Emory Clinical Cardiovascular Research Institute, Department of Medicine, Division of Cardiology, Emory University School of Medicine, Atlanta, Georgia; Department of Epidemiology, Rollins School of Public Health, Emory University, Atlanta, Georgia.
Emory Clinical Cardiovascular Research Institute, Department of Medicine, Division of Cardiology, Emory University School of Medicine, Atlanta, Georgia.
Am J Cardiol. 2020 Dec 1;136:1-8. doi: 10.1016/j.amjcard.2020.09.019. Epub 2020 Sep 15.
High sensitive cardiac troponin I (hs-cTnI) increases with inducible myocardial ischemia in patients with coronary artery disease (CAD). We aimed to assess if the change in hs-cTnI levels with exercise stress testing is associated with major adverse cardiac events (MACE). A cohort of 365 (age 62 ± 9 years, 77% men) patients with stable CAD underwent 99mTc sestamibi myocardial perfusion imaging with treadmill testing. Plasma hs-cTnI level was measured at rest and at 45 min after stress. Multivariable Fine & Gray's subdistribution hazards models were used to determine the association between the change in hs-cTnI and MACE, a composite end point of cardiovascular death, myocardial infarction, and unstable angina requiring revascularization. During a median follow-up of 3 years, 39 (11%) patients experienced MACE. After adjustment, for each two-fold increment in hs-cTnI with stress, there was a 2.2 (95% confidence interval 1.3-3.6)-fold increase in the hazard for MACE. Presence of both a high resting hs-cTnI level (>median) and ≥ 20% stress-induced hs-cTnI elevation was associated with the highest incidence of MACE (subdistribution hazards models 4.6, 95% confidence interval 1.6 to 13.0) compared with low levels of both. Risk discrimination statistics significantly improved after addition of resting and change in hs-cTnI levels to a model including traditional risk factors and inducible ischemia (0.67 to 0.71). Conversely, adding inducible ischemia by SPECT did not significantly improve the C-statistic from a model including traditional risk factors, baseline and change in hs-cTnI (0.70 to 0.71). In stable CAD patients, higher resting levels and elevation of hs-cTnI with exercise are predictors of adverse cardiovascular outcomes beyond traditional cardiovascular risk factors and presence of inducible ischemia.
高敏心肌肌钙蛋白 I（hs-cTnI）在患有冠状动脉疾病（CAD）的患者中随可诱导性心肌缺血而增加。我们旨在评估运动应激试验中 hs-cTnI 水平的变化是否与主要不良心脏事件（MACE）相关。一个由 365 名（年龄 62 ± 9 岁，77%为男性）稳定型 CAD 患者组成的队列接受了 99mTc sestamibi 心肌灌注成像和跑步机测试。在休息时和应激后 45 分钟测量血浆 hs-cTnI 水平。使用多变量 Fine & Gray 亚分布风险模型来确定 hs-cTnI 变化与 MACE（心血管死亡、心肌梗死和需要血运重建的不稳定型心绞痛的复合终点）之间的关联。在中位数为 3 年的随访期间，39 名（11%）患者发生了 MACE。经过调整，hs-cTnI 在应激时每增加两倍，MACE 的风险就增加 2.2 倍（95%置信区间 1.3-3.6）。高静息 hs-cTnI 水平（>中位数）和≥20%的应激诱导 hs-cTnI 升高的存在与 MACE 的最高发生率相关（亚分布风险模型 4.6，95%置信区间 1.6 至 13.0），与两者低值相比。在包含传统危险因素和诱发性缺血的模型中加入静息和 hs-cTnI 水平后，风险判别统计数据显著改善（从 0.67 增加到 0.71）。相反，在包含传统危险因素、基线和 hs-cTnI 变化的模型中添加 SPECT 诱导的缺血并不能显著提高 C 统计量（从 0.70 增加到 0.71）。在稳定型 CAD 患者中，较高的静息水平和运动时 hs-cTnI 的升高是传统心血管危险因素和诱发性缺血存在之外不良心血管结局的预测因素。
