Department of Propedeutics of Internal Medicine, Faculty of Medicine, Medical University, Varna, 9002, Bulgaria.
Clinic of Internal Medicine, University Hospital St. Marina - Varna, Varna, 9010, Bulgaria.
Rheumatol Int. 2024 Oct;44(10):1837-1848. doi: 10.1007/s00296-024-05693-3. Epub 2024 Aug 24.
Ankylosing Spondylitis (AS) stands as a chronic inflammatory arthritis within the spondyloarthritis spectrum, notably increasing cardiovascular (CV) risk and mortality through accelerated atherosclerosis compared to the non-affected population. While evidence in some studies supports a higher cardiovascular morbidity in AS patients, results from other studies reveal no significant disparities in atherosclerotic markers between AS individuals and healthy controls. This discrepancy may arise from the complex interaction between traditional CV risk factors and AS inflammatory burden. Endothelial dysfunction, a recognized antecedent of atherosclerosis prevalent among most individuals with AS, demonstrates the synergistic impact of inflammation and conventional risk factors on endothelial injury, consequently hastening the progression of atherosclerosis. Remarkably, endothelial dysfunction can precede vascular pathology in AS, suggesting a unique relationship between inflammation, atherosclerosis, and vascular damage. The role of adhesion molecules in the development of atherosclerosis, facilitating leukocyte adherence and migration into vascular walls, underscores the predictive value of soluble intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) levels for cardiovascular events. Despite significant progress in comprehending the pathogenesis of AS and its associated cardiovascular implications, the interplay among inflammation, endothelial dysfunction, and atherosclerosis remains partially elucidated. Investigations into the efficacy of therapeutic approaches involving angiotensin receptor blockers and statins have demonstrated reduced cardiovascular risk in AS patients, underscoring the imperative for additional research in this domain.
强直性脊柱炎（AS）是一种属于脊柱关节炎谱系的慢性炎症性关节炎，与未受影响的人群相比，通过加速动脉粥样硬化，显著增加了心血管（CV）风险和死亡率。虽然一些研究中的证据表明 AS 患者的心血管发病率更高，但其他研究的结果显示，AS 个体与健康对照组之间的动脉粥样硬化标志物没有显著差异。这种差异可能源于传统 CV 危险因素和 AS 炎症负担之间的复杂相互作用。内皮功能障碍是大多数 AS 患者普遍存在的动脉粥样硬化的公认前兆，它展示了炎症和传统危险因素对内皮损伤的协同影响，从而加速了动脉粥样硬化的进展。值得注意的是，内皮功能障碍可以在 AS 之前出现血管病理学，表明炎症、动脉粥样硬化和血管损伤之间存在独特的关系。黏附分子在动脉粥样硬化发展中的作用促进了白细胞黏附和迁移到血管壁，突出了可溶性细胞间黏附分子-1（ICAM-1）和血管细胞黏附分子-1（VCAM-1）水平对心血管事件的预测价值。尽管在理解 AS 的发病机制及其相关心血管影响方面取得了重大进展，但炎症、内皮功能障碍和动脉粥样硬化之间的相互作用仍部分阐明。对涉及血管紧张素受体阻滞剂和他汀类药物的治疗方法的疗效的研究表明，AS 患者的心血管风险降低，这突显了在这一领域进行更多研究的必要性。
