[Tumor necrosis factor-alpha: a mediator in the pathogenesis of cardiac insufficiency]. / Factor de necrosis tumoral-alpha: un mediador en la patogénesis de la insuficiencia cardiaca.

An increasing body of experimental and clinical work suggesting that tumor necrosis factor alpha plays a pathogenic role in heart failure continues to accumulate. This cytokine is produced in failing but not in normal hearts and experimentally, it's expression is induced by hemodynamic conditions of pressure or volume overload. Specific receptors for this cytokine are present in the heart and dynamic regulation in tumor necrosis factor receptor expression occurs in failing myocardium. In addition, tumor necrosis factor alpha may exert major cardiac effects that contribute to the development of the failing phenotype: induces negative contractil dysfunction, promotes fibrosis, induces cardiomyopathy in experimental animals and it is a major mediator of apoptosis in vivo and in vitro. The knowledge gained from studying the role of tumor necrosis factor alpha in cardiac function draws attention to a series of molecules previously unrecognized as potential mediators in the pathogenesis of heart failure.

[Heterotopic heart transplantation: 13-year experience at the Methodist Hospital of the Baylor Medical College]. / Trasplante cardiaco heterotópico: experiencia de trece años en el Hospital Metodista del Colegio de Medicina de Baylor.

UNLABELLED: In order to evaluate our experience in heterotopic cardiac transplantation, we conducted a retrospective analysis of the clinical files of patients who underwent this procedure. RESULTS: A total of 405 heart transplants were performed in our institution. In 24 (5.9%), the grafts were placed heterotopically. In group I (12 patients), the indication was irreversible pulmonary hypertension and in group II (remaining 12 patients), it was marginal grafts or size mismatch. Both groups demonstrated similar demographics and the survival rate was slightly better in group I. Nine patients from group I demonstrated an early reduction in pulmonary pressures which normalized in one year. CONCLUSIONS: The heterotopic heart supports the function of the native ventricles. In 9 patients, the heterotopic heart enables the reversal of a state of pulmonary hypertension previously thought to be irreversible. This finding supports the use of pulmonary vaso-dilators on a chronic basis or the use of a left ventricular assist device pre-transplant with the intention of normalizing pulmonary pressures and allowing the patients to become candidates for orthotopic cardiac transplantation and thereby avoiding the necessity of heterotopic cardiac transplantation.