Lack of statin therapy is associated with plaque instability in non-culprit non-ischemic lesions of diabetic patients – data from the COMBINE OCT-FFR study

Abstract

Abstract Background Effect of statin therapy on coronary plaque stabilisation and reducing adverse cardiovascular events is well known both in primary and secondary prevention. Nevertheless, there is a paucity of data presenting the impact of statins on plaque morphology as assessed by optical coherence tomography (OCT). Purpose The goal of this analysis was to evaluate the plaque morphology using OCT within non-culprit, non-ischaemic coronary lesions in diabetes mellitus (DM) patients with or without statin pre-treatment. Methods All patients of the COMBINE (FFR-OCT) trial underwent fractional flow reserve (FFR) measurement followed by OCT in FFR negative lesions. OCT recorded the presence of thin-cap fibroatheroma (TCFA), plaque rupture (PR), plaque erosion (PE) and calcified nodule (CN). Results From the 391 patients, 82 (21%) had no statin at baseline. OCT was performed in 463 lesions of which 96 lesions assessed in statin naive and 367 lesions in statin treated group. The median angiographic diameter stenosis was 50% and the median FFR value was 0.88 in both groups (p=0.953 and p=0.448, respectively). Myocardial infarction (MI) at presentation was 16.6% and did not differ between groups (p=0.380). Patients without statin pre-treatment were characterized by lower rate of known hypercholesterolemia (47.6% vs. 63.0%; p=0.011), male gender (52.4% vs. 65.7%; p=0.027), active smokers (8.5% vs. 22.3%; p=0.004) and previous MI (22.0% vs. 35.3%; p=0.022) as compared to patients with statin pre-treatment, respectively. The results of the qualitative OCT findings see in Table 1. Conclusions Non-ischemic lesions of DM patients without statin pre-treatment showed more vulnerable and instable plaque features like wider lipid arc, thinner fibrotic cap and a higher prevalence of lipid-rich plaque, TCFA and PR suggesting a stabilizing effect of statins on non-ischemic atherosclerotic lesions. Funding Acknowledgement Type of funding source: Private grant(s) and/or Sponsorship. Main funding source(s): The trial is founded from the Department of Cardiology Zwolle Heart-centrum with support from a non-restricted grant from St Jude Medical (now Abbott)