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高敏心肌肌钙蛋白与心肌梗死的通用定义。

High-Sensitivity Cardiac Troponin and the Universal Definition of Myocardial Infarction.

机构信息

BHF Centre for Cardiovascular Science (A.R.C., P.D.A., A.S.V.S., A.A., F.E.S., A.V.F., K.K.L., K.A.A.F., D.E.N., N.L.M.), University of Edinburgh, United Kingdom.

Christchurch Heart Institute, University of Otago, New Zealand (P.D.A.).

出版信息

Circulation. 2020 Jan 21;141(3):161-171. doi: 10.1161/CIRCULATIONAHA.119.042960. Epub 2019 Oct 7.

DOI:10.1161/CIRCULATIONAHA.119.042960
PMID:31587565
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6970546/
Abstract

BACKGROUND

The introduction of more sensitive cardiac troponin assays has led to increased recognition of myocardial injury in acute illnesses other than acute coronary syndrome. The Universal Definition of Myocardial Infarction recommends high-sensitivity cardiac troponin testing and classification of patients with myocardial injury based on pathogenesis, but the clinical implications of implementing this guideline are not well understood.

METHODS

In a stepped-wedge cluster randomized, controlled trial, we implemented a high-sensitivity cardiac troponin assay and the recommendations of the Universal Definition in 48 282 consecutive patients with suspected acute coronary syndrome. In a prespecified secondary analysis, we compared the primary outcome of myocardial infarction or cardiovascular death and secondary outcome of noncardiovascular death at 1 year across diagnostic categories.

RESULTS

Implementation increased the diagnosis of type 1 myocardial infarction by 11% (510/4471), type 2 myocardial infarction by 22% (205/916), and acute and chronic myocardial injury by 36% (443/1233) and 43% (389/898), respectively. Compared with those without myocardial injury, the rate of the primary outcome was highest in those with type 1 myocardial infarction (cause-specific hazard ratio [HR] 5.64 [95% CI, 5.12-6.22]), but was similar across diagnostic categories, whereas noncardiovascular deaths were highest in those with acute myocardial injury (cause specific HR 2.65 [95% CI, 2.33-3.01]). Despite modest increases in antiplatelet therapy and coronary revascularization after implementation in patients with type 1 myocardial infarction, the primary outcome was unchanged (cause specific HR 1.00 [95% CI, 0.82-1.21]). Increased recognition of type 2 myocardial infarction and myocardial injury did not lead to changes in investigation, treatment or outcomes.

CONCLUSIONS

Implementation of high-sensitivity cardiac troponin assays and the recommendations of the Universal Definition of Myocardial Infarction identified patients at high-risk of cardiovascular and noncardiovascular events but was not associated with consistent increases in treatment or improved outcomes. Trials of secondary prevention are urgently required to determine whether this risk is modifiable in patients without type 1 myocardial infarction.

CLINICAL TRIAL REGISTRATION

https://www.clinicaltrials.gov. Unique identifier: NCT01852123.

摘要

背景

更敏感的心肌肌钙蛋白检测方法的引入导致在急性冠状动脉综合征以外的急性疾病中发现心肌损伤的情况增多。心肌梗死的通用定义推荐使用高敏心肌肌钙蛋白检测,并根据发病机制对心肌损伤患者进行分类,但人们对实施该指南的临床意义还不太了解。

方法

在一项逐步楔形群随机对照试验中,我们在连续 48282 例疑似急性冠状动脉综合征患者中实施了高敏心肌肌钙蛋白检测和通用定义的建议。在预先设定的二次分析中,我们比较了 1 年时的主要结局(心肌梗死或心血管死亡)和次要结局(非心血管死亡)在不同诊断类别中的差异。

结果

实施该方案使 1 型心肌梗死的诊断增加了 11%(510/4471),2 型心肌梗死增加了 22%(205/916),急性和慢性心肌损伤分别增加了 36%(443/1233)和 43%(389/898)。与无心肌损伤的患者相比,1 型心肌梗死患者的主要结局发生率最高(特定病因风险比[HR] 5.64 [95% CI,5.12-6.22]),但不同诊断类别之间的发生率相似,而急性心肌损伤患者的非心血管死亡发生率最高(特定病因 HR 2.65 [95% CI,2.33-3.01])。尽管在实施 1 型心肌梗死患者的治疗方案后,抗血小板治疗和冠状动脉血运重建适度增加,但主要结局并未改变(特定病因 HR 1.00 [95% CI,0.82-1.21])。识别出 2 型心肌梗死和心肌损伤的患者虽然发生心血管和非心血管事件的风险较高,但并未导致检查、治疗或结局的改变。

结论

实施高敏心肌肌钙蛋白检测和心肌梗死的通用定义可以识别出发生心血管和非心血管事件风险较高的患者,但并未与治疗的一致性增加或改善结局相关。迫切需要进行二级预防试验,以确定在没有 1 型心肌梗死的患者中,这种风险是否可以改变。

临床试验注册

https://www.clinicaltrials.gov。唯一标识符:NCT01852123。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/759f/6970546/3a0c4438bc62/cir-141-161-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/759f/6970546/0c0b3e4fdf4d/cir-141-161-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/759f/6970546/c3e368b7bda6/cir-141-161-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/759f/6970546/1365e5d39f48/cir-141-161-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/759f/6970546/3a0c4438bc62/cir-141-161-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/759f/6970546/0c0b3e4fdf4d/cir-141-161-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/759f/6970546/c3e368b7bda6/cir-141-161-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/759f/6970546/1365e5d39f48/cir-141-161-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/759f/6970546/3a0c4438bc62/cir-141-161-g006.jpg

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