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FK 506 (FK) has a strong immunosuppressive effect, but a low-grade, dose-dependent nephrotoxicity and diabetogenicity, which means that reducing the dose of FK is of considerable interest. Lipo-prostaglandin E1 (LPGE1) is a preparation of PGE1 that has potent immunosuppressive properties, and its duration of action is longer than that of ordinary PGE1. The purpose of this study was to investigate whether LPGE1 can enhance the immunosuppressive effect of FK. Heterotopic cardiac transplantations to the neck vessels were performed, and recipient rats were treated with intramuscular injections of FK and LPGE1 once daily for 10 days. All grafts without any treatment were rejected within 14 days. In comparison, the FK doses of 0.07, 0.2 and 1.0 mg/kg/day for 10 days significantly increased the long-term graft survival (>100 days) to 8%, 44% and 100%, respectively. The addition of LPGE1 to the first two dosages caused a further significant increase in the graft survival, to 18% and 80%, respectively, when compared with the control. LPGE1 appears to enhance the immunosuppressive effect of FK.

The predominant causes of late graft loss and death after cardiac transplantation are graft rejection and infection. The histopathological classification of acute rejection is based on cellular phenomena such as lymphocytic infiltration and myocyte damage. The adverse prognostic importance of vascular or humoral rejection has been reported, but there is no well-documented treatment available. In our experience, comprising 151 orthotopic transplants, five patients presented with graft rejection characterized by a lymphocytic vasculitis that did not respond to conventional therapy. Because of a deteriorating condition, in spite of vigorous antirejection treatment that included inotropic drugs and circulatory support. plasmapheresis was tried as a last, desperate means to stop the process from developing further. The clinical symptoms rapidly subsided in all five patients after the first couple of plasma exchanges. All of the patients are alive and well after 2-3.5 years of follow-up. Although the mechanism of action is unclear, plasmapheresis was beneficial in these critically ill patients.

The purpose of this study was to evaluate the cardiac damage by cardiac myosin light chain I after transplantation. This study included 30 patients who underwent cardiac operations and who were divided into three groups. These groups consisted of (1) control group, 15 valvular patients without coronary disease (no electrocardiography changes and creatine kinase MB isoenzyme of 100 micrograms/L or less); (2) infarction group, eight patients (six coronary bypass and two valvular patients with perioperative infarction pattern in the electrocardiography and creatine kinase MB isoenzyme of 100 micrograms/L or more; and (3) transplantation group, seven transplant patients (six heart and one heart-lung). The peak cardiac myosin light chain I value in the transplantation group (32.9 +/- 3.4 micrograms/L) was comparable to the infarction group (27.6 +/- 2.6 micrograms/L), and both of them were significantly higher than the control group (9.2 +/- 0.9 micrograms/L) (p < 0.01). Peak cardiac myosin light chain I levels in the control and transplantation groups correlated with the ischemic time (r = 0.48, p < 0.05 and r = 0.67, p < 0.05, respectively). The total dose of dopamine in the transplantation group correlated with the peak cardiac myosin light chain I (r = 0.67, p < 0.05), and with the cardiac myosin light chain I value on day 7 (r = 0.88, p < 0.01). This study suggests that circulating cardiac myosin light chain I estimations are useful to evaluate myocardial damage after transplantation during postoperative week 1.

Sudden mediastinal haemorrhage one month after heart transplantation in an 18-year-old youth was found to originate from a rupture of the ascending aorta associated with mycotic aortitis. Aortic continuity was restored with a Dacron graft. Cultures from the resected vessel wall showed Candida albicans. The patient recovered, and 11 months later is well.

The incidence of chordal tissue in endomyocardial biopsies from heart transplant recipients and the possibility of an association between this incidence and tricuspid regurgitation or tricuspid valvular abnormalities were prospectively investigated. The biopsies were performed to detect rejection. Postoperative echocardiography and Doppler were done according to routine schedule and always when chordal tissue was found histologically, for specific evaluation of the tricuspid valve function. Chordal tissue was detected in 24 of 1,265 bites at 206 biopsies during the study period. Echocardiographically there was no significant increase in tricuspid regurgitation and no major valvular abnormality in any patient after biopsy showing chordal tissue. The presence of chordal tissue in biopsy specimens implies that the tricuspid valve is potentially at risk in biopsy. Our results, however, also showed that occasional capture of chordal tissue by the bioptome did not necessarily result in tricuspid valve dysfunction.

Heart transplantation is well established therapy for end-stage heart failure, where no other treatment is available. From 1983 to the end of 1993, 620 heart transplantations were performed in the Nordic countries, the main causes of heart failure being dilated cardiomyopathy and ischaemic heart disease. The 1-year and 5-year actuarial survival rates were above 80 per cent and 70 per cent, respectively, which are higher than corresponding figures reported by the International Society of Heart and Lung Transplantation. The indications and contra-indications for heart transplantation, pre-operative evaluation and outcome are discussed in the article.

The morbidity of cytomegalovirus (CMV) infection and toxoplasmosis was evaluated in 75 heart transplant recipients. Among the 73 patients who survived more than one week after transplantation, 16 (22%) acquired primary CMV infection and 30 (41%) had evidence of secondary infection. All CMV seronegative recipients receiving hearts from seropositive donors developed CMV infection. The majority of infections (42/46) occurred during the first 4 months after transplantation. Overall, the incidence of symptomatic CMV disease was 44%. The infections were generally mild and only 1 death was attributed to primary CMV disease complicated by bacterial septicaemia and multiple organ failure. The severity of CMV disease was greatest among those with primary infection. There were 3 cases of toxoplasmosis. Two patients were toxoplasma seronegative before transplantation and developed clinical and serological signs of infection 2-3 months after transplantation despite receiving organs from seronegative donors. Of toxoplasma seronegative recipients receiving allografts from seropositive donors 3/4 were prophylactically treated with pyrimethamine for 6 weeks. None developed clinical or serological signs of toxoplasmosis while one patient who received trimethoprim-sulfamethoxazole had a subclinical infection.

The purpose of this study was to investigate the occurrence of major tricuspid insufficiency caused by endomyocardial biopsy in heart transplant recipients. Endomyocardial biopsy was used for the detection of rejection and Doppler echocardiography was performed at regular intervals. Six of 96 heart transplant patients (6.3%) had sudden appearance of large tricuspid regurgitation, all of which were directly related to a preceding biopsy. Chordal tissue was identified histologically in biopsy samples of all six patients. All patients developed symptoms of right ventricular failure which was confirmed by right heart catheterization. Three patients subsequently underwent valvuloplasty for ruptured chordae tendineae of either of the three leaflets. Two of these three patients were free from symptoms during follow-up, but the third patient developed moderate tricuspid regurgitation and clinical symptoms. It is concluded that endomyocardial biopsy, although it is the most useful tool for detection of rejection, should be used with caution with regard to anatomical structures and the risk of damage to the tricuspid valve must not be neglected. It is also concluded that valvuloplasty of the tricuspid valve can be successfully performed in a transplanted heart.