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Pericoronary adipose tissue (PCAT) is a source of microRNAs (miRs) that act as messengers for intercellular communication. We investigated whether the PCAT surrounding significant coronary atherosclerotic lesions shows specific miR expression patterns compared with PCAT surrounding plaque-free segments. We included 49 patients with 3-vessel coronary artery disease (CAD) and 19 patients with severe valvular disease but no CAD, who underwent elective cardiac surgery. The PCAT was harvested from two sites: adjacent to a significant atherosclerotic coronary lesion and from plaque-free segments. miR-133a, miR-21, miR-26b, miR-9, and miR-143 levels in PCAT cells were quantified by real-time reverse transcription polymerase chain reaction (data expressed as arbitrary units). Expression of miR-133, miR-21, and miR-26b in adipose tissue at a site without atherosclerotic lesion was much lower in patients with CAD than in those without CAD (0.82 ± 1.37 vs 1.86 ± 0.52, P < .001, 0.45 ± 1.3 vs 1.51 ± 1.11, P < .001, 0.3 ± 1.25 vs 1.2 ± 0.73, P = .02, respectively). In addition, miR-133, miR-21, and miR-143 in CAD patients showed significantly greater expression in PCAT from atherosclerotic lesion compared with plaque-free segments (1.32 ± 0.96 vs 0.82 ± 0.37 (P = .011), 0.91 ± 1.7 vs 0.3 ± 1.25 (P = .012), 1.2 ± 1.59 vs 0.43 ± 0.54 (P < .001), respectively). Our findings open new perspectives for the role of PCAT in the pathophysiology of atherosclerosis and should be further investigated.

Background Pericoronary adipose tissue (PCAT) plays a key role in the pathogenesis of atherosclerosis. PCAT is a source of microRNAs (miRs) that acts as messengers for intercellular communication. In this study, we investigated whether the PCAT surrounding coronary occlusive atherosclerotic lesions shows specific miR expression patterns compared to PCAT surrounding plaque-free segments. Purpose To evaluate the expression of miRs that are known to be implicated in the pathophysiology of atherosclerosis. Methods We included 49 patients (38 men, age 65±9 years) with 3-vessel coronary artery disease, who underwent elective coronary bypass surgery. The PCAT was harvested from two sites: adjacent to an occlusive atherosclerotic coronary lesion, and a plaque-free segment. miR-133a, miR-21, miR-26b, miR-9 and miR-143 levels in PCAT cells were quantified by real-time reverse transcription polymerase chain reaction. Results miR-26b, miR-21 and miR-143 showed significantly greater expression in PCAT samples taken from around atheromatous plaque (154±295 versus 37±96, p=0.014, for miR-26b; 122±265 versus 29±79, p=0.014, for miR-21; and 181±356 versus 31±50, p=0.03, for miR-143) (Figure 1). In addition, the expression of miR-143, miR-26b and miR-21 in PCAT from atherosclerotic plaque showed robust positive correlations with body.mass index (r=0.451, p=0.001, r=0.41, p=0.03 and r=0.416, p=0.003 respectively), Conclusions Analysis of PCAT located in proximity to atherosclerotic plaque showed a different pattern of miR expression compared to PCAT in a plaque-free segment. Our findings open new perspectives for the role of PCAT in the pathophysiological mechanisms of atherosclerotic disease and should be further investigated. Funding Acknowledgement Type of funding sources: None.

A 52-year-old woman presented with malignant ventricular arrthythmogenesis intraoperatively during kyphoplasty for an osteoporotic fracture of a lumbar vertebra. No previous cardiovascular condition was known. Causes of arrhythmogenesis associated with the procedure were excluded. Due to her positive family history for dilated cardiomyopathy, upcoming thoughts were made for unmasking a previous asymptomatic cardiomyopathy. Nevertheless, an intracardiac cement embolism was diagnosed and, finally, the patient underwent an open heart surgery with successful removal of the cardiac cement while no new arrhythmogenic episode was recorded during follow up.