Ho Daniel, Alfaris Ibrahim, Joury Abdulaziz, Cecere Renzo, Giannetti Nadia
Centre for Outcomes Research and Evaluation, Research Institute of the McGill University Health Centre, 2155 Rue Guy, Montréal, QC H3H 2L9, Canada.
Division of Cardiology, McGill University Health Centre, McGill University, 1001 Bd Décarie, Montréal, QC H4A 3J1, Canada.
Eur Heart J Case Rep. 2024 May 6;8(5):ytae234. doi: 10.1093/ehjcr/ytae234. eCollection 2024 May.
Excluding spontaneous coronary artery dissection (SCAD) as an aetiology of acute coronary syndrome in young adults is imperative.
A previously healthy 39-year-old woman experienced sudden severe chest pain, ST-segment elevation on electrocardiogram, necessitating high-dose aspirin and urgent transfer to a revascularization centre. Suffering ventricular tachycardia (VT) and ventricular fibrillation (VF), she underwent two rounds of advanced life support and venoarterial extracorporeal membrane oxygenation. Diagnosed with left main coronary artery (LMCA) SCAD, she was initially started on conservative therapy for declining left ventricular ejection fraction. However, she continued to experience an escalating anginal symptoms, worsening biomarkers, and LMCA SCAD progression, which urged the need for surgical intervention with coronary artery bypass graft surgery (CABG). Following her CABG, she experienced a worsening of her functional mitral regurgitating, which she underwent transcatheter edge-to-edge repair of her severe mitral regurgitation. Despite being listed for orthotopic heart transplantation (OHTx), her low body mass index and elevated antibodies necessitated the HeartMate III left ventricular assist device (LVAD) for bridge to transplant. After treating frequent VT episodes with medications, she eventually received a LVAD as a bridge to cardiac transplantation. Within 1 year of her receiving LVAD, she underwent a successful OHTx.
The pathogenesis of SCAD involves intramural haematoma formation through intimal tears or vasa vasorum haemorrhage. Adverse outcomes that could occur in SCAD patients include cardiac arrest, cardiogenic shock, reduced left ventricle systolic function, and occasionally serious cardiac arrhythmia-such as VF-which can lead to sudden cardiac death. Although most SCAD cases heal spontaneously, revascularization can be considered in case of worsening SCAD progression. Advanced therapeutic intervention including mechanical circulatory support and OHTx should be considered in refractory cases.
排除自发性冠状动脉夹层（SCAD）作为年轻成人急性冠状动脉综合征的病因至关重要。
一名既往健康的39岁女性突发严重胸痛，心电图显示ST段抬高，需要大剂量阿司匹林治疗并紧急转至血管重建中心。她出现室性心动过速（VT）和室颤（VF），接受了两轮高级生命支持和静脉-动脉体外膜肺氧合治疗。诊断为左主干冠状动脉（LMCA）SCAD，最初因左心室射血分数下降开始接受保守治疗。然而，她持续出现心绞痛症状加重、生物标志物恶化以及LMCA SCAD进展，这促使需要进行冠状动脉旁路移植术（CABG）手术干预。CABG术后，她的功能性二尖瓣反流恶化，因此接受了经导管二尖瓣缘对缘修复术治疗严重二尖瓣反流。尽管被列入原位心脏移植（OHTx）名单，但她的低体重指数和抗体升高使得需要使用HeartMate III左心室辅助装置（LVAD）作为移植桥梁。在用药物治疗频繁发作的VT后，她最终接受了LVAD作为心脏移植的桥梁。在接受LVAD的1年内，她成功接受了OHTx。
SCAD的发病机制涉及通过内膜撕裂或滋养血管出血形成壁内血肿。SCAD患者可能出现的不良后果包括心脏骤停、心源性休克、左心室收缩功能降低，偶尔还会出现严重心律失常，如VF，可导致心源性猝死。尽管大多数SCAD病例可自愈，但如果SCAD进展恶化，可考虑进行血管重建。对于难治性病例，应考虑包括机械循环支持和OHTx在内的高级治疗干预。
