Department of Internal Medicine, University Hospital Basel, Switzerland.
Am J Med. 2012 May;125(5):491-498.e1. doi: 10.1016/j.amjmed.2011.10.031.
It is unknown to what extent noncardiac causes, including renal dysfunction, may contribute to high-sensitivity cardiac troponin T levels.
In an observational international multicenter study, we enrolled consecutive patients presenting with acute chest pain to the emergency department. Of 1181 patients enrolled, 572 were adjudicated by 2 independent cardiologists to have a noncardiac cause of chest pain. Multiple linear regression analyses were used to determine the important predictors of log-transformed high-sensitivity cardiac troponin T. Kaplan-Meier curve was used to assess the prognostic significance of high-sensitivity cardiac troponin T>0.014 μg/L (99th percentile).
A total of 88 patients (15%) had high-sensitivity cardiac troponin T>0.014 μg/L. Less than 50% of cardiac troponins could be explained by known cardiac or noncardiac diseases. In decreasing order of importance, age, estimated glomerular filtration rate, hypertension, previous myocardial infarction, and chronic kidney disease (adjusted r(2) 0.44) emerged as significant factors in linear regression analysis to predict high-sensitivity cardiac troponin T. High-sensitivity cardiac troponin T was best explained by a linear curve with age as ≤0.014 μg/L. Patients with high-sensitivity cardiac troponin T levels>0.014 μg/L were at increased risk for all-cause mortality (hazard ratio 3.0; 95% confidence interval, 0.8-10.6; P=.02) during follow-up.
Among the known covariates, age and not renal dysfunction is the most important determinant of high-sensitivity cardiac troponin T. Because known cardiac and noncardiac factors, including renal dysfunction, explain less than 50% of high-sensitivity cardiac troponin T levels among patients with a noncardiac cause of chest pain, unknown or underestimated cardiac involvement during the acute presenting condition seems to be the major cause of elevated high-sensitivity cardiac troponin T.
目前尚不清楚包括肾功能不全在内的非心脏原因在多大程度上可能导致高敏心肌肌钙蛋白 T 水平升高。
在一项观察性的国际多中心研究中，我们连续纳入因急性胸痛就诊于急诊科的患者。在纳入的 1181 例患者中，有 572 例由 2 位独立的心脏病专家判定为胸痛的非心脏原因。采用多元线性回归分析确定高敏心肌肌钙蛋白 T 的对数转换的重要预测因子。Kaplan-Meier 曲线用于评估高敏心肌肌钙蛋白 T＞0.014μg/L（第 99 百分位数）的预后意义。
共有 88 例患者（15%）的高敏心肌肌钙蛋白 T＞0.014μg/L。不到 50%的心肌肌钙蛋白可以用已知的心脏或非心脏疾病来解释。按重要性降序排列，年龄、估计肾小球滤过率、高血压、既往心肌梗死和慢性肾脏病（校正 r（2）为 0.44）在多元线性回归分析中是预测高敏心肌肌钙蛋白 T 的重要因素。高敏心肌肌钙蛋白 T 与年龄呈线性关系，以年龄≤0.014μg/L 时最佳。高敏心肌肌钙蛋白 T 水平＞0.014μg/L 的患者在随访期间全因死亡率增加（风险比 3.0；95%置信区间，0.8-10.6；P=0.02）。
在已知的混杂因素中，年龄而非肾功能不全是高敏心肌肌钙蛋白 T 的最重要决定因素。由于已知的心脏和非心脏因素，包括肾功能不全，仅能解释胸痛非心脏原因患者中不到 50%的高敏心肌肌钙蛋白 T 水平，在急性发病时未知或低估的心脏受累似乎是导致高敏心肌肌钙蛋白 T 升高的主要原因。
