Pathophysiology of Spontaneous Coronary Artery Dissection Determines Anticoagulation Strategy.
Pathophysiology of Spontaneous Coronary Artery Dissection Determines Anticoagulation Strategy.
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DOI：
10.7759/cureus.17437
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发表时间：
2021-08
期刊：
影响因子：
--
通讯作者：
Houck P
中科院分区：
文献类型：
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作者：
Houck P
自发性冠状动脉夹层是一种罕见的疾病，缺乏令人信服的病理生理证据。科学声明和最先进的文章表明血管出血引起的血管内血肿是病因。证据是基于光学相干断层扫描有限的侵入性评估。因此，这一假设建议停用抗凝治疗。机械剪切力，腔内压力不支持出血血管关闭高腔压血管。内皮在炎症、血栓形成和修复中的作用提示其病理生理是内皮细胞修复失败，缺乏修复作为破坏的中心。眼泪随之产生，并能自发地重新愈合。病理标本中炎症细胞的缺乏以及与另一种鲜为人知的疾病纤维肌肉发育不良的关联，支持了这两种实体的病因学，即未能替代内皮细胞。内皮是炎症和血栓形成的支点。愈合裂口的能力支持保守疗法。抗凝血剂和抗血小板剂可以减少内皮细胞被破坏后产生的血栓和炎症。这些药物将替代衰竭的内皮细胞，使血栓形成得到控制，减少炎症，促进愈合。这篇论文和最新的文章没有提供临床结果数据。两者都支持保守干预。然而，抗凝建议却在相反的领域。内皮修复失败提示他汀类药物、运动、戒烟等额外治疗将增加循环干细胞，可能减少未来事件并减缓纤维肌肉发育不良的进展。了解这种疾病和新疗法的未来方向需要测量修复机制，如循环内皮祖细胞的数量。
Spontaneous coronary dissection is an uncommon disorder, lacking convincing pathophysiologic evidence. Scientific statements and state-of-the-art articles suggest intramural hematoma from bleeding vasa vasorum is the cause. Evidence is based on limited invasive evaluation with optical coherence tomography. This assumption, therefore, suggests anti-coagulation be discontinued. Mechanical shear forces, intraluminal pressures do not support bleeding vasa vasorum closing a higher luminal pressure vessel. The endothelium’s role in inflammation, thrombosis, and repair suggests the pathophysiology is failure to repair endothelium with the lack of repair as the nidus of disruption. A tear ensues and can spontaneously reseal. The lack of inflammatory cells in pathological specimens and association with another poorly understood disease fibromuscular dysplasia supports the etiology of both entities as failure to replace endothelium. The endothelium is the fulcrum of both inflammation and thrombosis. The ability to heal the rift supports conservative therapy. Anticoagulants and antiplatelet reduce thrombosis and inflammation which will ensue when the endothelium is disrupted. These agents will substitute for the failed endothelium allowing thrombosis to be kept in check, reduce inflammation, and promote healing. This thesis and the state-of-the-art articles do not present clinical outcome data. Both support conservative interventions. Anticoagulation recommendations are however in opposite realms. Failure to repair endothelium suggest additional therapies of statins, exercise, smoking cessation will increase circulating stem cells may reduce future events and slow the progression of fibromuscular dysplasia. Future directions in understanding this disease and new therapies requires measurement of repair mechanisms such as the quantity of circulating endothelial progenitor cells.