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Calcium Burden, Vascular Inflammation, and Plaque Vulnerability
Quick Takes
- High calcified plaque burden is associated with a significantly lower level of pericoronary adipose tissue attenuation, indicating that advanced calcification is associated with a lower level of vascular inflammation.
- Plaque vulnerability appears to increase as calcium starts accumulating, then decreases with advanced calcification.
Study Questions:
Is calcified plaque burden (CPB) associated with vascular inflammation and plaque vulnerability?
Methods:
Patients with coronary artery disease, including those with non–ST-elevation myocardial infarction, acute coronary syndrome (ACS), or stable angina who completed computed tomography angiography and optical coherence tomography (OCT) prior to coronary intervention were included in the present analysis. Participants were divided into four groups, including those without calcification at the culprit lesion and three groups based on CPB (low-CPB group [0 < CPB < 1.98%], intermediate-CPB group [1.98 < CPB < 7.96%], and high-CPB group [7.96% < CPB]). CPB was calculated as plaque volume divided by vessel volume in the culprit lesion. Pericoronary adipose tissue (PCAT) attenuation as a measure of vascular inflammation and OCT-derived vulnerable features were measured among the four groups.
Results:
There were a total of 578 patients including 183 patients without calcification and 395 patients with calcification in the culprit lesion (132 patients in the low-CPB group, 132 patients in the intermediate-CPB group, and 131 patients in the high-CPB group). Patients with high CPB were older, more likely to be on statins, had lower rates of ACS, and had more culprit lesions located in the left anterior descending artery. No significant difference in the level of high-sensitivity C-reactive protein was observed among the four groups. The highest CPB tertile was associated with lower PCAT attenuation in the culprit vessel compared to other groups. The prevalence of features of plaque vulnerability, including lipid-rich plaque, was also lowest in the highest CPB tertile. In the patients with calcification, higher age, statin use, and lower PCAT attenuation were independently associated with CPB.
Conclusions:
The authors conclude that greater calcium burden is associated with a lower level of vascular inflammation and plaque vulnerability. Greater calcium burden may represent advanced stable plaque without significant inflammatory activity.
Perspective:
The present study suggests the importance of understanding the trajectory of plaque formation with a goal to understanding the interplay between vascular inflammation and plaque stability, leading to tailored management of unstable plaque and associated cardiovascular events.
Clinical Topics: Noninvasive Imaging
Keywords: Plaque, Atherosclerotic, Inflammation, Tomography, Optical Coherence
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