Grewal Dennis, Mohammad Adeba, Swamy Pooja, Abudayyeh Islam, Mamas Mamas A, Parwani Purvi
Division of Cardiology, Department of Cardiology, Loma Linda University Medical Center, Loma Linda, CA 92354, United States.
Keele Cardiovascular Research Group, Centre for Prognosis Research, Institutes of Applied Clinical Science and Primary Care and Health Sciences, Keele University, Stoke on Trent, Manchester M139PT, United Kingdom.
World J Cardiol. 2020 Sep 26;12(9):468-474. doi: 10.4330/wjc.v12.i9.468.
Coronary artery vasospasm (CAV) is a reversible, transient form of vasoconstriction with clinical manifestations ranging from stable angina to acute coronary syndromes (ACS). Vasospasm of epicardial coronary arteries or associated micro-vasculature can lead to total or subtotal occlusion and has been demonstrated in nearly 50% of patients undergoing angiography for suspected ACS. The mechanism for CAV has been described in literature, but in a subgroup of patients presenting with intracranial hemorrhage, it appears to be multifactorial. These patients tend to have electrocardiographic changes, elevation of cardiac biomarkers of injury and neurogenic stress cardiomyopathy.
A 44-year-old woman presented with severe headaches and tonic-clonic seizures. She was found to have diffuse subarachnoid hemorrhage (SAH) requiring ventricular drain placement, coil embolization and induced hypertension. She subsequently developed chest pain with ST elevations in anterior precordial leads, elevated cardiac enzymes and apical ballooning with left ventricular ejection fraction of 35% on transthoracic echocardiogram. Coronary angiogram revealed severe diffuse triple vessel stenoses secondary to CAV seen distally. Subsequent cardiac MRI notable for apical non-viability and scar formation.
This case highlights a unique etiology of acute myocardial infarction in a patient with SAH leading to ST elevations, diffuse triple vessel CAV and apical scar.
冠状动脉痉挛(CAV)是一种可逆的、短暂的血管收缩形式,其临床表现从稳定型心绞痛到急性冠状动脉综合征(ACS)不等。心外膜冠状动脉或相关微血管的痉挛可导致完全或不完全闭塞,在因疑似ACS接受血管造影的患者中,近50%已证实存在这种情况。CAV的机制在文献中已有描述,但在一组出现颅内出血的患者中,其机制似乎是多因素的。这些患者往往有心电图改变、心脏损伤生物标志物升高以及神经源性应激性心肌病。
一名44岁女性出现严重头痛和强直阵挛性发作。她被发现患有弥漫性蛛网膜下腔出血(SAH),需要进行脑室引流、弹簧圈栓塞和诱导性高血压治疗。随后,她出现胸痛,胸前导联ST段抬高,心肌酶升高,经胸超声心动图显示心尖部气球样变,左心室射血分数为35%。冠状动脉造影显示远端继发于CAV的严重弥漫性三支血管狭窄。随后的心脏磁共振成像显示心尖部无活力和瘢痕形成。
本病例突出了SAH患者急性心肌梗死的一种独特病因,导致ST段抬高、弥漫性三支血管CAV和心尖部瘢痕。