Relationship Between Coronary Artery Calcium and Atherosclerosis Progression Among Patients With Suspected Coronary Artery Disease.
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Hollenberg Emma J, Lin Fay, Blaha Michael J, Budoff Matthew J, van den Hoogen Inge J, Gianni Umberto, Lu Yao, Bax A Maxim, van Rosendael Alexander R, Tantawy Sara W, Andreini Daniele, Cademartiri Filippo, Chinnaiyan Kavitha, Choi Jung Hyun, Conte Edoardo, de Araújo Gonçalves Pedro, Hadamitzky Martin, Maffei Erica, Pontone Gianluca, Shin Sanghoon, Kim Yong-Jin, Lee Byoung Kwon, Chun Eun Ju, Sung Ji Min, Gimelli Alessia, Lee Sang-Eun, Bax Jeroen J, Berman Daniel S, Sellers Stephanie L, Leipsic Jonathon A, Blankstein Ron, Narula Jagat, Chang Hyuk-Jae, Shaw Leslee J
Аннотация
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.