Association of Coronary Artery Calcium Score With Qualitatively and Quantitatively Assessed Adverse Plaque
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Patients with stable chest pain seen in a cardiology clinic underwent computed tomography and assessment of coronary artery calcium score (CACS). Among patients with a zero CACS, 14% had nonobstructive disease, 2% had obstructive disease, 2% had visually assessed adverse plaques, and 13% had low-attenuation plaque burden >4%. Of the patients with myocardial infarctions, 10% had a zero CACS.
- Among patients with stable chest pain, a zero CACS is associated with a good prognosis but does not guarantee the absence of obstructive coronary artery disease, nonobstructive plaque, or an adverse plaque phenotype.
abstract
This abstract is available on the publisher's site.
Access this abstract nowAIMS
Coronary artery calcification is a marker of cardiovascular risk, but its association with qualitatively and quantitatively assessed plaque subtypes is unknown.
METHODS AND RESULTS
In this post-hoc analysis, computed tomography (CT) images and 5-year clinical outcomes were assessed in SCOT-HEART trial participants. Agatston coronary artery calcium score (CACS) was measured on non-contrast CT and was stratified as zero (0 Agatston units, AU), minimal (1-9 AU), low (10-99 AU), moderate (100-399 AU), high (400-999 AU), and very high (≥1000 AU). Adverse plaques were investigated by qualitative (visual categorization of positive remodelling, low-attenuation plaque, spotty calcification, and napkin ring sign) and quantitative (calcified, non-calcified, low-attenuation, and total plaque burden; Autoplaque) assessments. Of 1769 patients, 36% had a zero, 9% minimal, 20% low, 17% moderate, 10% high, and 8% very high CACS. Amongst patients with a zero CACS, 14% had non-obstructive disease, 2% had obstructive disease, 2% had visually assessed adverse plaques, and 13% had low-attenuation plaque burden >4%. Non-calcified and low-attenuation plaque burden increased between patients with zero, minimal, and low CACS (P < 0.001), but there was no statistically significant difference between those with medium, high, and very high CACS. Myocardial infarction occurred in 41 patients, 10% of whom had zero CACS. CACS >1000 AU and low-attenuation plaque burden were the only predictors of myocardial infarction, independent of obstructive disease, and 10-year cardiovascular risk score.
CONCLUSION
In patients with stable chest pain, zero CACS is associated with a good but not perfect prognosis, and CACS cannot rule out obstructive coronary artery disease, non-obstructive plaque, or adverse plaque phenotypes, including low-attenuation plaque.
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Additional Info
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Association of coronary artery calcium score with qualitatively and quantitatively assessed adverse plaque on coronary CT angiography in the SCOT-HEART trial
Eur Heart J Cardiovasc Imaging 2021 Sep 16;[EPub Ahead of Print], M Osborne-Grinter, J Kwiecinski, M Doris, P McElhinney, S Cadet, PD Adamson, AJ Moss, S Alam, A Hunter, ASV Shah, NL Mills, T Pawade, C Wang, JR Weir-McCall, G Roditi, EJR van Beek, LJ Shaw, ED Nicol, D Berman, PJ Slomka, DE Newby, MR Dweck, D Dey, MC WilliamsFrom MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.
There has been substantial evolution of the ability of coronary CT angiography (CCTA) to comprehensively image atherosclerosis. From its earliest incarnations imaging obstructive stenoses and coronary artery calcium (CAC), contemporary CCTA imaging can interrogate many characteristics of individual plaques and better characterize non-obstructive plaques.
From a clinical perspective, the role of this comprehensive evaluation of plaque characteristics in management is still in evolution. Also somewhat unsettled is the role of CAC imaging alone, and whether it can be used as a screen to assess who should move on to more comprehensive CCTA imaging (with its higher radiation exposure and need for contrast) in symptomatic patients as well as in asymptomatic patients.
In the current study, the authors use the CCTA and CAC data from the SCOT-HEART trial database (symptomatic patients with stable chest pain and suspected CAD) to examine the relationship between CAC and many other plaque characteristics, as well as to the 5-year outcomes. There were 2 fundamental findings of interest. First, 36% of the patients had a CAC score of zero. However, this did not preclude the presence of atherosclerosis, as 13% to 14% of those with CAC of zero had evidence of non-obstructive CAD and/or low attenuation plaque (potentially more unstable). The implication is that for symptomatic patients, CAC alone may be insufficient to identify very low risk patients and make decisions about more aggressive lipid lowering therapy. CAC alone may have a larger role in asymptomatic patients, to assist in decision making about primary prevention strategies.
The second finding of interest was that among those with high or very high CAC scores, well known to have a more unfavorable outcome, there was also a substantial burden of non-calcified low attenuation and higher risk plaques. Although we think of calcified plaques as those that are more stable, the higher risk of MI and CV death in such patients is suggested to be driven by the high burden of non-calcified high-risk plaques that accompany the CAC-causing plaques.
The large data set from this trial and others and the ever-evolving sophistication and comprehensiveness of analyses, such as this one, have contributed substantially to enhancing our understanding or coronary atherosclerosis and its management.