Fulminant micro and macroangiopathic sequalae in a patient with COVID-19.
Fulminant micro and macroangiopathic sequalae in a patient with COVID-19.
复制标题
DOI：
10.1093/ehjcr/ytaa372
复制
发表时间：
2020-12
期刊：
影响因子：
--
通讯作者：
McCann GP
中科院分区：
文献类型：
--
作者：
Bhandari SS;Yeo J;Kotecha D;McCann GP
一名既往健康的49岁南亚裔男性，在COVID-19大流行高峰期就诊于我们的急诊科，有2天的呼吸困难和干咳史，之前有急性腹泻病。临床检查显示体温38.6℃，血压150/105 mmHg，心率129 bpm，呼吸频率40/min，空气氧饱和度96%。胸片显示双侧肺斑片状影（图1A）。初步实验室检查显示白细胞计数升高11.5[正常范围（NR） 4-11 Â 109 L]，中性粒细胞计数升高9.27 (NR 1.5-7.5 Â 109 L)， c反应蛋白升高129 (NR< 5mg/L)， d -二聚体升高7.7 （NR< 0.5 μg/mL）。国际标准化比值及心肌肌钙蛋白正常。患者在重症监护病房接受经验治疗：克拉霉素500mg每日2次静脉滴注，复方莫昔拉夫1.2 g每日3次，地塞米松6mg每日1次，持续气道正压通气，同时给予抗血栓预防治疗。患者接受了SARS-CoV-2聚合酶链反应测试，结果表明他患有活性COVID-19。第6天，患者出现左臂肿胀。超声证实左颈内静脉及腋窝静脉有血栓，随后给予达特帕林12 500单位抗凝治疗，每日1次。第10天，患者出现中枢性胸痛。心电图示前st段抬高、q波（在线补充资料，图S1），高敏肌钙蛋白- i 27 266 （NR< 14 ng/L）。超声心动图显示中度左心室收缩功能不全伴心尖运动障碍。计算机断层肺血管造影显示胸膜下组织实变区伴片状周围磨玻璃混浊伴多发双侧肺栓塞（图1B）。进行心脏磁共振成像以确定心脏损伤的病因。T1测图显示间隔水肿，射血分数保留（63%），但伴有心尖运动障碍和晚期钆增强，证实心外膜右室侧的心尖心肌梗死（MI）和中间隔斑片状微梗死（图1C，视频1）。腺苷应激灌注用于评估可逆性心肌缺血，结果显示心肌血流明显充血（高达5mL/g/min），伴有斑块状的心尖和中隔灌注不足（图1D），提示微血管疾病。随后的冠状动脉造影显示冠状动脉通畅（在线补充资料，图S2和S3）。该病例突出了日益被认可的大血管（静脉和肺动脉血栓形成，根尖心肌梗死）和微血管并发症（斑块性微心肌梗死伴非匹配应激灌注不足）。尽管抗凝4天仍发生心脏并发症，越来越多的证据表明，COVID-19血管后遗症与免疫复合物沉积和局部血管炎症有关，而不是血栓栓塞。
A previously fit 49-year-old male of South Asian ethnicity, presented to our emergency department at the height of the COVID-19 pandemic with a 2-day history of dyspnoea and a dry cough, preceded by an acute diarrhoeal illness. Clinical examination revealed a temperature of 38.6 C, blood pressure of 150/105 mmHg, heart rate of 129 bpm, and a respiratory rate of 40/min with oxygen saturations of 96% on air. A chest radiograph showed bilateral patchy lung opacities (Figure 1A). Initial laboratory tests showed an elevated white cell count of 11.5 [normal range (NR) 4–11 Â 109 L], neutrophil count of 9.27 (NR 1.5–7.5 Â 109 L), C-reactive protein of 129 (NR< 5mg/L), and a D-dimer of 7.7 (NR< 0.5 μg/mL). International normalized ratio and cardiac troponin were normal. The patient was treated empirically with intravenous clarithromycin 500mg twice daily, coamoxiclav 1.2 g three times daily, dexamethasone 6mg once daily, and continuous positive airway pressure ventilation, along with antithrombotic prophylaxis on the intensive care unit. The patient underwent a SARS-CoV-2 polymerase chain reaction test which demonstrated that he had active COVID-19. On Day 6, the patient developed left arm swelling. Ultrasound confirmed a thrombus in the left internal jugular vein and axillary vein and was subsequently anticoagulated with dalteparin 12 500 units once daily. On Day 10, the patient developed central chest pain. Electrocardiogram showed anterior ST-segment elevation and Q-waves (Supplementary material online, Figure S1), high-sensitive troponin-I was 27 266 (NR< 14 ng/L). An echocardiogram showed moderate left ventricular systolic dysfunction with apical akinesia. A computed tomography pulmonary angiogram showed subpleural organizing areas of consolidation with patchy peripheral ground-glass opacities with multiple bilateral pulmonary emboli (Figure 1B). Cardiac magnetic resonance imaging was undertaken to establish the aetiology of the cardiac injury. T1 mapping showed septal oedema with preserved ejection fraction (63%) but with apical akinesia and late gadolinium enhancement confirming apical myocardial infarction (MI) and patchy micro-infarction in the mid septum on the epicardial right ventricular side (Figure 1C, Video 1). Adenosine stress perfusion, to assess reversible myocardial ischaemia revealed marked hyperaemic myocardial blood flow (up to 5mL/g/min) with patchy apical and mid septal hypoperfusion (Figure 1D) suggesting microvascular disease. Subsequent coronary angiography revealed unobstructed coronary arteries (Supplementary material online, Figures S2 and S3). This case highlights the increasingly recognised macrovascular (venous and pulmonary arterial thrombosis, apical MI) and microvascular complications (patchy micro MI with non-matching stress hypoperfusion). The cardiac complications occurred despite 4 days of anticoagulation and there is increasing evidence that the vascular sequalae of COVID-19 are related to immune complex deposition and localized vascular inflammation rather than thromboembolism.