Anatomic complexity and lipid plaque burden in NSTE-ACS smoker patients with or without COPD: Insights from the SCAP trial

Background: The effects of COPD on coronary artery lesions are unknown. The Screening for COPD in ACS patients (SCAP) trial enrolled acute coronary syndrome (ACS) patients with smoking habit without known COPD to detect undiagnosed COPD (UCOPD). Purpose: To evaluate the anatomic complexity (Syntax score) and plaque lipid core burden index (LCBI through near infrared spectroscopy (NIRS)) in patients hospitalized for no ST-elevated (NSTE)-ACS enrolled in the SCAP trial. Methods: The SCAP trial study protocol mandated to perform Syntax score and suggested to perform NIRS in the culprit lesion and at least in one non-culprit lesion, in all patients presenting with NSTE-ACS. LCBI and Max LCBI 4 mm were calculated in all analyzed vessels by two independent investigators. Results: SCAP trial enrolled 78 patients with NSTE-ACS. NIRS was performed in 65 patients on a total of 151 vessels. The number of diseased vessels and the Syntax score were comparable between the two groups (UCOPD and no COPD). The LCBI and max LCBI 4mm were significantly higher in the UCOPD group. The same result was found in culprit and in non-culprit coronary arteries (LCBI culprit: UCOPD 119 [102-146]; no COPD 71 [50-119], p=0.01; LCBI non culprit: UCOPD 111 [69-144]; no COPD 77 [46-104], p=0.002; LCBI max 4 mm culprit: UCOPD 424 [399-464]; no COPD 286 [178-385], p<0.001; LCBI max 4 mm nonculprit: UCOPD 337 [286-408]; no COPD 233 [151-333], p<0.001). The number of vessel with max LCBI 4 mm>400 was significantly higher in the UCOPD group (Table presented) compared to the no COPD group (52% of UCOPD vessels; 15% of no COPD vessels, p<0.001). Conclusions: Patients with UCOPD hospitalized for NSTE-ACS showed a comparable Syntax score and a higher LCBI and max LCBI 4 mm compared to smoker patients without COPD both in culprit and non-culprit lesions. UCOPD increases plaque vulnerability through a higher lipid content, likely consequent to higher inflammation and endothelial dysfunction.