急性心肌梗死中心肌肌钙蛋白 I 清除更快、峰值更高的可能机制与肌钙蛋白 T 相比。

A Possible Mechanism behind Faster Clearance and Higher Peak Concentrations of Cardiac Troponin I Compared with Troponin T in Acute Myocardial Infarction.

机构信息

Department of Laboratory Medicine, Institute of Biomedicine, Sahlgrenska Academy, University of Gothenburg, Sahlgrenska University Hospital, Gothenburg, Sweden.

Department of Anesthesiology and Intensive Care Medicine, Institute of Clinical Sciences at the Sahlgrenska Academy, University of Gothenburg, Sahlgrenska University Hospital, Gothenburg, Sweden.

出版信息

Clin Chem. 2020 Feb 1;66(2):333-341. doi: 10.1093/clinchem/hvz003.

DOI:10.1093/clinchem/hvz003

PMID:32040581

Abstract

BACKGROUND

Although cardiac troponin I (cTnI) and troponin T (cTnT) form a complex in the human myocardium and bind to thin filaments in the sarcomere, cTnI often reaches higher concentrations and returns to normal concentrations faster than cTnT in patients with acute myocardial infarction (MI).

METHODS

We compared the overall clearance of cTnT and cTnI in rats and in patients with heart failure and examined the release of cTnT and cTnI from damaged human cardiac tissue in vitro.

RESULTS

Ground rat heart tissue was injected into the quadriceps muscle in rats to simulate myocardial damage with a defined onset. cTnT and cTnI peaked at the same time after injection. cTnI returned to baseline concentrations after 54 h, compared with 168 h for cTnT. There was no difference in the rate of clearance of solubilized cTnT or cTnI after intravenous or intramuscular injection. Renal clearance of cTnT and cTnI was similar in 7 heart failure patients. cTnI was degraded and released faster and reached higher concentrations than cTnT when human cardiac tissue was incubated in 37°C plasma.

CONCLUSION

Once cTnI and cTnT are released to the circulation, there seems to be no difference in clearance. However, cTnI is degraded and released faster than cTnT from necrotic cardiac tissue. Faster degradation and release may be the main reason why cTnI reaches higher peak concentrations and returns to normal concentrations faster in patients with MI.

摘要

背景

虽然心肌中的肌钙蛋白 I（cTnI）和肌钙蛋白 T（cTnT）形成复合物并与肌节中的细肌丝结合，但在急性心肌梗死（MI）患者中，cTnI 的浓度往往更高，恢复正常浓度的速度也比 cTnT 更快。

方法

我们比较了大鼠和心力衰竭患者中 cTnT 和 cTnI 的总体清除率，并在体外研究了 cTnT 和 cTnI 从受损人心肌组织中的释放。

结果

将大鼠的心肌组织研磨后注射到大鼠的股四头肌中，以模拟具有明确发病时间的心肌损伤。注射后 cTnT 和 cTnI 同时达到峰值。cTnI 在 54 小时后恢复到基线浓度，而 cTnT 则需要 168 小时。静脉或肌肉内注射后，溶解的 cTnT 或 cTnI 的清除率没有差异。7 例心力衰竭患者的 cTnT 和 cTnI 肾清除率相似。当将人心肌组织在 37°C 血浆中孵育时，cTnI 比 cTnT 更快地降解和释放，并且达到更高的浓度。