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C 反应蛋白在预测心梗后左心室收缩功能障碍和心力衰竭中的作用。

The usefulness of C-reactive protein for the prediction of post-infarct left ventricular systolic dysfunction and heart failure.

机构信息

Department of Cardiology and Internal Medicine, Collegium Medicum, Nicolaus Copernicus University, Bydgoszcz, Poland.

出版信息

Kardiol Pol. 2018;76(5):821-829. doi: 10.5603/KP.a2018.0091. Epub 2018 Apr 10.

Abstract

Acute myocardial infarction (MI) provokes a systemic inflammatory response that may contribute to the development of left ventricular systolic dysfunction (LVSD) and heart failure (HF). Patients with post-infarct HF with concomitant LVSD have the most unfavourable long-term prognosis. Measurement of C-reactive protein (CRP) concentration reflecting an involvement of inflammatory pathways in post-infarct myocardial damage offers an attractive strategy to improve risk stratification and clinical decision-making for early management of high-risk patients. Despite growing evidence for the prognostic value of CRP both as a single factor and as a component of multi-marker approach in MI, CRP measurement is not yet incorporated into current guidelines. This may be due to conflicting results reported in existing studies related to various limitations in study designs, such as retrospective case control design, prior myocardial damage, CRP measurement with low-sensitivity assays, non-homogenous populations with acute coronary syndromes, different treatment strategies, small sample sizes, and the lack of left ventricular ejection fraction assessment and long-term clinical and echocardiographic monitoring. As a result, previous studies have not provided conclusive evidence of the prognostic value of CRP for post-infarct LVSD or HF. Future studies with an adequate design including upstream mediators of inflammation as inflammatory markers are needed to identify the best biomarker-based strategies for identifying high-risk patients. Further clinical trials involving anti-inflammatory therapies target-ing different pathways of inflammatory activation in MI should test the inflammatory hypothesis of post-infarct LVSD and HF. Identifying high-risk patients with persistent post-infarct inflammatory response may allow incorporation of pathophysiological guidance for implementation of personalised treatment approaches.

摘要

急性心肌梗死(MI)会引发全身性炎症反应,这可能导致左心室收缩功能障碍(LVSD)和心力衰竭(HF)的发展。伴有 LVSD 的梗死后 HF 患者的长期预后最差。测量反映炎症途径参与梗死后心肌损伤的 C 反应蛋白(CRP)浓度提供了一种有吸引力的策略,可以改善风险分层,并为高危患者的早期管理提供临床决策。尽管 CRP 作为单一因素以及作为 MI 多指标方法的组成部分的预后价值的证据不断增加,但 CRP 测量尚未纳入当前指南。这可能是由于现有研究报告的结果存在冲突,这些研究存在研究设计方面的各种局限性,例如回顾性病例对照设计、先前存在心肌损伤、使用低灵敏度检测方法测量 CRP、急性冠状动脉综合征人群不均一、不同的治疗策略、样本量小以及缺乏左心室射血分数评估和长期临床及超声心动图监测。因此,以前的研究并未为 CRP 对梗死后 LVSD 或 HF 的预后价值提供确凿的证据。需要进行设计合理的未来研究,包括将炎症的上游介质作为炎症标志物,以确定基于最佳生物标志物的策略,用于识别高危患者。进一步的临床试验涉及针对 MI 中炎症激活不同途径的抗炎治疗,应测试梗死后 LVSD 和 HF 的炎症假说。确定持续存在梗死后炎症反应的高危患者,可能允许纳入病理生理学指导,以实施个性化治疗方法。

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