Plaque Changes Visible in MI Patients After High-Intensity Statin Use

January 1, 2019

By David Douglas

NEW YORK (Reuters Health) - Optical coherence tomography (OCT) shows alteration in the composition of coronary atherosclerotic plaques in ST-elevation myocardial infarction (STEMI) patients receiving high-intensity statin treatment, according to international researchers.

"Our study is in full support of routine high-intensity statin therapy in STEMI patients as it demonstrates a consistent stabilization of presumably high-risk plaques by increasing cap thickness, reducing macrophage accumulations and lipid content in only one year," said Dr. Lorenz Raeber of Bern University Hospital in Switzerland.

OCT, he told Reuters Health by email, "is a great technology to visualize what statins can achieve in diseased coronary arteries."

In a paper online December 12 in JACC: Cardiovascular Interventions, Dr. Raeber and colleagues note that preclinical investigations and human pathological studies have demonstrated plaque-stabilizing effects of statins, but "in vivo evidence remains elusive."

To investigate further, the team used intravascular ultrasound and OCT in 103 patients in the acute phase of STEMI to examine two non-infarct-related coronary arteries. The patients then went on to receive rosuvastatin for 13 months. Serial OCT imaging was available in 153 arteries of 83 patients.

On subsequent examination, median LDL-cholesterol had decreased from 128 mg/dL to 73.6 mg/dL. Measurement in 31 lesions in 27 patients showed that minimum fibrous-cap thickness (FCT) increased significantly from 64.9 um to 87.9 um. There was a highly significant reduction in macrophage-line arc and a decrease in mean lipid arc.

In analyses of 191 lesions, nine of 13 thin-cap fibroatheromata (TCFAs) at baseline (69.2%) regressed to non-TCFA morphology, and two of 178 non-TCFA lesions (1.1%) progressed to TCFAs.

These findings, say the researchers, "provide novel in vivo evidence of changes in non-culprit 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."

However, Dr. Raeber concluded, "The study confirms in a purely visual manner what many patients and doctors doubt: statins stabilize coronary plaques."

In an accompanying editorial, Dr. Marc D. Feldman of UT Health San Antonio, in Texas, and colleagues, note that the authors' "application of a computer-assisted, semi-automated method for measuring fibrous cap thickness is an improvement over manual measurements and plaque classification of both thin-cap and thick-cap fibroatheromas. The semi-automatic assessment also showed better inter-observer reliability and reproducibility."

"Approaches that improve the identification of TCFA and vulnerable plaques," they conclude, "provide valuable diagnostic methodologies to all interventional cardiologists."


J Am Coll Cardiol Intv 2018.

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