Troponin and Cardiac Events in Stable Ischemic Heart Disease and Diabetes.
Troponin and Cardiac Events in Stable Ischemic Heart Disease and Diabetes.
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DOI：
10.1056/nejmoa1415921
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发表时间：
2015-08-13
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影响因子：
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通讯作者：
BARI 2D Study Group
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作者：
Everett BM;Brooks MM;Vlachos HE;Chaitman BR;Frye RL;Bhatt DL;BARI 2D Study Group
心肌肌钙蛋白浓度可用于鉴别急性冠脉综合征患者是否能从紧急血运重建中获益。我们假设它们可能用于稳定性缺血性心脏病患者，以确定那些心血管事件的高风险患者，这些患者也可能从及时的冠状动脉血运重建中获益。我们采用高灵敏度测定法测量了2285例2型糖尿病和稳定性缺血性心脏病患者的基线心肌肌钙蛋白T浓度，这些患者均参加了2型糖尿病旁路血管成形术血运重建研究试验。我们检测了肌钙蛋白T浓度与心血管原因、心肌梗死或卒中死亡复合终点之间的相关性;然后我们评估了随机分配到即时血运重建是否降低了肌钙蛋白T浓度异常（≥14 ng/L）患者与肌钙蛋白T浓度正常（<14 ng/L）患者的复合终点发生率。在2285例患者中，2277例（99.6%）基线时肌钙蛋白T浓度可检测（≥3 ng/L），897例（39.3%）基线时肌钙蛋白T浓度异常。在基线肌钙蛋白T浓度异常的患者中，复合终点的5年发生率为27.1%，而在基线肌钙蛋白T浓度正常的患者中，复合终点的5年发生率为12.9%。在校正了心血管危险因素、糖尿病严重程度、心电图异常和冠状动脉解剖结构的模型中，肌钙蛋白T浓度异常患者的复合终点风险比为1.85（95%置信区间[CI]，1.48 - 2.32; P<0.001）。在肌钙蛋白T浓度异常的患者中，与单独药物治疗相比，随机分配至迅速血运重建组并未导致复合终点发生率显著降低（风险比，0.96; 95%CI，0.74 - 1.25）。心肌肌钙蛋白T浓度是2型糖尿病和稳定性缺血性心脏病患者心血管原因、心肌梗死或卒中死亡的独立预测因子。异常肌钙蛋白T值为14 ng/L或更高并不能确定一个亚组的患者受益于随机分配，以促进冠状动脉血运重建。（由美国国立卫生研究院和罗氏诊断公司资助;巴里二维ClinicalTrials.gov编号，NCT 00006305。）
Cardiac troponin concentrations are used to identify patients who would benefit from urgent revascularization for acute coronary syndromes. We hypothesized that they might be used in patients with stable ischemic heart disease to identify those at high risk for cardiovascular events who might also benefit from prompt coronary revascularization. We measured the cardiac troponin T concentration at baseline with a high-sensitivity assay in 2285 patients who had both type 2 diabetes and stable ischemic heart disease and were enrolled in the Bypass Angioplasty Revascularization Investigation in Type 2 Diabetes trial. We tested for an association between the troponin T concentration and a composite end point of death from cardiovascular causes, myocardial infarction, or stroke; we then evaluated whether random assignment to prompt revascularization reduced the rate of the composite end point in patients with an abnormal troponin T concentration (≥14 ng per liter) as compared with those with a normal troponin T concentration (<14 ng per liter). Of the 2285 patients, 2277 (99.6%) had detectable (≥3 ng per liter) troponin T concentrations and 897 (39.3%) had abnormal troponin T concentrations at baseline. The 5-year rate of the composite end point was 27.1% among the patients who had had abnormal troponin T concentrations at baseline, as compared with 12.9% among those who had had normal baseline troponin T concentrations. In models that were adjusted for cardiovascular risk factors, severity of diabetes, electrocardiographic abnormalities, and coronary anatomy, the hazard ratio for the composite end point among patients with abnormal troponin T concentrations was 1.85 (95% confidence interval [CI], 1.48 to 2.32; P<0.001). Among patients with abnormal troponin T concentrations, random assignment to prompt revascularization, as compared with medical therapy alone, did not result in a significant reduction in the rate of the composite end point (hazard ratio, 0.96; 95% CI, 0.74 to 1.25). The cardiac troponin T concentration was an independent predictor of death from cardiovascular causes, myocardial infarction, or stroke in patients who had both type 2 diabetes and stable ischemic heart disease. An abnormal troponin T value of 14 ng per liter or higher did not identify a subgroup of patients who benefited from random assignment to prompt coronary revascularization. (Funded by the National Institutes of Health and Roche Diagnostics; BARI 2D ClinicalTrials.gov number, NCT00006305.)