Initial clinical experience with the HeartWare left ventricular assist system: a single-center report.

BACKGROUND: The HeartWare ventricular assist device (HVAD) system (HeartWare International Inc, Framingham, MA) is a new centrifugal continuous-flow ventricular assist device. The aim of the present study is to review our institutional experience with this novel device. METHODS: We reviewed the files of 50 patients (39 men, 11 women) with a mean age of 50.6 ± 11.8 years (range, 19 to 70 years) who underwent HVAD implantation between July 2009 and November 2011. Two patients underwent HeartWare BIVAD implantation. The underlying heart diseases were end-stage ischemic heart disease (n = 12), acute myocardial infarction (n = 9), dilated cardiomyopathy (n = 27) and acute myocarditis (n = 2). Interagency Registry for Mechanically Assisted Circulatory Support (INTERMACS) profiles were level 1 (n = 11), 2 (n = 5), 3 (n = 10), and 4 (n = 24). RESULTS: After a cumulative support duration of 11,086 days, Kaplan-Meier analysis revealed a survival of 82.0%, 77.9%, 75.5%, at 1, 12, and 24 months, respectively. Causes of early death were right heart failure (n = 4), multiorgan failure (n = 2), septic shock (n = 2), and major neurologic complications (n = 4). One late death occurred due to a right heart failure. Comparison between patients operated on in cardiogenic shock (INTERMACS 1 and 2) and patients who underwent elective HVAD implantation (INTERMACS 3 and 4) revealed a survival of 61.5% and 44.1% for the INTERMACS 1 and 2 group and 90.3% and 87.1% for the INTERMACS 3 and 4 group at 1 and 12 months, respectively (odds ratio, 4.67; p = 0.003). One patient was weaned from the system after 2 years. Eleven patients (22%) were successfully bridged to transplantation. Mean time to transplantation was 209 days (range, 72 to 427 days). Posttransplant survival at the 1-year follow-up was 90.9% (11 patients). CONCLUSIONS: Our experience with HVAD shows satisfying results with an excellent posttransplantation survival. Moreover, the stratified survival based on the level of preoperative stability shows better outcomes in patients undergoing elective HVAD implantation.

Medically refractory pulmonary hypertension: treatment with nonpulsatile left ventricular assist devices.

BACKGROUND: Severe pulmonary hypertension refractory to medical treatment is a contraindication to orthotopic heart transplantation in most centers. We report our experience in treating severe pulmonary hypertension with mechanical left ventricular unloading using implantable nonpulsatile left ventricular assist devices (LVAD) with continuous flow properties. METHODS: In ten patients with severe pulmonary hypertension, refractory to medical treatment, an implantable nonpulsatile LVAD was placed for continuous mechanical left ventricular support. Pulmonary hemodynamics were assessed by right heart catheterization prior to and during LVAD implantation, and after orthotopic heart transplantation. RESULTS: The mean (+/-SD) interval of nonpulsatile support was 182 (+/-118) days. Pulmonary artery pressure (mean +/- SD) significantly decreased from 42 +/- 13 to 24 +/- 5 mm Hg (p < 0.005), the transpulmonary gradient (mean +/- SD) decreased from 20 +/- 6 to 11 +/-5 mm Hg (p < 0.005), and the pulmonary vascular resistance (mean +/- SD) from 4.8 +/- 1.8 to 2.2 +/- 0.8 Wood units (p < 0.005) during an interval of one to six months of LVAD support. No significant increases in pulmonary artery pressure, transpulmonary gradient, and pulmonary vascular resistance were observed during an interval of three to six months after orthotopic heart transplantation. CONCLUSIONS: This study supports that LVAD support and continuous nonpulsatile mechanical unloading of the left ventricle can reverse medically unresponsive pulmonary hypertension and render patients eligible for orthotopic heart transplantation.

Ischemic preconditioning by unstable angina reduces the release of CK-MB following CABG and stimulates left ventricular HSP-72 protein expression.

BACKGROUND AND AIM: Whether the CK-MB reducing effect of ischemic preconditioning (IP) by unstable angina within 24 to 48 hours before CABG is achieved by early or by delayed preconditioning of left ventricular myocardium in humans is unknown. We investigated whether IP is associated with phosphorylation of p38 MAPK (characteristic for early preconditioning) or with increased protein expression of HSP-72 (characteristic for delayed preconditioning) at the time of CABG in patients. METHODS: Nineteen patients were grouped according to the occurrence of ischemic episodes within 48 hours before CABG. The patients without angina were assigned to the control group (CON, n = 10) whereas patients who had experienced angina within 48 hours before CABG were assigned to the preconditioned group (IP, n = 9). The effect of IP on the CABG induced maximal release of creatine kinase (CK) and CK-MB was examined. Left ventricular biopsy specimens taken immediately before cross clamping from ischemic (ISCH) and from reference (REF) areas were processed to analyze p38 MAPK phosphorylation and HSP-72-protein expression. RESULTS: While IP significantly reduced CK-MB (18.7 +/- 1.3 vs. 13.8 +/- 1.5 U/L, mean +/- SEM, p < 0.05), it only tended to reduce CK (292.7 +/- 32.8 vs. 274.1+/-31.1 U/L, p = NS, mean +/- SEM). CK-MB release for any given cross-clamp time was significantly reduced by IP (regression lines: CON, y= 0.4x+ 2, r= 0.8; IP, y= 0.1x+ 10, r= 0.2; p < 0.01, ANCOVA). There was no effect of IP on left ventricular p38 MAPK phosphorylation. IP increased left ventricular HSP-72-protein expression in ischemic areas when compared to reference areas (1.78 +/- 0.35 vs. 2.58 +/- 0.65, REF vs. ISCH, PhosphorImager units x10(6), mean +/- SEM, p < 0.05, ANCOVA). CONCLUSIONS: Thus, in the human left ventricular myocardium there is a second window of protection lasting for at least 48 hours, while at that time the early phase of preconditioning has already gone.