Incidence, Predictors, and Outcomes of New-Onset Left Ventricular Systolic Dysfunction After Orthotopic Liver Transplantation.

BACKGROUND: Adverse cardiovascular events after liver transplantation (LT) are relatively common and are a significant source of early mortality. Although new-onset systolic dysfunction after LT is a reported phenomenon, there is little data regarding its incidence, risk factors, and outcomes. METHODS AND RESULTS: This single-center retrospective study included all adult patients from January 2002 to March 2015 with deceased-donor LT and available preoperative transthoracic echocardiograms (TTEs). In total, 1,760 patients were included in the study, 602 (34.2%) of whom had a postoperative TTE. The primary end point was development of new-onset cardiomyopathy, defined as a new left ventricular ejection fraction (LVEF) of <40% within 180days of transplant. Sixty-nine (11.4%) of the patients who received post-LT TTE had a reduction in LVEF to <40% within 6 months. Clinical parameters of donor and recipient did not show significant impact on development of post-LT LV systolic dysfunction (LVSD). Presence of wall motion abnormalities (P = .004) on preoperative TTE was predictive of development of post-LT LVSD. These patients did not have longer hospitalizations, but they had worse survival. CONCLUSIONS: Post-LT LV systolic dysfunction occurs at higher rates than previously suspected and may develop more frequently in patients with underlying cardiac structural abnormalities, which appear to adversely affect post-LT survival.

The effects of pulmonary valve replacement on QRS duration in repaired tetralogy of Fallot patients with pulmonary regurgitation.

INTRODUCTION: Chronic pulmonary regurgitation (PR) following surgical correction in Tetralogy of Fallot (TOF) leads to right ventricular (RV) dysfunction, arrhythmias and sudden cardiac death (SCD). Pulmonary valve replacement (PVR) decreases PR and improves RV function, but data regarding QRS duration reduction remain scarce. METHODS: All adult TOF patients undergoing transcatheter PVR or surgical PVR from 2010 to 2016 were included. Clinical characteristics and QRS duration were measured and compared to post-intervention QRS duration using an institutional software and manually verified. Significantly wide QRS was defined as QRS >140 ms. RESULTS: Of 133 PVR patients, 85 had TOF and 27 (21.1%) had QRS > 140 ms (14 transcatheter, 13 surgical) and were included in this analysis. A 6 ms decrease in QRS duration was seen at 3-year follow-up (168.0 ±â€¯3.5 ms vs. 161.8 ±â€¯3.5 ms, p = .04). There was a significant decrease in the median RV size (defined as RV/LV diameter ratio) pre-intervention to 3-year post-intervention: (0.96 vs 0.89, p = .03). The median PR decreased significantly from moderate-severe to mild post-intervention (p < .0001). CONCLUSIONS: Replacement of the pulmonary valve in high risk TOF patients reduces QRS duration at 3 years. Further study is needed to assess whether this QRS duration reduction may identify patients at lower risk of ventricular arrhythmias.

Evacetrapib: Another CETP Inhibitor for Dyslipidemia With No Clinical Benefit.

Evacetrapib is a cholesteryl ester transfer protein (CETP) inhibitor that has been recently studied as a cholesterol modifying agent to reduce cardiovascular risk and mortality in high risk cardiovascular disease patients. Evacetrapib acts to decrease lipid exchange through CETP inhibition. CETP acts to transfer cholesteryl esters from high-density lipoprotein-cholesterol (HDL-C) to low-density lipoprotein cholesterol (LDL-C) and very-low-density lipoprotein (VLDL-C). HDL-C is involved in reverse cholesterol transport and its blood levels have been shown to be inversely correlated with cardiovascular risk. Thus, a pharmacologic agent that can elevate HDL-C has been seen as an exciting area of research. In recent studies, evacetrapib was shown to be safe and efficacious. It produced an increase in HDL-C up to 128% and a 35% decrease in LDL-C, in comparison to placebo. In addition, evacetrapib was also shown to be more potent than previous CETP inhibitors. HDL-C particles treated with evacetrapib remained functional and had improved cholesterol efflux. A previously studied CETP inhibitor, torcetrapib, exhibited side effects of hyperaldosteronism, manifesting in electrolyte disturbances, and hypertension. These detrimental effects were not seen with evacetrapib. Recently, the results of evacetrapib's phase III ACCELERATE trial showed no significant reduction in major adverse cardiovascular events or mortality, and the drug will not be marketed. Although beneficial cholesterol effects were seen with this drug, more needs to be known to understand what role, if any, evacetrapib has in the reduction of cardiovascular risk.