Ansari Salman, Trujillo Robert, McClelland Robyn L, Budoff Matthew J
California University of Science and Medicine - School of Medicine, Colton, CA, USA.
Department of Biostatistics, University of Washington, Seattle, WA, USA.
Int J Cardiovasc Imaging. 2025 Jul 22. doi: 10.1007/s10554-025-03462-2.
Cigarette smoking is a known contributor to cardiovascular disease (CVD) and is associated with increased prevalence of coronary artery calcium. However, despite this clinical significance, calcium deposition in other vascular beds, specifically the aortic arch, has yet to be thoroughly investigated among cigarette smokers.The study population comprised participants who underwent non-contrast chest CT scans in MESA exam 5 (2010-2012). Aortic arch calcium (AAC) is defined as calcification in the transverse aortic arch, as measured using the Agatston method on chest CT scans. Log-transformed AAC scores were used for all analyses. Multivariable linear regression models were fit to assess the relationship between log-AAC and cigarette smoking status (never-smoked, former smoker, current smoker). Cox proportional hazard models were fit to investigate the relationship between log-AAC and incident CVD and mortality for those with a history of smoking (former & current smokers). All models were adjusted for demographic and traditional clinical risk factors. After excluding those with missing variables or prevalent CVD prior to the chest CT, 2,191 participants were included in the final analysis, of which 1,091 self-identified as never smokers, 918 as former smokers, and 182 as current smokers. Estimated mean log-AAC was 0.58 (p < 0.001) log-Agatston units higher in former smokers compared with never smokers [95% CI: 0.40-0.77], and 1.10 (p < 0.001) log-Agatston units higher in current smokers compared with never smokers [95% CI: 0.76-1.40]. Among ever-smokers (current or former smokers), a one log-Agatston unit increase in AAC was associated with a 20.6% (p = 0.002) greater risk for CVD events [95% CI: 7.4 - 35.5%] and a 12% (p = 0.020) greater risk for mortality [95% CI: 2 - 23%]. This study demonstrated an association between cigarette smoking and AAC scores, with significant differences in AAC among current, former, and never smokers. Furthermore, AAC is associated with incident cardiovascular events and mortality among those with a history of smoking.
吸烟是心血管疾病（CVD）的一个已知诱因，且与冠状动脉钙化患病率增加有关。然而，尽管具有这一临床意义，但在吸烟者中，其他血管床（特别是主动脉弓）的钙沉积尚未得到充分研究。研究人群包括在MESA检查5（2010 - 2012年）中接受非增强胸部CT扫描的参与者。主动脉弓钙化（AAC）定义为横断主动脉弓的钙化，通过胸部CT扫描上的阿加斯顿方法进行测量。所有分析均使用对数转换后的AAC分数。采用多变量线性回归模型来评估对数转换后的AAC与吸烟状态（从不吸烟、既往吸烟者、当前吸烟者）之间的关系。采用Cox比例风险模型来研究对数转换后的AAC与有吸烟史（既往吸烟者和当前吸烟者）者发生CVD和死亡率之间的关系。所有模型均针对人口统计学和传统临床风险因素进行了调整。在排除胸部CT检查前有变量缺失或患有CVD的参与者后，最终分析纳入了2191名参与者，其中1091人自称从不吸烟，918人是既往吸烟者，182人是当前吸烟者。与从不吸烟者相比，既往吸烟者的估计平均对数转换后的AAC高0.58（p < 0.001）阿加斯顿对数单位[95%置信区间：0.40 - 0.77]，与从不吸烟者相比，当前吸烟者的估计平均对数转换后的AAC高1.10（p < 0.001）阿加斯顿对数单位[95%置信区间：0.76 - 1.40]。在曾经吸烟者（当前吸烟者或既往吸烟者）中，AAC每增加一个阿加斯顿对数单位，发生CVD事件的风险增加20.6%（p = 0.002）[95%置信区间：7.4 - 35.5%]，死亡风险增加12%（p = 0.020）[95%置信区间：2 - 23%]。这项研究表明吸烟与AAC分数之间存在关联，当前吸烟者、既往吸烟者和从不吸烟者之间的AAC存在显著差异。此外，在有吸烟史者中，AAC与发生心血管事件和死亡率有关。
