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Updated: Aug 6, 2026

Identifying Coronary Artery Calcification on Non-gated Computed Tomography Scans
Published on: August 28, 2018
Relationship of clinical presentation and calcification of culprit coronary artery stenoses
J A Beckman1, J Ganz, M A Creager
1Cardiovascular Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA. jbeckman@partners.org
Insights
Coronary artery calcification in culprit lesions is less extensive in acute coronary syndromes (myocardial infarction, unstable angina) than in stable angina. This finding impacts understanding acute coronary syndromes and calcium-based stenosis identification.
Area of Science:
- Cardiovascular Medicine
- Interventional Cardiology
- Atherosclerosis Research
Background:
- Coronary artery calcification (CAC) is linked to atherosclerosis but shows variability.
- The clinical significance of CAC in individual coronary stenoses is not fully understood.
- The relationship between CAC extent and acute coronary syndromes (ACS) requires further investigation.
Purpose of the Study:
- To test the hypothesis that culprit lesions in myocardial infarction (MI) or unstable angina (UA) are less calcified than in stable angina (SA).
- To investigate the association between the degree of coronary stenosis calcification and clinical presentation.
Main Methods:
- Intravascular ultrasound imaging was performed on culprit stenoses in 78 patients post-stenting.
- Patients were categorized into stable angina (n=17), unstable angina (n=43), and myocardial infarction (n=18).
- Coronary calcification was quantified using the arc of calcium via a computer-based protractor, measuring maximal and average calcification in stented segments.
Main Results:
- Maximal arc of calcium decreased progressively from SA (91±10°) to UA (59±8°) and MI (49±11°, P=0.014).
- Average arc of calcium was greatest in SA (32±7°), less in UA (15±4°), and least in MI (10±5°, P=0.014).
- These associations remained significant after adjusting for potential confounding factors.
Conclusions:
- Acute coronary syndromes are associated with significantly less calcification in culprit stenoses compared to stable angina.
- Findings suggest a potential biological difference in plaque composition between ACS and SA.
- The results have implications for understanding ACS pathogenesis and for diagnostic methods relying on calcium detection.
Abstract:
Coronary artery calcification is increased in the presence of atherosclerosis. However, there is great variability in the calcification of individual coronary stenoses, and the clinical significance of this finding remains unknown. We tested the hypothesis that culprit lesions associated with myocardial infarction or unstable angina are less calcified than are stenoses associated with stable angina. The study consisted of 78 patients who underwent intravascular ultrasound imaging of culprit stenoses after the placement of a stent. Seventeen patients presented with stable angina; 43, with unstable angina; and 18, with myocardial infarction. The extent of coronary calcification was measured by the angle of its arc and was quantified with a computer-based protractor. The arc of calcium was measured in the stented area at the point of maximal calcification and also as an average of the calcification found at proximal, middle, and distal stent segments. The maximal arc of calcium decreased progressively from patients with stable angina (91+/-10 degrees ) to those with unstable angina (59+/-8 degrees ) and to those with myocardial infarction (49+/-11 degrees, P=0.014). Similarly, the average arc of calcium was greatest (32+/-7 degrees ) in patients with stable angina, less (15+/-4 degrees ) in patients with unstable angina, and least (10+/-5 degrees ) in patients with acute myocardial infarction (P=0.014). These associations remained significant after adjustment for other factors that potentially affect arterial calcification. Acute coronary syndromes are associated with a relative lack of calcium in the culprit stenoses compared with stenoses of patients with stable angina. These findings have implications for the understanding of the biology of acute coronary syndromes as well as for the identification of coronary stenoses by methods that rely solely on the presence of calcium.
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