Ventricular assist devices: pharmacological aspects of a mechanical therapy.

Heart failure (HF) is a global epidemic that continues to cause significant morbidity and mortality despite advances in medical therapy. Ventricular assist device technology has emerged as a therapeutic option to bridge patients with end-stage HF to heart transplantation or as an alternative to transplantation in selected patients. In some patients, mechanical unloading induced by ventricular assist devices leads to improvement of myocardial function and a possibility of device removal. The implementation of this advanced technology requires multiple pharmacological interventions, both in the perioperative and long-term periods, in order to minimize potential complications and improve patient outcomes. We herein review the latest available evidence supporting the use of specific pharmacological interventions and current practices in the care of these patients: anticoagulation, bleeding management, pump thrombosis, infections, arrhythmias, right ventricular failure, hypertension, desensitization protocols, among others. Areas of uncertainty and ground for future research are also highlighted.

Impact of donor left ventricular hypertrophy on survival after heart transplant.

Left ventricular hypertrophy (LVH) of the donor heart is believed to increase the risk of allograft failure after transplant. However this effect is not well quantified, with variable findings from single-center studies. The United Network for Organ Sharing database was used to analyze the effect of donor LVH on recipient survival. Three cohorts, selected in accordance with the American Society of Echocardiography guidelines, were examined: recipients of allografts without LVH (<1.1 cm), with mild LVH (1.1-1.3 cm) and with moderate-severe LVH (≥ 1.4 cm). The study group included 2626 patients with follow-up of up to 3.3 years. Mild LVH was present in 38% and moderate-severe LVH in 5.6% of allografts. Predictors of mortality included a number of donor and recipient characteristics, but not LVH. However, a subgroup analysis showed an increased risk of death in recipients of allografts with LVH and donor age >55 years, and in recipients of allografts with LVH and ischemic time ≥ 4 h. In the contemporary era, close to half of all transplanted allografts demonstrate LVH, and survival of these recipients is similar to those without LVH. However, the use of allografts with LVH in association with other high-risk characteristics may result in increased mortality.

Effect of blood product transfusion-induced tolerance on incidence of cardiac allograft rejection.

BACKGROUND: Blood product transfusion has been successfully used in solid-organ transplantation to induce tolerance. Whether a similar protective effect of blood product transfusion exists in heart transplantation is controversial. OBJECTIVE: To investigate the effect of cellular blood product transfusion within 2 weeks posttransplantation on the incidence of cellular and antibody-mediated rejection. PATIENTS AND METHODS: Patients were grouped on the basis of number of blood transfusions; group 1 received no transfusions, and groups 2, 3, and 4 each received an incremental number of transfusion units. All endomyocardial biopsy samples were routinely studied using immunofluorescence in the first 12 weeks posttransplantation. RESULTS: Baseline characteristics including age, sex, body mass index, history of diabetes, donor characteristics, and pretransplantation laboratory values were similar except that group 4 had a higher rate of previous sternotomy and longer ischemic time during transplantation. Approximately 9200 endomyocardial biopsy samples composed the data. Short- and long-term freedom from the International Society for Heart & Lung Transplantation grade 3A or higher cellular rejection and from antibody-mediated rejection were comparable between groups. CONCLUSIONS: Blood transfusions within the first 2 weeks post-transplantation do not seem to confer any protective effect against posttransplantation cellular rejection or antibody- mediated rejection. Whether other unmeasured confounding factors mask their effect requires further prospective studies.

Impact of donor cause of death on transplant outcomes: UNOS registry analysis.

Donor cause of death (DCOD) has been described to influence allograft survival. Whether this effect is independent of other donor characteristics and whether it is similar across different solid organ allografts is not known. The aim of our study was to determine the impact of DCOD on organ utilization and on transplantation outcomes-graft rejection, function, and survival. The registry data were provided by the United Network for Organ Sharing/Organ Procurement and Transplantation Network. Stroke, head trauma, and anoxia were the cause of brain death in 97% of the more than 86,000 donors whose data were recorded between 1989 and 2008. In univariate analysis, stroke DCOD was associated with worse graft survival across all organs. After adjustment in a multivariable analysis, modest differences persisted in survival of heart, kidney, and liver allografts. DCOD also appeared to affect the incidence of allograft rejection. Anoxia DCOD was associated with significantly less rejection relative to donor death caused by head trauma and stroke. In summary, this multi-institutional study confirms that DCOD is a modest predictor of survival and rejection of solid organ allografts of different types.