急性冠状动脉综合征和非急性冠状动脉综合征患者的临床概况和肌钙蛋白 I 的敏感性:一项观察性研究。

Shruthi M Kulkarni, Rashmi Roongta, Seena Sankar
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TnI was used as the index test of sensitivity to diagnose ACS and either echocardiography or coronary angiogram in those available as the reference gold standard. They were classified into two groups of normal and elevated TnI, and further divided into those with ACS and no ACS. Data on clinical parameters and aetiology of elevated TnI in patients without ACS were analysed. Results Of the 254 patients studied, 114 patients (45%) had normal TnI and 140 (55%) had elevated TnI. Seventy-eight patients had ACS, 66 (84.6%) of whom had elevated TnI and 12 (15.38%) had normal TnI. Seventy-four (52.85%) of 140 patients with elevated TnI had alternate causes of TnI elevation; the most common being sepsis, acute kidney injury (AKI) and heart failure without ACS. All-cause mortality was significantly higher in patients with elevated TnI with or without ACS. There was no cardiac mortality among patients with ACS with normal TnI. 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引用次数: 0

摘要

背景 在没有心肌缺血的情况下,各种临床症状都可能导致肌钙蛋白升高。肌钙蛋白升高代表可能发生了心肌坏死,其本身并不能说明病因。确定肌钙蛋白升高的原因及其在预测急性冠状动脉综合征(ACS)和心脏病死亡率方面的敏感性和特异性,是确定这些患者最佳治疗方法的重要一步。方法 我们回顾性地收集了在急诊科、内科病房、冠心病监护病房(CCU)或重症监护病房(ICU)接受肌钙蛋白 I(TnI)检测作为临床评估一部分并最终确诊的住院患者的数据。TnI被用作诊断ACS的敏感性指标,而超声心动图或冠状动脉造影则被用作诊断ACS的参考金标准。他们被分为 TnI 正常和升高两组,并进一步分为有 ACS 和无 ACS 两组。分析了无 ACS 患者的临床参数和 TnI 升高的病因。结果 在研究的 254 例患者中,114 例(45%)TnI 正常,140 例(55%)TnI 升高。78 名患者患有 ACS,其中 66 人(84.6%)TnI 升高,12 人(15.38%)TnI 正常。在 140 名 TnI 升高的患者中,有 74 人(52.85%)的 TnI 升高有其他原因;最常见的原因是败血症、急性肾损伤 (AKI) 和无 ACS 的心力衰竭。无论是否患有 ACS,TnI 升高患者的全因死亡率都明显较高。在 TnI 正常的 ACS 患者中,没有心脏病死亡率。TnI 预测 ACS 的敏感性和特异性分别为 84.6%(95% CI 74.7%-91.8%)和 58%(95% CI 50.3%-65.3%)。结论 除心肌梗死外,多种疾病都可能导致 TnI 升高。因此,鉴于 TnI 的特异性较低,在缺乏其他支持证据的情况下,根据 TnI 值诊断 ACS 患者时应谨慎。无论病因如何,TnI 升高都预示着预后较差,并可用于预测全因死亡率和心源性死亡率。
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Clinical profile of patients and sensitivity of troponin I in patients with and without acute coronary syndrome: An observational study.

Background Various clinical conditions can cause troponin elevation in the absence of myocardial ischaemia. Elevated troponin represents the likely occurrence of myocardial necrosis and does not itself provide any indication of the aetiology. Identifying the cause for troponin elevation and its sensitivity and specificity in predicting acute coronary syndrome (ACS) and cardiac mortality is an important step in determining the optimal management for these patients. Methods We retrospectively collected data of inpatients who had troponin I (TnI) testing as part of their clinical assessment, either in the emergency department, medical wards, coronary care unit (CCU) or intensive care unit (ICU) with their final diagnosis. TnI was used as the index test of sensitivity to diagnose ACS and either echocardiography or coronary angiogram in those available as the reference gold standard. They were classified into two groups of normal and elevated TnI, and further divided into those with ACS and no ACS. Data on clinical parameters and aetiology of elevated TnI in patients without ACS were analysed. Results Of the 254 patients studied, 114 patients (45%) had normal TnI and 140 (55%) had elevated TnI. Seventy-eight patients had ACS, 66 (84.6%) of whom had elevated TnI and 12 (15.38%) had normal TnI. Seventy-four (52.85%) of 140 patients with elevated TnI had alternate causes of TnI elevation; the most common being sepsis, acute kidney injury (AKI) and heart failure without ACS. All-cause mortality was significantly higher in patients with elevated TnI with or without ACS. There was no cardiac mortality among patients with ACS with normal TnI. Sensitivity and specificity of TnI for predicting ACS was 84.6% (95% CI 74.7%-91.8%) and 58% (95% CI 50.3%-65.3%), respectively. Conclusion A variety of conditions apart from myocardial infarction can lead to elevated TnI. Hence, caution should be exercised while diagnosing a patient with ACS based on TnI value in the absence of other supporting evidence given its low specificity. Elevated TnI portends a worse prognosis regardless of the aetiology and has a role in predicting all-cause and cardiac mortality.

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