Highly Selective PPARα (Peroxisome Proliferator-Activated Receptor α) Agonist Pemafibrate Inhibits Stent Inflammation and Restenosis Assessed by Multimodality Molecular-Microstructural Imaging.

BACKGROUND New pharmacological approaches are needed to prevent stent restenosis. This study tested the hypothesis that pemafibrate, a novel clinical selective PPARα (peroxisome proliferator-activated receptor α) agonist, suppresses coronary stent-induced arterial inflammation and neointimal hyperplasia. METHODS AND RESULTS Yorkshire pigs randomly received either oral pemafibrate (30 mg/day; n=6) or control vehicle (n=7) for 7 days, followed by coronary arterial implantation of 3.

Elevated Heart Rate in Combination with Elevated Blood Pressure Predicts Lower Cardiovascular Mortality in Acute Decompensated Heart Failure.

Despite its clinical relevance, a subclass of acute decompensated heart failure (ADHF) with elevated blood pressure, known as hypertensive ADHF (HT-ADHF), has been less intensively evaluated. This study aimed to characterize the prognostic nature and pathophysiology of HT-ADHF. A total of 509 consecutive patients with first-time ADHF hospitalization were subjects of the study.

Successful Coronary Flow Restoration by Stent-Free Strategy Using the Pull-Back Method of Cutting Balloon in Spontaneous Coronary Artery Dissection.

This report describes a 46-year-old woman with ST-elevation myocardial infarction due to spontaneous coronary artery dissection. Because continuous chest pain and ST-segment elevation in electrocardiography indicated ongoing cardiac ischemia, the urgent revascularization strategy was used using a novel method of cutting balloon angioplasty, "the pull-back of inflated cutting balloon," which led to the successful coronary flow restoration and complete healing of dissected coronary artery in 1 year. The pull-back of the inflated cutting balloon method is a useful therapeutic option in the treatment of patients with spontaneous coronary artery dissection with ongoing cardiac ischemia.

PARP9 and PARP14 cross-regulate macrophage activation via STAT1 ADP-ribosylation.

Despite the global impact of macrophage activation in vascular disease, the underlying mechanisms remain obscure. Here we show, with global proteomic analysis of macrophage cell lines treated with either IFNγ or IL-4, that PARP9 and PARP14 regulate macrophage activation. In primary macrophages, PARP9 and PARP14 have opposing roles in macrophage activation.

Macrophages in Vascular Inflammation: Origins and Functions.

Macrophages influence various processes of cardiovascular inflammation. Whether they are of embryonic or post-natal hematopoietic origin, their balance in differential activation may direct the course of inflammation. Accelerated macrophage activation and accumulation through a pro-inflammatory signaling pathway may result in extensive tissue damage, adverse repair, and worsened clinical outcomes.