PDF(Pubmed)
Abstract：
Acute Coronary Syndrome (ACS) significantly contributes to cardiovascular death worldwide. ACS may arise from the disruption of an atherosclerotic plaque, ultimately leading to acute ischemia and myocardial infarction. In the pathogenesis of atherosclerosis, inflammation assumes a pivotal role, not solely in the initiation and complications of atherosclerotic plaque formation, but also in the myocardial response to ischemic insult. Acute inflammatory processes, coupled with time to reperfusion, orchestrate ischemic and reperfusion injuries, dictating infarct magnitude and acute left ventricular (LV) remodeling. Conversely, chronic inflammation, alongside neurohumoral activation, governs persistent LV remodeling. The interplay between chronic LV remodeling and recurrent ischemic episodes delineates the progression of the disease toward heart failure and cardiovascular death. Colchicine exerts anti-inflammatory properties affecting both the myocardium and atherosclerotic plaque by modulating the activity of monocyte/macrophages, neutrophils, and platelets. This modulation can potentially result in a more favorable LV remodeling and forestalls the recurrence of ACS. This narrative review aims to delineate the role of inflammation across the different phases of ACS pathophysiology and describe the mechanistic underpinnings of colchicine, exploring its purported role in modulating each of these stages.
摘要：
急性冠脉综合征(ACS)是全球心血管死亡的重要原因。ACS可能起因于动脉粥样硬化斑块的破坏,最终导致急性缺血和心肌梗死。在动脉粥样硬化的发病机制中，炎症起着关键作用，不仅仅是动脉粥样硬化斑块形成的开始和并发症，而且在心肌对缺血性损伤的反应中。急性炎症过程，再加上再灌注的时间，协调缺血和再灌注损伤，指示梗死程度和急性左心室（LV）重塑。相反，慢性炎症，除了神经体液激活，支配持续性左心室重塑。慢性LV重塑和复发性缺血发作之间的相互作用描绘了疾病向心力衰竭和心血管死亡的进展。秋水仙碱通过调节单核细胞/巨噬细胞的活性发挥影响心肌和动脉粥样硬化斑块的抗炎特性，中性粒细胞，和血小板。这种调节可能会导致更有利的LV重塑并阻止ACS的复发。这篇叙述性综述旨在描述炎症在ACS病理生理学不同阶段的作用，并描述秋水仙碱的机制基础。探索其在调节每个阶段中的所谓作用。
