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A new study published in the Journal of the American College of Cardiology suggests that higher levels of coronary artery calcium are associated with reduced vascular inflammation and decreased plaque vulnerability. These findings may signal that heavily calcified plaques, often considered markers of advanced atherosclerosis, represent a stable, less inflammatory state of coronary disease.
The study explored the complex relationship between coronary artery calcium, vascular inflammation, and plaque vulnerability. While previous research has established that coronary artery calcification is integral to atherosclerosis, this new study adds depth to our understanding by showing that increased calcium burden is linked to stability, not plaque rupture. In contrast, non-calcified plaques, which are more prone to rupture, are associated with higher levels of inflammation and an increased risk of acute coronary syndromes (ACS).
These findings have significant implications for cardiovascular risk assessment and prevention strategies. For decades, coronary calcification has been used as a key imaging biomarker to identify high-risk individuals. However, this research underscores the importance of not only tracking calcification but also addressing vascular inflammation, which can lead to plaque destabilization and acute events. As statin therapy has been shown to increase plaque calcification and thus reduce cardiovascular events, the role of inflammation in plaque vulnerability is becoming more pronounced. The editorial accompanying the study emphasizes the need for new biomarkers, such as the Fat Attenuation Index (FAI), to more accurately assess coronary inflammation.
Understanding the interplay between calcification and inflammation could refine how clinicians approach the management of atherosclerosis, leading to more precise and effective treatments for preventing heart attacks and other cardiovascular events.