Inflammation in acute coronary syndromes
Inflammation in acute coronary syndromes
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DOI：
10.36503/chcmj1(1)-03
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发表时间：
2004
期刊：
影响因子：
--
通讯作者：
A. Maseri;D. Cianflone
中科院分区：
文献类型：
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作者：
A. Maseri;D. Cianflone
炎症作为缺血性心脏病的一种可能的致病成分和治疗靶点，正成为一个有趣的研究热点。然而，炎症和缺血性心脏病之间的潜在联系至少存在于三个层面。首先，多年来人们已经知道炎症反应在缺血/再灌注损伤中起主要作用，减少炎症反应可以限制心肌损伤[1]。其次，炎症是慢性动脉粥样硬化过程的一个非常常见的特征，Virchow于1856年首次描述了这一点，最近由Ross[3]进行了全面的综述。最后，在大约一半的急性冠脉综合征（ACS）患者中，炎症可能是不稳定的急性致病因素，独立于动脉粥样硬化和缺血负担bbb。可能有几种实际的炎症触发因素，个体炎症反应可能不同，并且在流行病学研究中，炎症与心血管事件发展相关的机制可能是多种的，并且不一定在所有患者中都相同。炎症反应可能通过调节某些个体的缺血和坏死的后果，通过突然发展的不稳定性，或通过其他个体的动脉粥样硬化来影响预后。本文综述了炎症在ACS中的独立作用以及炎症标志物的短期和中期预后价值。不稳定性沉淀ACS的最后一个共同途径是心外膜动脉和阻力性冠状血管的冠状动脉血栓形成和血管收缩的可变组合，叠加在可变的动脉粥样硬化背景上（图1）。血栓形成是最明显的急性成分，因为它的频繁持续使其在尸检、血管镜检查和血管造影中都能检测到。然而，痉挛和血管收缩是短暂的，只能在硝酸盐缓解严重狭窄时偶然发现，或在使用刺激试验时设计发现[7,8]；冠状动脉微血管收缩只能通过特殊的研究来推断和揭示。与血管收缩相比，血栓形成也是一个更有效的治疗靶点，因为当全身给予血管扩张药物时，通常不能对抗血栓局部释放的物质的收缩作用。欧洲心脏杂志增刊（2002）4（增刊B）， B8-B13
Inflammation is becoming an intriguing focus of research as a possible pathogenetic component and therapeutic target in ischaemic heart disease. However, the potential links between inflammation and ischaemic heart disease are present at three levels at least. First, the inflammatory response has been known for many years to play a major role in ischaemia/reperfusion injury, and its reduction can limit myocardial damage[1]. Second, inflammation is a very common feature of the chronic atherosclerotic process, as first described by Virchow in 1856[2] and recently comprehensively reviewed by Ross[3]. Finally, inflammation may be an acute pathogenetic component of instability in approximately half of patients with acute coronary syndromes (ACS), independently of the atherosclerotic and ischaemic burdens[4]. There may be several actual triggers of inflammation, the individual inflammatory response may vary, and the mechanisms through which inflammation correlates with the development of cardiovascular events in epidemiological studies may be multiple and not necessarily the same in all patients. The inflammatory response may influence prognosis through modulating the consequences of ischaemia and necrosis in some individuals, through sudden development of instability, or through atherogenesis in others. The present review focuses on the independent role of inflammation in ACS and on the short-term and mid-term prognostic value of inflammatory markers. The final common pathway through which instability precipitates ACS is represented by a variable combination of coronary thrombosis and vasoconstriction in epicardial arteries and in resistive coronary vessels, superimposed on a variable atherosclerotic background (Fig. 1)[5]. Thrombosis is the most obvious acute component, because its frequent persistence makes it detectable at autopsy, angioscopy and angiography. Spasm and vasoconstriction are transient, however, and can only be detected by chance, when critical stenoses are relieved by nitrates[6], or by design, when provocative tests are used[7,8]; coronary microvascular constriction can only be inferred and revealed by special studies[9]. Thrombosis is also a much more effective therapeutic target as compared with vasoconstriction, because vasodilator drugs, when given systemically, usually do not counter the constrictor effect of substances released by thrombi locally[6]. European Heart Journal Supplements (2002) 4 (Supplement B), B8–B13