Coronary Plaque Changes in STEMI Patients Treated With Statins
Can optical coherence tomography (OCT), a high-resolution modality to measure plaque characteristics, detect potential effects of statins on plaque characteristics among patients with ST-segment elevation myocardial infarction (STEMI)?
In the IBIS-4 (Integrated Biomarker Imaging Study-4), patients underwent intravascular ultrasonography and OCT of two noninfarct-related coronary arteries in the acute phase of STEMI. Patients were treated with high-dose rosuvastatin for 13 months. Serial OCT imaging was available in 153 arteries from 83 patients. Fibrous cap thickness was measured by using a semi-automated method. Co-primary endpoints consisted of the change in minimum fibrous cap thickness (measured in fibroatheromas) and change in macrophage line arc.
Among the 83 STEMI patients, at 13 months, median low-density lipoprotein cholesterol (LDL-C) had decreased from 128 mg/dl to 73.6 mg/dl. A total of 27 patients (31 arteries) had evidence of fibroatheroma at both time points. Minimum fibrous cap thickness, measured in 31 lesions from 27 patients, increased from 64.9 ± 19.9 mm to 87.9 ± 38.1 mm (p = 0.008). In all investigated arteries (n = 153), macrophage line arc decreased from 9.6 degrees ± 12.8 degrees to 6.4 degrees ± 9.6 degrees (p < 0.0001). A linear association was observed between LDL-C and change in the macrophage line arc, but not with the change in LDL-C and changes in minimum fibrous cap thickness. The secondary endpoint, mean lipid arc, decreased from 55.9 degrees ± 37 degrees to 43.5 degrees ± 33.5 degrees. In lesion-level analyses (n = 191), 9 of 13 thin-cap fibroatheromata at baseline (69.2%) regressed to non–thin-cap fibroatheromata morphology, whereas 2 of 178 non–thin-cap fibroatheromata lesions (1.1%) progressed to thin-cap fibroatheromatas.
The investigators concluded that in this study, increases in minimum fibrous cap thickness, reduction in macrophage accumulation, and frequent regression of thin-cap fibroatheromatas were observed in nonculprit lesions of patients with STEMI treated with high-intensity statin therapy.
This study provides mechanistic data, which observed that high-intensity statin use was associated with increased fibrous cap thickness and reduction in macrophages in nonculprit lesions among STEMI patients. Additional studies in other patient groups to understand changes in plaque morphology that are associated with clinical benefit are warranted.
Keywords: Acute Coronary Syndrome, Atherosclerosis, Biological Markers, Cholesterol, LDL, Diagnostic Imaging, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Macrophages, Myocardial Infarction, Plaque, Atherosclerotic, Primary Prevention, Tomography, Optical Coherence, Ultrasonography, Interventional
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