High-Intensity Statins Affect Coronary Plaque Composition After STEMI
Patients with diabetes had a greater increase in minimum fibrous cap thickness and had a smaller minimum fibrous cap thickness than those without diabetes.
Patients using a high-intensity statin after a ST-elevation myocardial infarction (STEMI) experienced a significant increase in minimum fibrous cap thickness, a reduction in macrophage accumulation, and more frequent regression of thin-cap fibroatheromas to other plaque phenotypes in nonculprit lesions, according to a study published in the JACC Cardiovascular Imaging.
Researchers working on the Integrated Biomarker Imaging Study-4 (IBIS-4, ClinicalTrials.gov Identifier: NCT00962416) analyzed a subpopulation of patients receiving high-intensity statins after STEMI using multimodality intracoronary imaging to assess changes in optical coherence tomography.
Patients received a 40 mg dose of rosuvastatin unless adverse events were reported. Optical coherence tomography was completed at baseline and at a 13-month follow up. Plaques were classified as fibroatheroma, thin-cap fibroatheroma, thick-cap fibroatheroma, fibrocalcific, or fibrous.
The study endpoints were changes in fibrous cap thickness and macrophage accumulation angels. Changes in mean fibrous cap thickness, lipid pool arc, and plaques types were also analyzed.
Of the 83 patients included in the study, 9.6% were women and the average age was 59 years old. By the follow-up, median low-density lipoprotein cholesterol had decreased from 128 mg/dL to 73.6 mg/dL. Additionally, all arteries had a decrease in the arc of macrophage lines from a mean score of 9.6 degrees (±12.8 degrees) to 6.4 degrees (±9.6 degrees; P <.001), and an association was found between changes in low density lipoprotein cholesterol and the arc of macrophage lines (P =.012).
Patients with diabetes had a greater increase in minimum fibrous cap thickness (P=.003) and had a smaller minimum fibrous cap thickness than those without diabetes. Overall, mean fibrous cap thickness increased to 313.8±88.7 µm from 248.6 ± 65.8 µm, mean lipid arc decreased to 43.5±33.5 degrees from 55.9±37.0 degrees, and while 92.6% of lesions remained in the same category from baseline to follow-up, two thirds of thin-cap fibroatheroma converted to another phenotype.
At the lesion level, the minimum fibrous cap thickness increased to 94.2±39.9 µm from 74.0±32.3 µm, and the mean arc of macrophage lines decreased by 31.7%.
Some limitations of this study are the lack of control group, the sample being a subset of a larger study, and the lack of validation on patterns assessed by optical coherence tomography. Future studies need to evaluate the specific mechanisms behind statin treatment success and the clinical relevance of optical coherence tomography coronary atheroma compositions categorizations.
The researchers concluded that these findings “provide novel in vivo evidence of changes in nonculprit lesions among STEMI patients receiving intensive statin therapy but should be interpreted in the context of the modest sample size and limitations inherent to observational studies.”
Räber L, Konstantinos KC, Yamaji K, et al. Changes in coronary plaque composition in patients with acute myocardial infarction treated with high-intensity statin therapy (IBIS-4): a serial optical coherence tomography study [published online December 12, 2018]. JACC Cardiovasc Imaging. doi: 10.1016/j.jcmg.2018.08.024