T hrombus generation leading to cardiovascular event (CVE) occurrence involves a complex interplay among platelets, coagulation factors, and leukocytes (1,2). It has been reported that a distinct pathophysiological state of heightened platelet activation, hypercoagulability, and inflammation marks the departure from stable coronary artery disease to an unstable state—a situation that may be referred to as a “thrombo-inflammatory syndrome” (1). It is well known that patients with atrial fibrillation (AF) commonly have coexistent arterial disease and that the risk of stroke, thromboembolism, and other cardiovascular thrombotic events is high among these patients (3). More recently, a link between inflammation, platelet activation, and coagulation has also been described in patients with AF (4). Therefore, AF may be another example of a thromboinflammatory syndrome. Various markers have been widely used to indicate the presence of a thromboinflammatory syndrome. One is urinary 11-dehydro-thromboxane B2 (11-dhTxB2), which serves as a direct marker of platelet cyclooxygenase (COX)-1 activity, and indirectly as a marker of platelet activation. However, it is

中文翻译：

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PCSK9 作为心血管危险因素的探索

导致心血管事件 (CVE) 发生的血栓生成涉及血小板、凝血因子和白细胞之间复杂的相互作用 (1,2)。据报道，血小板活化升高、高凝状态和炎症的独特病理生理状态标志着从稳定型冠状动脉疾病转变为不稳定状态——这种情况可能被称为“血栓炎症综合征”(1)。众所周知，房颤 (AF) 患者通常同时存在动脉疾病，并且这些患者发生中风、血栓栓塞和其他心血管血栓事件的风险很高 (3)。最近，在 AF 患者中也描述了炎症、血小板活化和凝血之间的联系 (4)。所以，AF 可能是血栓炎症综合征的另一个例子。各种标志物已被广泛用于指示血栓炎症综合征的存在。一种是尿 11-脱氢血栓烷 B2 (11-dhTxB2)，它作为血小板环氧化酶 (COX)-1 活性的直接标志物，间接作为血小板活化的标志物。然而，它是