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Background: Although triiodothyronine deficiency has been described after cardiopulmonary bypass, data supporting its use have been conflicting. A double-blind, randomized, placebo-controlled study was undertaken to further define the effect of triiodothyronine on hemodynamics and outcome after coronary artery bypass grafting. Methods: A total of 170 patients undergoing elective coronary artery bypass grafting were enrolled and completed the study from November 1996 through March 1998. On removal of the aortic crossclamp, patients were randomized to receive either intravenous triiodothyronine (0.4 @mg/kg bolus plus 0.1 @mg/kg infusion administered over a 6-hour period, n = 81) or placebo (n = 89). Outcome variables included hemodynamic profile and inotropic drug/pressor requirements at several time points (mean +/- standard error of the mean), perioperative morbidity (arrhythmia/ischemia/infarction), and mortality. Results: Despite similar baseline characteristics, patients randomized to triiodothyronine had a higher cardiac index and lower inotropic requirements after the operation. Subjects receiving triiodothyronine demonstrated a significantly lower incidence of postoperative myocardial ischemia (4% vs 18%, P = .007) and pacemaker dependence (14% vs 25%, P = .013). Seven patients in the placebo group required postoperative mechanical assistance (intra-aortic balloon pump, n = 4; left ventricular assist device, n = 3), compared with none in the triiodothyronine group (P = .01). There were 2 deaths in the placebo group and no deaths in the triiodothyronine group. Conclusions: Parenteral triiodothyronine given after crossclamp removal during elective coronary artery bypass grafting significantly improved postoperative ventricular function, reduced the need for treatment with inotropic agents and mechanical devices, and decreased the incidence of myocardial ischemia. The incidence of atrial fibrillation was slightly decreased, and the need for postoperative pacemaker support was reduced. (J Thorac Cardiovasc Surg 1999;117:1128-35)

Background: Inhaled nitric oxide has been shown to be a potent and selective pulmonary vasodilator. Reports of increases in left ventricular end-diastolic pressure and episodes of pulmonary edema during the clinical use of inhaled nitric oxide in patients with preexisting left ventricular dysfunction have raised concerns that this agent may have myocardial depressant effects. We therefore undertook a study of the effects of inhaled nitric oxide on myocardial contractility in a porcine model of ventricular failure and pulmonary hypertension. Methods: After inducing heart failure in 10 pigs by rapid ventricular pacing, hemodynamic measurements and pressure-volume diagrams (by the conductance method) were obtained in six animals at baseline and during administration of inhaled nitric oxide at concentrations of 20 and 40 ppm. Myocardial contractile state was assessed by the end-systolic pressure-volume relationship and preload-recruitable stroke work, whereas diastolic function was measured in terms of the end-diastolic pressure-volume relationship and the pressure decay time constant T. Results: Baseline hemodynamics reflected heart failure and pulmonary hypertension, and inhaled nitric oxide induced significant reductions in mean pulmonary artery pressure and pulmonary vascular resistance. Although left ventricular end-diastolic pressure increased during administration of inhaled nitric oxide, no changes were observed in measures of systolic or diastolic function. Conclusions: Inhaled nitric oxide reduced pulmonary vascular resistance but did not alter myocardial contractility or diastolic function. Increases in left ventricular end-diastolic pressure during inhaled nitric oxide therapy are therefore not due to myocardial depression and may be related to increases in volume delivery to the left side of the heart resulting from reduced pulmonary vascular resistance. (J Thorac Cardiovasc Surg 1998;115:700-8)

A great number of patients suffer and die of the sequelae of acute and chronic heart failure each year. Although advances in medical and surgical therapy have benefited many of these patients, most have disease that is refractory to any definitive therapy. For these patients cardiac transplantation is the only remaining hope. Unfortunately, because of the increasing demand for donor organs in the face of a fixed and limited supply, this option is available to only a small percentage of these patients. Even in patients accepted for transplantation, a significant waiting list mortality has been observed. A variety of VADs have been developed since the first successful case of mechanical cardiac assistance more than 30 years ago. These devices differ in basic mechanical function, method of insertion, and degree of implantability and thus have different indications and potential applications. Whereas the intraaortic balloon pump and centrifugal pumps are effective short-term support modalities, extracorporeal and implantable pulsatile devices have been used successfully for long-term support of patients with reversible and nonreversible cardiac failure. Although these pumps have most commonly been used as bridges to transplantation, increasing clinical experience has supported the notion of long-term mechanical assistance as a definitive therapy for patients with end-stage heart disease. Although complications, particularly infection and thromboembolism, pose significant challenges and long-term device reliability remains to be fully determined, available implantable devices appear to be capable of providing effective long-term support. As data are obtained from currently ongoing trials comparing VAD support with medical therapy for end-stage heart failure, ethical and economic issues will assume increasing importance.