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Identifying Coronary Artery Calcification on Non-gated Computed Tomography Scans
Published on: August 28, 2018
Relationship Between Coronary Artery Calcium and Atherosclerosis Progression Among Patients With Suspected Coronary
Emma J Hollenberg1, Fay Lin2, Michael J Blaha3
1Dalio Institute of Cardiovascular Imaging, New York-Presbyterian Hospital and Weill Cornell Medicine, New York, New York, USA; Emory University School of Medicine, Atlanta, Georgia, USA.
Insights
Coronary artery calcium (CAC) scores alone do not fully capture atherosclerotic plaque burden or risk. Serial computed tomographic angiography reveals plaque progression and varying risk across CAC score subgroups.
Area of Science:
- Cardiovascular Imaging
- Radiology
- Preventive Cardiology
Background:
- Coronary artery calcium (CAC) scoring is used to assess cardiovascular risk.
- Its sufficiency in identifying all atherosclerotic plaque burden and progressive risk in symptomatic patients is unclear.
Purpose of the Study:
- To quantify noncalcified plaque and plaque volume progression in relation to CAC scores.
- To assess serial plaque progression and associated coronary artery disease (CAD) event risk.
Main Methods:
- Serial coronary computed tomographic angiography (CTA) in 698 symptomatic patients over 3.5–4.0 years.
- Quantification of atherosclerotic plaque composition and volume.
- Analysis of CAD event risk using Cox proportional hazard models.
Main Results:
- Plaque volume and obstructive CAD prevalence increased significantly with higher baseline CAC scores.
- Patients with CAC < 100 had prevalent nonobstructive, noncalcified plaque.
- Plaque progression varied by CAC score, with disproportionate noncalcified plaque growth in lower CAC groups and calcified plaque growth in higher CAC groups.
- CAD event risk showed a graded increase with higher CAC scores.
Conclusions:
- CAC scoring imperfectly characterizes total atherosclerotic disease burden.
- CAC subgroups demonstrate distinct patterns of plaque progression and stratify long-term prognostic risk.
Background:
Among symptomatic patients, it remains unclear whether a coronary artery calcium (CAC) score alone is sufficient or misses a sizeable burden and progressive risk associated with obstructive and nonobstructive atherosclerotic plaque.
Objectives:
Among patients with low to high CAC scores, our aims were to quantify co-occurring obstructive and nonobstructive noncalcified plaque and serial progression of atherosclerotic plaque volume.
Methods:
A total of 698 symptomatic patients with suspected coronary artery disease (CAD) underwent serial coronary computed tomographic angiography (CTA) performed 3.5 to 4.0 years apart. Atherosclerotic plaque was quantified, including by compositional subgroups. Obstructive CAD was defined as ≥50% stenosis. Multivariate linear regression models were used to measure atherosclerotic plaque progression by CAC scores. Cox proportional hazard models estimated CAD event risk (median of 10.7 years of follow-up).
Results:
Across baseline CAC scores from 0 to ≥400, total plaque volume ranged from 30.4 to 522.4 mm3 (P < 0.001) and the prevalence of obstructive CAD increased from 1.4% to 49.1% (P < 0.001). Of those with a 0 CAC score, 97.9% of total plaque was noncalcified. Among patients with baseline CAC <100, nonobstructive CAD was prevalent (40% and 89% in CAC scores of 0 and 1-99), with plaque largely being noncalcified. On the follow-up coronary CTA, volumetric plaque growth (P < 0.001) and the development of new or worsening stenosis (P < 0.001) occurred more among patients with baseline CAC ≥100. Progression varied compositionally by baseline CAC scores. Patients with no CAC had disproportionate growth in noncalcified plaque, and for every 1 mm3 increase in calcified plaque, there was a 5.5 mm3 increase in noncalcified plaque volume. By comparison, patients with CAC scores of ≥400 exhibited disproportionate growth in calcified plaque with a volumetric increase 15.7-fold that of noncalcified plaque. There was a graded increase in CAD event risk by the CAC with rates from 3.3% for no CAC to 21.9% for CAC ≥400 (P < 0.001).
Conclusions:
CAC imperfectly characterizes atherosclerotic disease burden, but its subgroups exhibit pathogenic patterns of early to advanced disease progression and stratify long-term prognostic risk.
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