Markers in Acute Coronary Syndrome: Distal Coronary Embolism at Percutaneous Coronary Intervention

(1) Introduction: Distal coronary emboli occur in up to 15-30.5% of patients undergoing percutaneous coronary intervention (PCI) for acute myocardial infarction (AMI) and are associated with poor myocardial reperfusion in the territory of the infarct-related artery. The objective of this study was to analyze the possible laboratory, clinical and imaging indicators of distal coronary embolism detected with an angiography at the time of PCI with stent implantation for acute coronary syndrome (ACS). (2) Methods: This analysis included 137 patients with ACS. The levels of cardiac enzymes (creatine kinase [CK], muscle-brain fraction of CK, high-sensitivity troponin T [hsTnT]), inflammatory markers (high-sensitivity C-reactive protein, white blood cell counts), sex steroids (total 17β-estradiol, total testosterone, dehydroepiandrosterone sulfate [DHEA-S]), serum lipids and oxidized low-density lipoproteins (oxLDL) were measured and analyzed for their relationship with the incidence of distal coronary embolism at PCI. (3) Results: Slow coronary blood flow was detected in the coronary artery subject to intervention in 9.4% (<i>n</i> = 13) of patients. Triglyceride (TG), high-density lipoprotein (HDL), glucose and serum DHEA-S levels were found to be associated with distal coronary embolization and slow coronary flow at PCI with stenting (DHEA-S: 1.316, OR 1.044-1.659, <i>p</i> = 0.020; TG: 1.130, OR 0.990-1.300, <i>p</i> = 0.072; HDL: 2.326, OR 0.918-5.8977, <i>p</i> = 0.075; glucose: 1.130, OR 0.990-1.300, <i>p</i> = 0.072). In the multivariable model, only DHEA-S after PCI tended to indicate a risk of distal coronary embolism (DHEA-S: <i>p</i> = 0.071; TG: <i>p</i> = 0.339; glucose: <i>p</i> = 0.582; HDL: <i>p</i> = 0.502). (4) Conclusions: Patients with ACS with higher triglyceride levels are at risk of developing slow blood flow after percutaneous intervention with stent implantation. Elevated DHEA-S possibly reflects sympathoadrenal and hypothalamus-pituitary-adrenal hyperactivity associated with ACS and coronary intervention.