Heart failure in remission for more than 13 years after removal of a left ventricular assist device.

Mechanical cardiac unloading with use of a left ventricular assist device (LVAD) is associated with substantial improvements in left ventricular function and enables subsequent LVAD explantation in some patients. We describe the case of a 35-year-old man with dilated nonischemic cardiomyopathy who was supported with an LVAD for 9 months. After the device was removed, he led a normal life for 13 years and 4 months. However, at 49 years of age, he presented with new signs and symptoms of heart failure, necessitating implantation of a 2nd LVAD. Afterwards, he has remained asymptomatic. This case is unique in that the patient lived a normal life for longer than a decade before renewed left ventricular decompensation necessitated repeat LVAD therapy. Histologic examination revealed few changes between the first device's removal in 1999 and the 2nd device's implantation in 2012.

Nitric oxide versus prostaglandin E1 for reduction of pulmonary hypertension in heart transplant candidates.

BACKGROUND: We sought to directly compare the effects of prostaglandin E1 (PGE1) and nitric oxide (NO) in testing for pulmonary hypertension reversibility in heart transplant candidates. METHODS: We included 19 heart transplant candidates who fulfilled at least 1 of 3 criteria: pulmonary vascular resistance (PVR) of >4 Wood units; transpulmonary gradient (TPG) of >12 mmHg; or systolic pulmonary artery pressure (PAP) of >60 mmHg. Patients randomly received either PGE1 (0.05, 0.2 and 0.5 microg/kg/min) or NO (40, 60 and 80 ppm) and were crossed-over to the second medication after receiving the maximal dose of the first. RESULTS: With PGE1, TPG decreased by 21% (baseline 20.3 +/- 6.8 mmHg; final 16.0 +/- 7.0 mmHg) compared to a 34% decrease with NO (baseline 20.8 +/- 6.2 mmHg; final 13.8 +/- 5.4 mmHg) (p = 0.13). PVR decreased by 42% with PGE1 (baseline 6.2 +/- 4.0 Wood units; final 3.6 +/- 1.8 Wood units) and by 47% with NO (baseline 6.0 +/- 3.9 Wood units; final 3.2 +/- 1.6 Wood units) (p = 0.87). Mean systemic pressure decreased with PGE1 (baseline 76.1 +/- 10.5 mmHg; final 69.4 +/- 12.2 mmHg; -9%) but not with NO administration (baseline 70.2 +/- 14.7 mmHg; final 71.6 +/- 10.9 mmHg; +2%) (p = 0.01). TPG was lowered to <12 mmHg in 14 patients. Of these, 6 (46%) responded to both PGE1 and NO, 4 (27%) responded only to PGE1, and 4 (27%) responded only to NO. CONCLUSIONS: The effects of PGE1 and NO on pulmonary hypertension are comparable, with PGE1 having more systemic hypotensive effects. Due to variability of patient responses, we recommend multiple rather than single-agent pharmacologic testing for the reversibility of pulmonary hypertension.

SEQUENTIAL ELECTROCARDIOGRAPHIC ANALYSIS OF STONE HEART SYNDROME IN A PATIENT SUPPORTED SIX DAYS WITH AN ABDOMINAL LEFT VENTRICULAR ASSIST DEVICE (ALVAD).

A 21-year-old male patient underwent aortic and mitral valve replacement for progressive cardiac failure due to acute bacterial endocarditis. Ischemic myocardial contracture developed during attempts to restore cardiac activity following hypothermic, ischemic, cardioplegic arrest. An abdominal left ventricular assist device (ALVAD) was implanted and supported the circulation for nearly six days prior to cardiac transplantation. The preoperative EKG showed sinus tachycardia with left anterior hemiblock. Postoperatively, there was complete electromechanical dissociation. The postoperative EKG showed a superior and leftward shift of the axis. There was a marked loss of QRS voltage and variable degrees of atrioventricular block. At times, only P waves were present. On the fourth postoperative day, there was an axis shift to the extreme right. Prior to transplantation, sinus rhythm returned, and the axis shifted leftward once again. The common denominator of all the abnormal postoperative electrocardiograms was the conspicuous low voltage that probably signified early and extensive myocardial damage. To our knowledge, this is the first instance wherein a sequential electrocardiographic analysis of stone heart syndrome has been undertaken.