Background— Bleeding is an important cause of morbidity and mortality in patients with continuous-flow left ventricular assist devices (LVADs). Reduced pulsatility has been implicated as a contributing cause. The aim of this study was to assess the effects of different degrees of pulsatility on the incidence of nonsurgical bleeding. Methods and Results— The Utah Transplantation Affiliated Hospitals (U.T.A.H.) heart failure and transplant program databases were queried for patients with end-stage heart failure who required support with the continuous-flow LVAD HeartMate II (Thoratec Corp, Pleasanton, CA) between 2004 and 2012. Pulsatility was evaluated by means of the LVAD parameter pulsatility index (PI) and by the echocardiographic assessment of aortic valve opening during the first 3 months of LVAD support. PI was analyzed as a continuous variable and also stratified according to tertiles of all the PI measurements during the study period (low PI: <4.6, intermediate PI: 4.6–5.2, and high PI: >5.2). Major nonsurgical bleeding associated with a decrease in hemoglobin ≥2 g/dL (in the absence of hemolysis) was the primary end point. A total of 134 patients (median age of 60 [interquartile range: 49–68] years, 78% men) were included. Major bleeding occurred in 33 (25%) patients (70% gastrointestinal, 21% epistaxis, 3% genitourinary, and 6% intracranial). In multivariable analysis, PI examined either as a categorical variable, low versus high PI (hazard ratio, 4.06; 95% confidence interval, 1.35–12.21; P =0.04), or as a continuous variable (hazard ratio, 0.60; 95% confidence interval, 0.40–0.92; P =0.02) was associated with an increased risk of bleeding. Conclusions— Reduced pulsatility in patients supported with the continuous-flow LVAD HeartMate II is associated with an increased risk of nonsurgical bleeding, as evaluated by PI.

Objective To prospectively investigate the longitudinal effects of continuous-flow left ventricular assist device (LVAD) unloading on myocardial structure and systolic and diastolic function. Background The magnitude, timeline and sustainability of changes induced by continuous-flow LVAD on the structure and function of the failing human heart are unknown. Methods Eighty consecutive patients with clinical characteristics consistent with chronic heart failure requiring implantation of a continuous-flow LVAD were prospectively enrolled. Serial echocardiograms (1, 2, 3, 4, 6, 9 and 12 months) and right heart catheterizations were performed after LVAD implant. Cardiac recovery was assessed on the basis of improvement in systolic and diastolic function indices on echocardiography that were sustained during LVAD turn-down studies. Results After 6 months of LVAD unloading, 34% of patients had a relative LVEF increase above 50% and 19% of patients, both ischemic and nonischemic, achieved an LVEF≥40%. LV systolic function improved as early as 30 days, the greatest degree of improvement was achieved by 6 months of mechanical unloading and persisted over the 1- year follow up. LV diastolic function parameters also improved as early as 30 days post LVAD unloading and this improvement persisted over time. LV end-diastolic and end-systolic volumes decreased as early as 30 days post LVAD unloading (113 vs. 77ml/m2, p<0.01 and 92 vs. 60ml/m2, p<0.01, respectively). LV mass decreased as early as 30 days post LVAD unloading (114 vs. 95g/m2, p<0.05) and continued to do so over the 1-year follow-up but did not reach values below the normal reference range suggesting no atrophic remodeling after prolonged LVAD unloading. Conclusion Continuous-flow LVAD unloading induced in a subset of patients, both ischemic and nonischemic, early improvement in myocardial structure and systolic and diastolic function that was largely completed within 6 months, with no evidence of subsequent regression.

Chemotherapy related cardiac dysfunction (CRCD) is a serious complication of anticancer therapy. CRCD can be classified into two types. Type I CRCD is exemplified by anthracyline- induced cardiac dysfunction and type II CRCD is exemplified by trastuzumab- induced cardiac dysfunction. The mechanism of cardiac toxicity in both types is not well defined. Certain risk factors may play a role in developing the cardiac injury, most importantly, the cumulative dose when dealing with anthracycline induced cardiotoxicity. Establishing an early diagnosis and initiating early treatment may be an important step in preventing irreversible cardiac injury especially in type I CRCD. Currently there are no guidelines developed specifically for the treatment of chemotherapy induced cardiomyopathy (CIC), however a few small studies support the use of neurohormonal antagonists in the treatment and prevention of CIC. Large multi- centers trials are needed to establish guidelines for CIC. Until then, we advocate following the American College of Cardiology/ American Heart Association (ACC/AHA) and Heart Failure Society of America (HFSA) guidelines. Additionally, a close collaboration between the patient’s cardiologist and oncologist is strongly recommended in order to establish a long term plan for the patient.

The use of high-dose inotropic support to maintain donor stability appears to have a higher trend for early post-transplant MN without an impact on clinical outcomes. With the current growing shortage of organ donors, it appears reasonable to use donors on high-dose inotropic support.