CMR can be performed safely in non-MRI-conditional CIEDs using a standardized protocol. Use of a wideband pulse sequence for LGE imaging yields a high rate of studies unaffected by artifact.

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 180 days 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.

ST-segment elevation myocardial infarction (STEMI) is the most serious manifestation of acute coronary syndrome. A variety of noncardiac conditions can mimic STEMI on electrocardiography (ECG). We describe a case of gastrointestinal distention and ileus masquerading as STEMI on ECG and posits a mechanism for this effect. ( Level of Difficulty: Intermediate. )

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.