure, VT and couplets predict increased mortality. When compared with hydralazine-isosorbide dinitrate, enalapril decreases both the persistence of baseline VT at 3 months and the emergence of new VT at 1 and 2 years. The reduction in VT prevalence parallels a reduction in sudden death. The effect of enalapril on survival over hydralazine-isosorbide dinitrate may be related to its ability to reduce prevalence of ventricular arrhythmia.

To better understand the phenomenon of acute rejection in the current era of heart transplantation, complete rejection data (918 rejection episodes) from 25 institutions were analyzed for all 911 patients undergoing primary heart transplantation between January 1, 1990, and July 1, 1991. During a mean follow-up of 8.1 months (maximum, 18 months), 54% of the patients had one or more rejection episodes. The mean cumulative number of rejection episodes per patient was 0.8 at 3 months, 1.10 at 6 months, and 1.3 at 12 months after transplantation. By univariate analysis, female donor hearts (irrespective of recipient sex) (p < 0.01) and the use of induction therapy (p < 0.01) were associated with greater cumulative rejection frequency. By multivariate analysis, younger donor age and female donor gender were risk factors for earlier rejection. Solution of the multivariate equation predicted an 85% probability of rejection at 1 month for a 5-year-old female with a female donor and 50% for a 50-year-old man with a male donor. Inferences: (1) In the current era, over 40% of patients appear to be free of rejection during the first year after transplantation. (2) Younger recipient age and female donors are associated with earlier onset of allograft rejection, but the precise immunologic basis for these observations remains unknown. (3) In this experience, induction therapy did not delay the onset of first rejection nor did it reduce the cumulative number of rejection episodes. Further studies are indicated to examine the need for induction therapy.

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.

Bleeding is the most serious complication of thrombolytic therapy and limits its usefulness. We have reported a case of epidural hematoma, a rare occurrence after combined therapy with tissue plasminogen activator (TPA) and heparin. We emphasize that in patients treated with thrombolytic agents, any trauma may increase the risk of bleeding. The sudden onset of back pain and neurologic deficits should alert the clinician to the possibility of spinal hematoma with cord compression.

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.

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.

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.