Summary Coronary artery disease (CAD) is characterised by progressive atherosclerotic plaque leading to flow-limiting stenosis, while myocardial infarction (MI) occurs due to plaque rupture or erosion with abrupt coronary artery occlusion. Multiple inflammatory pathways influence plaque stability, but direct assessment of endothelial inflammation at the site of coronary artery stenosis has largely been limited to pathology samples or animal models of atherosclerosis. We describe a technique for isolating and characterising endothelial cells (ECs) and EC microparticles (EMPs) derived directly from the site of coronary artery plaque during balloon angioplasty and percutaneous coronary intervention. Coronary artery endothelial cells (CAECs) were identified using imaging flow cytometry (IFC), and individual CAEC and EMP expression of the pro-atherogenic adhesion molecule vascular cell adhesion molecule-1 (VCAM-1) was assessed immediately following angioplasty. Patients with MI registered 73 % higher VCAM-1 expression on their CAECs and 79 % higher expression on EMPs compared to patients with stable CAD. In contrast, VCAM-1 expression was absent on ECs in the peripheral circulation from these same subjects. VCAM-1 density was significantly higher on CAECs and EMPs among patients with MI and positively correlated with markers of myocardial infarct size. We conclude that increased VCAM-1 expression on EC and formation of EMP at the site of coronary plaque is positively correlated with the extent of vascular inflammation in patients with myocardial infarction.

No abstract

The purpose of this study was to identify plasma metabolites associated with superior endurance running performance. In 2016, participants at the Western States Endurance Run (WSER), a 100-mile (161-km) foot race, underwent non-targeted metabolomic testing of their post-race plasma. Metabolites associated with faster finish times were identified. Based on these results, runners at the 2017 WSER underwent targeted metabolomics testing, including lipidomics and choline levels. The 2017 participants’ plasma metabolites were correlated with finish times and compared with non-athletic controls. In 2016, 427 known molecules were detected using non-targeted metabolomics. Four compounds, all phosphatidylcholines (PCs) were associated with finish time (False Discovery Rate (FDR) < 0.05). All were higher in faster finishers. In 2017, using targeted PC analysis, multiple PCs, measured pre- and post-race, were higher in faster finishers (FDR < 0.05). The majority of PCs was noted to be higher in runners (both pre- and post-race) than in controls (FDR < 0.05). Runners had higher choline levels pre-race compared to controls (p < 0.0001), but choline level did not differ significantly from controls post-race (p = 0.129). Choline levels decreased between the start and the finish of the race (p < 0.0001). Faster finishers had lower choline levels than slower finishers at the race finish (p = 0.028).

No abstract

Neurogenic thoracic outlet syndrome (NTOS) is an etiologically and clinically diverse disorder caused by compression of the brachial plexus traversing the thoracic outlet. Athletes who perform repetitive overhead activities are at risk of developing NTOS with sport-specific symptoms. This article reviews the controversial NTOS nomenclature, common sites of anatomic compression, and red flag symptoms that require immediate intervention. It also reviews the congenital, traumatic, and functional etiologies of NTOS, with a discussion of the differential diagnosis, diagnostic criteria, and workup for NTOS. Nonsurgical treatment is highlighted with an emphasis on thoracic outlet syndrome-specific physical therapy and updates on injection options and ultrasound guided hydrodissection. This article compares nonsurgical versus surgical functional outcome data with an emphasis on athletes with NTOS. Functional assessment tools and performance metrics for athletes are reviewed, as well as return to sport considerations.