Heterogeneity in the Association Between the Presence of Coronary Artery Calcium and Cardiovascular Events: A Machine-Learning Approach in the MESA Study.
Heterogeneity in the Association Between the Presence of Coronary Artery Calcium and Cardiovascular Events: A Machine-Learning Approach in the MESA Study.
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DOI：
10.1161/circulationaha.122.062626
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发表时间：
2023-01-10
期刊：
影响因子：
37.8
通讯作者：
Watson, Karol E.
中科院分区：
文献类型：
--
作者：
Inoue, Kosuke;Seeman, Teresa E.;Horwich, Tamara;Budoff, Matthew J.;Watson, Karol E.
冠状动脉钙化（CAC）已被广泛认为是心血管疾病（CVD）的重要预测因子。鉴于资源有限，重要的是要确定谁将获得最大的好处，从检测阳性CAC筛查。然而，证据是有限的，积极的CAC对CVD的负担是否不同的多维个体特征。我们试图调查阳性CAC和CVD事件之间的关联的异质性。该队列研究纳入了来自梅萨（多种族动脉粥样硬化研究）的年龄≥45岁且无心血管疾病的成人。在以1：1的比例进行倾向评分匹配后，我们应用机器学习因果森林模型来（1）评估阳性CAC与CVD事件之间关联的异质性，以及（2）预测当CAC>0（相对于CAC=0）时，在个体水平上10年CVD风险的增加。然后，我们将CAC>0时CVD风险的估计增加与2013年美国心脏病学会/美国心脏协会汇总队列方程计算的10年动脉粥样硬化CVD（ASCVD）绝对风险进行了比较。在我们的倾向评分匹配分析中，我们的因果森林模型显示了CAC>0和CVD事件之间的关联的异质性。我们发现，当CAC>0时，估计CVD风险增加的剂量-反应关系具有较高的10年ASCVD风险。当CAC>0时，几乎所有ASCVD临界风险或更高的个体（2428例中的2293例[94.4%]）显示CVD风险增加≥2.5%。即使在900名ASCVD风险较低的成年人中，689名（69.2%）在CAC>0时显示CVD风险增加≥2.5%;这些个体更可能是男性，西班牙裔，并且比其他人有不利的CVD风险因素。当CAC>0时，CVD风险的预期增加在个体间是异质的。此外，当CAC>0时，近70%的ASCVD低风险人群显示CVD风险大幅增加，这突出了在这些低风险人群中进行CAC筛查的必要性。未来的研究需要评估CAC测量的目标个体是否不仅基于绝对ASCVD风险，而且还基于CAC>0时CVD风险的预期增加改善心血管结局。
Coronary artery calcium (CAC) has been widely recognized as an important predictor of cardiovascular disease (CVD). Given the finite resources, it is important to identify individuals who would receive the most benefit from detecting positive CAC by screening. However, the evidence is limited as to whether the burden of positive CAC on CVD differs by multidimensional individual characteristics. We sought to investigate the heterogeneity in the association between positive CAC and incident CVD. This cohort study included adults from MESA (Multi-Ethnic Study of Atherosclerosis) ages ≥45 years and free of cardiovascular disease. After propensity score matching in a 1:1 ratio, we applied a machine learning causal forest model to (1) evaluate the heterogeneity in the association between positive CAC and incident CVD, and (2) predict the increase in CVD risk at 10-years when CAC>0 (versus CAC=0) at the individual level. We then compared the estimated increase in CVD risk when CAC>0 to the absolute 10-year atherosclerotic CVD (ASCVD) risk calculated by the 2013 American College of Cardiology/American Heart Association pooled cohort equations. Across 3328 adults in our propensity score–matched analysis, our causal forest model showed the heterogeneity in the association between CAC>0 and incident CVD. We found a dose–response relationship of the estimated increase in CVD risk when CAC>0 with higher 10-year ASCVD risk. Almost all individuals (2293 of 2428 [94.4%]) with borderline risk of ASCVD or higher showed ≥2.5% increase in CVD risk when CAC>0. Even among 900 adults with low ASCVD risk, 689 (69.2%) showed ≥2.5% increase in CVD risk when CAC>0; these individuals were more likely to be male, Hispanic, and have unfavorable CVD risk factors than others. The expected increases in CVD risk when CAC>0 were heterogeneous across individuals. Moreover, nearly 70% of people with low ASCVD risk showed a large increase in CVD risk when CAC>0, highlighting the need for CAC screening among such low-risk individuals. Future studies are needed to assess whether targeting individuals for CAC measurements based on not only the absolute ASCVD risk but also the expected increase in CVD risk when CAC>0 improves cardiovascular outcomes.