1 Department of Anesthesiology Washington University School of Medicine in St. Louis MO.
3 Cardiovascular Division Department of Internal Medicine Mayo Clinic and Medical School Rochester MN.
J Am Heart Assoc. 2019 Mar 19;8(6):e008626. doi: 10.1161/JAHA.118.008626.
Background The recent introduction of high-sensitivity cardiac troponin (hs-cTn) assays has allowed clinicians to measure hs-cTn before and after cardiac stress testing, but the hs-cTn release pattern and potential utility in identifying inducible myocardial ischemia are unclear. We thus conducted a systematic review and meta-analysis to improve our understanding of hs-cTn release associated with exercise and pharmacological stress testing. Methods and Results Studies published between January 2008 and July 2016 that reported hs-cTn change values (high-sensitivity cardiac troponin T [hs-cTnT] or high-sensitivity cardiac troponin I [hs-cTnI]) in relation to cardiac stress testing were searched and reviewed by 2 independent screeners. Primary outcomes were pooled estimates of absolute and relative hs-cTn changes after cardiac stress test, stratified by the presence of inducible myocardial ischemia. This meta-analysis included 11 studies (n=2432 patients). After exercise stress testing, hs-cTnT increased by 0.5 ng/L or 11% (6 studies, n=406) and hs-cTnI by 2.4 ng/L or 41% (4 studies, n=365) in patients with inducible myocardial ischemia versus hs-cTnT by 1.1 ng/L or 18% (8 studies, n=629; P=0.29) and hs-cTnI by 1.8 ng/L or 72% (4 studies, n=831; P=0.61) in patients who did not develop inducible myocardial ischemia. After pharmacological stress test, hs-cTnT changed by -0.1 ng/L or -0.4% (6 studies, n=251) and hs-cTnI by 2.4 ng/L or 32% (2 studies, n=108) in patients with inducible myocardial ischemia versus hs-cTnT by 0.7 ng/L or 11% (5 studies, n=443, P=0.44) and hs-cTnI by 1.7 ng/L or 38% (2 studies, n=116; P=0.62) in patients who did not develop inducible myocardial ischemia. Conclusions hs-cTn rising patterns after exercise and pharmacological stress testing appear inconsistent and comparably small, and do not appear to be correlated with inducible myocardial ischemia.
背景 高敏心肌肌钙蛋白（hs-cTn）检测方法的应用，使临床医生可以在心脏负荷试验前后测量 hs-cTn。但 hs-cTn 的释放模式以及在识别可诱导性心肌缺血中的潜在作用尚不清楚。因此，我们进行了一项系统评价和荟萃分析，以加深对运动和药物负荷试验相关 hs-cTn 释放的理解。
方法 本研究检索并回顾了 2008 年 1 月至 2016 年 7 月间发表的相关研究，这些研究报道了 hs-cTn 变化值（高敏肌钙蛋白 T [hs-cTnT]或高敏肌钙蛋白 I [hs-cTnI]）与心脏负荷试验的关系。2 位独立筛查者对主要结果进行了评估，即有无可诱导性心肌缺血患者心脏负荷试验后 hs-cTn 的绝对和相对变化的汇总估计值。该荟萃分析纳入了 11 项研究（n=2432 例患者）。与无可诱导性心肌缺血患者相比，运动负荷试验后 hs-cTnT 增加 0.5ng/L（6 项研究，n=406）或 11%，hs-cTnI 增加 2.4ng/L（4 项研究，n=365）或 41%；而 hs-cTnT 增加 1.1ng/L（8 项研究，n=629）或 18%，hs-cTnI 增加 1.8ng/L（4 项研究，n=831）或 72%（P=0.29）。药物负荷试验后，与无可诱导性心肌缺血患者相比，hs-cTnT 降低 0.1ng/L（6 项研究，n=251）或 0.4%，hs-cTnI 增加 2.4ng/L（2 项研究，n=108）或 32%；而 hs-cTnT 增加 0.7ng/L（5 项研究，n=443）或 11%，hs-cTnI 增加 1.7ng/L（2 项研究，n=116）或 38%（P=0.44）。
结论 运动和药物负荷试验后 hs-cTn 的升高模式似乎不一致且幅度较小，且与可诱导性心肌缺血无关。
