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Intra-aortic balloon (IAB) counterpulsation has been utilized as an effective "bridge" to transplantation in patients with end-stage heart failure. To determine if patients with heart failure with nonischemic cardiomyopathy (NICM) derive the same benefit from IAB support as those with ischemic cardiomyopathy (ISCM), we evaluated 27 patients with NICM and 16 patients with ISCM who required IAB support while awaiting transplantation. Hemodynamic changes, effects on organ function (renal and hepatic), frequency of complications, and clinical outcomes were analyzed. Baseline demographics and hemodynamics were comparable in both groups (p = NS). Hemodynamics improved in both groups, immediately (15 to 30 min) following IAB insertion, with greater improvement (p0.05) in cardiac index and a trend toward greater reduction in filling pressures in the NICM group. Systemic vascular resistance fell to a similar degree in both groups. During continued IAB support (0.13 to 38 days in NICM, 1 to 54 days in ISCM), all hemodynamic changes persisted in both groups, with larger decrease (p0.05) in systemic vascular resistance and greater increase (p0.05) in cardiac index in the patients with NICM. The reduction in filling pressures, however, tended to be greater in patients with ISCM. Renal and hepatic function parameters improved to a similar extent in both groups. The frequency of complications and clinical outcome during IAB support were also similar in the two groups. These data confirm that IAB counterpulsation is a safe and effective "bridge" in patients with both NICM and ISCM with end-stage heart failure. The mechanism of sustained benefit in the two groups, however, may be different; afterload reduction appears to be more important in patients with NICM whereas reduction in filling pressures (increased coronary perfusion pressure) may be the main mechanism in patients with ISCM.

Patients with chronic heart failure frequently have pulmonary hypertension. Because severe preoperative pulmonary hypertension predicts a poor outcome after orthotopic transplantation, pulmonary vasoreactivity is evaluated frequently in the pretransplantation screening of heart failure patients. We prospectively evaluated the utility of the direct pulmonary vasodilator, prostaglandin E1, and compared it to the nonspecific vasodilators, nitroglycerin and sodium nitroprusside, in the evaluation of pulmonary hypertension in 39 heart transplantation candidates. Prostaglandin E1 significantly lowered pulmonary artery pressure, transpulmonary pressure gradient, and pulmonary vascular resistance. An adequate pulmonary vasodilator response (defined as a decline in transpulmonary pressure gradient to less than 15 mm Hg) occurred in 31 patients (79%). In a subgroup of nine patients also tested with nitroglycerin, greater reductions (p less than 0.01) in both transpulmonary pressure gradient and pulmonary vascular resistance occurred with prostaglandin E1, compared to nitroglycerin. Five of six patients who did not respond to nitroglycerin responded to prostaglandin E1. In another subgroup of 12 patients who were also evaluated with sodium nitroprusside, prostaglandin E1 produced a larger decline (p less than 0.05) in transpulmonary pressure gradient and pulmonary vascular resistance than did sodium nitroprusside. Six of eight patients who did not respond to sodium nitroprusside responded to prostaglandin E1. Based on pulmonary vasodilator response to prostaglandin E1, 27 patients were accepted on the transplantation waiting list, and eight patients underwent orthotopic transplantation. Postoperatively, acute right ventricular failure of the donor heart developed in none of these patients. Significant hemodynamic improvement occurred by 24 hours and persisted through 4 weeks of postoperative follow-up in all patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac events from graft arteriopathy, including myocardial infarction, heart failure resulting from previous myocardial infarction, and sudden death, may limit long-term survival after heart transplantation. To determine the incidence of cardiac events and the use of coronary arteriography in predicting these events, the long-term results (mean follow-up, 3.5 years; standard deviation +/- 2.0) of heart transplantation in 427 patients were reviewed. Cardiac events included 19 cases of myocardial infarction, 13 cases of sudden death, and 10 cases of congestive heart failure. All these events occurred after the first year except for three cases of sudden death and one case of myocardial infarction. Cumulative incidence of cardiac events per patient year was 0.9% within the first year, increasing to 1.9% by 5 years. Cardiac events accounted for 3.8% of the deaths by the end of the first year, rising to 18% of total mortality by 7 years after heart transplantation. In patients dying after the first year of transplantation, deaths from sequelae of coronary artery disease occurred in 36% (20/55). The relative risk ("odds ratio") of any cardiac event was 3.44 (p less than 0.05) in patients with angiographic evidence of obstructive disease compared with those without evidence of disease, risk of cardiac death 4.6 (p less than 0.05) and risk of sudden death, 2.4 (not significant). Of the 13 patients who died suddenly, five seen at autopsy were found to have had a recent myocardial infarction. Of all patients who died of heart disease, recent myocardial infarction was detected in nine who were seen at autopsy.(ABSTRACT TRUNCATED AT 250 WORDS)

