Use of High-Sensitivity Cardiac Troponin for the Exclusion of Inducible Myocardial Ischemia: A Cohort Study.

Use of High-Sensitivity Cardiac Troponin for the Exclusion of Inducible Myocardial Ischemia: A Cohort Study.
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DOI:
10.7326/m18-0670
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发表时间:
2018-12-04
影响因子:
39.2
通讯作者:
Quyyumi AA
Quyyumi AA
中科院分区:
医学1区
文献类型:
--
作者:
Hammadah M;Kim JH;Tahhan AS;Kindya B;Liu C;Ko YA;Al Mheid I;Wilmot K;Ramadan R;Alkhoder A;Choudhary F;Gafeer MM;Abdelhadi N;Pimple P;Sandesara P;Lima BB;Shah AJ;Ward L;Kutner M;Bremner JD;Sheps DS;Raggi P;Sperling LS;Vaccarino V;Quyyumi AA

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许多冠状动脉疾病(CAD)患者被常规转介进行监测负荷测试,尽管有反对的建议。目的:确定低水平静息高敏感性心肌肌钙蛋白I(hs-cTnI)是否能识别无诱发性心肌缺血的患者。观察性研究。一个大学附属医院网络。冠心病稳定的人:衍生组中有589人,验证队列中有118人。在跑台试验或药物负荷试验中,用~(99m)Tm单光子发射计算机断层扫描进行心肌灌注成像,以确定是否存在诱发性心肌缺血。在负荷试验后1周内测定静息血浆hs-cTnI,并计算诱发缺血的阴性预测值(NPV)。对发生心血管死亡和心肌梗死的衍生队列进行了3年的跟踪调查。在衍生队列中,101例hs-cTnI水平低于2.5pg/mL的患者中,有10例存在诱导性心肌缺血(NPV,90%[95%CI,83%至95%]),101例患者中有3例(NPV,97%[CI,92%至99%])至少累及10%的心肌。在验证队列中,hs-cTnI水平低于2.5pg/mL的32例患者中有4例存在诱导性缺血(NPV,88%[CI,71%至96%]),32例患者中有2例存在10%或更高的缺血(NPV,94%[CI,79%至99%])。经过中位数3年的随访,hs-cTnI水平低于2.5pg/m L的患者没有发生不良事件,相比之下,hs-cTnI水平在2.5pg/m L或以上的患者中有33例(7%)心血管死亡或发生心肌梗死。这些数据可能不适用于没有已知冠心病的人群或不稳定型心绞痛患者,适度的样本量保证了在更大的队列中进一步验证。非常低的hs-cTnI水平可能有助于排除稳定性冠心病患者的诱发性心肌缺血。美国国立卫生研究院。
Many patients with coronary artery disease (CAD) are routinely referred for surveillance stress testing despite recommendations against it. To determine whether low levels of resting high-sensitivity cardiac troponin I (hs-cTnI) can identify persons without inducible myocardial ischemia. Observational study. A university-affiliated hospital network. Persons with stable CAD: 589 in the derivation group and 118 in the validation cohort. Presence of inducible myocardial ischemia was determined by myocardial perfusion imaging with technetium-99m single-photon emission computed tomography during either treadmill or pharmacologic stress testing. Resting plasma hs-cTnI was measured within 1 week of the stress test, and the negative predictive value (NPV) for inducible ischemia was calculated. The derivation cohort was followed for 3 years for incident cardiovascular death and myocardial infarction. In the derivation cohort, 10 of 101 patients with an hs-cTnI level below 2.5 pg/mL had inducible myocardial ischemia (NPV, 90% [95% CI, 83% to 95%]) and 3 of 101 had inducible ischemia involving at least 10% of the myocardium (NPV, 97% [CI, 92% to 99%]). In the validation cohort, 4 of 32 patients with an hs-cTnI level below 2.5 pg/mL had inducible ischemia (NPV, 88% [CI, 71% to 96%]) and 2 of 32 had ischemia of 10% or greater (NPV, 94% [CI, 79% to 99%]). After a median follow-up of 3 years in the derivation cohort, no adverse events occurred in patients with an hs-cTnI level below 2.5 pg/mL, compared with 33 (7%) cardiovascular deaths or incident myocardial infarctions among those with an hs-cTnI level of 2.5 pg/mL or greater. The data may not be applicable to a population without known CAD or to persons with unstable angina, and the modest sample sizes warrant further validation in a larger cohort. Very low hs-cTnI levels may be useful in excluding inducible myocardial ischemia in patients with stable CAD. National Institutes of Health.