The relationship between coronary artery calcification and atheroma volume is not what it seems. So indicates a recent Cleveland Clinic analysis of serial coronary intravascular ultrasound (IVUS) images of patients participating in eight large clinical trials.
Findings of the analysis, published in the Journal of the American College of Cardiology, include the following:
- Patients with coronary artery disease (CAD) who are treated with statins experience an increase in coronary calcification, an effect that is independent of plaque progression or regression.
- Paradoxically, high-intensity statin therapy is associated with the largest increases in coronary calcification despite promoting atheroma regression.
“Patients prescribed the highest doses of statins, despite achieving low levels of cholesterol and demonstrating marked plaque regression, had changes in plaque calcification that were nearly double the changes in patients who received no statins, and greater than changes in those who received low-intensity statin therapy, both of which were associated with plaque progression,” says the study’s principal investigator, Rishi Puri, MBBS, PhD.
Dr. Puri is a consultant with the Atherosclerosis Imaging Core Laboratory within the Cleveland Clinic Coordinating Center for Clinical Research (C5Research). The studies included in the pooled analysis were run through C5Research.
Calcification as a mechanism of plaque stabilization?
The increase in calcification revealed by the analysis may represent a means by which statin therapy stabilizes coronary plaque to reduce the risk of cardiovascular events, says the study’s senior investigator, Steven Nissen, MD, who adds that this hypothesis remains to be proved.
“We found that as plaques were getting smaller with statins, they were calcifying,” explains Dr. Nissen, Chairman of the Robert and Suzanne Tomsich Department of Cardiovascular Medicine at Cleveland Clinic.
“It’s exactly the opposite of what you might think intuitively,” he continues. “This is an important observation that tells us that statins work to stabilize plaques by converting softer, cholesterol-laden plaques that are prone to rupture into more stable calcified plaques that are relatively inert. It explains the paradox of why serial measurement of calcium doesn’t necessarily work to track the progression of disease, and it explains to some extent how statins work.”
Not all calcium is the same
“These findings show that not all calcium within the coronary arteries is necessarily the same,” Dr. Puri notes. “Rather, it likely depends on the context of a patient’s therapy and its duration, as well as the specific clinical situation. Our findings strongly suggest a calcium-related healing effect following high-dose therapy with potent statins, which could be considered atheroprotective. Our imaging laboratory, along with others, has demonstrated in the past the possible adverse effects of ‘spotty calcification’ found within the coronary tree, the plaques of which seem more resistant to therapies and more frequently found within culprit lesions of patients presenting with acute coronary syndromes.”
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