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https://www.selleckchem.com/products/dynasore.html Vulnerable plaques are the primary cause of acute coronary syndrome (ACS). The association between in-vivo plaque vulnerability and adiponectin levels in ACS still remains to be determined. The purpose of this study was to investigate the correlation between adiponectin levels and vulnerable plaque features in ACS patients. We enrolled 107 ACS patients admitted to our institution; 83 with Non-ST elevation ACS (NSTE-ACS) and 24 with ST-elevation myocardial infarction (STEMI). Adiponectin levels were measured in these patients. Coronary angiography and subsequent optical coherence tomography (OCT) analysis of culprit lesions were performed. Adiponectin level was lower in patients with complex angiographic lesions, compared to those with non-complex lesions (7.13±3.04 vs. 8.94±2.84μg/ml, P=0.002). Adiponectin level was lower in patients with plaque rupture (PR), micro-thrombi, and thin cap fibroatheroma (TCFA), compared to those with non-vulnerable features (7.19±2.95 vs 8.79±3.02μg/ml, P=0.007 & 7.29±2.97 vs 8.44±3.09μg/ml, P=0.04 and 4.76±0.65 vs 9.74±2.35μg/ml, P<0.001μg/ml respectively). There was a significant negative correlation between adiponectin levels and lipid rich plaque extent and maximum lipid arc (r=-0.05, P<0.001 & r=-0.03, P=0.03, respectively). However, a significant positive correlation was observed between adiponectin levels and fibrous cap thickness (r=0.95, P<0.001). Low adiponectin levels were associated with complex angiographic lesions and vulnerable plaque features in ACS patients, where there was a significant correlation between it and PR, TCFA, and lipid rich plaque. Low adiponectin levels were associated with complex angiographic lesions and vulnerable plaque features in ACS patients, where there was a significant correlation between it and PR, TCFA, and lipid rich plaque. Pharmacotherapy is key in asthma control, including preventing lung function decline, in primary care. However, patie

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