Amyloid heart disease has been considered a contraindication for cardiac transplant based on the hypothesis that it is a systemic disease and that amyloid deposition would occur in the cardiac allograft. A survey was sent to all of the US centers and a limited number of Canadian and European centers listed with the International Registry. Twenty-four centers responded, and data were ultimately provided for a total of 10 patients (3 men, 7 women, mean age 48 years, range 30-60 years) who were transplanted for cardiac amyloid. The diagnosis of cardiac amyloidosis was made histologically on endomyocardial biopsy and/or examination of the explanted heart. Additional documented organ involvement included liver (two of 10), rectal (three of 10), renal (two of 10), gingiva (two of 10), and tongue (one of 10), although invasive biopsies were not performed in a majority of patients. A specific amyloid protein was identified in eight patients (seven lambda, one kappa immunoglobulin light chain). Although four of the surviving nine patients (one perioperative death) developed recurrent amyloid deposition in the allograft, it was detected solely by electron microscopy in two of these and had no clinical significance. There was, however, a progressive risk of major organ involvement with organ function impairment in this group (22% at 12 months, 50% at 24 months, 66% at 48 months). Although the immediate and early postoperative outcomes were not dissimilar between this group and patients undergoing transplantation for other cardiac diseases, late survival was reduced (39% at 48 months) compared with the larger population, but differences were not statistically significant due to the small amyloid sample size (p = 0.16).(ABSTRACT TRUNCATED AT 250 WORDS)

When examining survival rates following cardiac transplantation, it is important to examine the risk factors for both early (30-day) and late (greater than 30-day) survival as they may well be different. Factors affecting early survival appear related more to the preoperative condition of the patient (including degree of pulmonary hypertension) as well as advances that have been made in postoperative care. It is not immediately obvious why gender has such a profound effect on early survival and why primary graft failure rates appear higher in this group. Donor organ factors did not appear to relate to this difference. On the other hand, late survival appears to be influenced mainly by immunologic factors such as panel reactive antibody level and immunosuppressive protocol. A less dramatic effect of transpulmonary gradient appears to have a lasting effect on recipients even when they survive the initial 30-day period. Thus, pulmonary hypertension may have prolonged effects on the cardiac allograft which as yet we do not understand completely. The majority of late mortality is still due to graft atherosclerosis, infection, and acute cellular rejection, the latter 2 occurring most frequently within the first year after transplantation whereas death from graft atherosclerosis becomes most prominent beyond 5 years. Despite persistent improvements in 30-day survival, late survival following cardiac transplantation will only improve with the advent of better tissue matching and improved immunosuppression. The results with FK506, for example, are promising.

Amyloid heart disease has been considered a contraindication for heart transplant on the basis of the hypothesis that it is a systemic disease and that amyloid deposition would occur in the cardiac allograft. Despite these concerns, several centers have performed heart transplantation for amyloidosis in a limited number of cases. A survey was sent to all of the U.S. centers and a limited number of European centers listed with the Registry of the International Society for Heart Transplantation. Nineteen centers responded, and data were provided for a total of seven patients (three men and four women, with a mean age of 46 years, range, 30 to 60 years) who had transplants for cardiac amyloid. The diagnosis of cardiac amyloidosis was made histologically on endomyocardial biopsy and/or examination of the explanted heart. Additional organ involvement included liver (two cases), rectal (two cases), renal (one case), gingiva (one case), and tongue (one case). A specific amyloid protein was identified in five patients (four lambda, one kappa Ig light chain). Two patients developed recurrent amyloid in their allograft seen by electron microscopy at 3 1/2 and 4 months, respectively. One patient developed progressive diastolic dysfunction, but systolic function was preserved. This patient died 13 months after transplantation as a result of progressive liver infiltration with amyloid. One patient died immediately after operation. Five patients are alive and fully rehabilitated 32 +/- 12 months after transplant. On the basis of this small series, some patients with cardiac amyloidosis can undergo heart transplantation with good intermediate-term results.

This study was undertaken to investigate the impact of diabetes, which develops after heart transplantation, on infection and patient survival. Nondiabetic patients (366) underwent heart transplantation at our institution between June 1, 1980 and January 12, 1988. Of these patients, 29 (8%) developed posttransplantation diabetes (PTD), defined as a continued need for hypoglycemic agents. The PTD group did not differ significantly from the nondiabetic recipients in age, sex, or human leukocyte antigen type. The average age in the PTD group was 49 years. Average length of follow-up was 21 months (range 4 to 46 months). Eighteen patients are maintained on insulin. Eight patients are on oral hypoglycemic agents. Three patients died while on insulin. The average prednisone dosage in this group is 0.23 mg/kg/day. There have been 18 minor infections and four potentially serious nonlethal infections in the 27 PTD recipients. One lethal infection occurred 33 months after heart transplantation. The only other fatality was related to metastatic bladder cancer. This lethal infection rate of 3% compares with a rate of 11% in all nondiabetic recipients who have follow-up for 21 months. The 3-year actuarial survival of the PTD group is 75%, which compares favorably with the survival of nondiabetic patients. PTD cannot be predicted by sex, age, or human leukocyte type before transplantation, and it does not significantly increase the incidence of mortality or serious infection.