An Interesting Case of COVID-19 Induced Hypercoagulability Manifesting as Pulmonary Embolism and Apical Left Ventricular Thrombus

A. Azhar, A. Bk, O. Hadzipasic
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引用次数: 1

Abstract

Introduction: Recent data demonstrates a strong correlation between COVID-19 and hypercoagulability with the spectrum of thromboembolic manifestations, including deep vein thrombosis and pulmonary embolism (PE). Here we present a unique case of COVID-19 associated hypercoagulability manifesting as both PE and apical left ventricular (LV) thrombosis in the absence of underlying coronary artery disease (CAD). Case: A 71-year-old female with a diagnosis of mild COVID-19 pneumonia presented with worsening fatigue, cough, shortness of breath, and chest heaviness on the thirteenth day of her illness. The patient was hypoxic on presentation requiring 3 L supplemental oxygen. Laboratory analysis showed an extremely high D-dimer level (greater than 20,000 ng/mL). Hence, computed tomography angiography of the chest was performed, showing evidence of right lower lobe segmental and subsegmental PE along with bilateral multifocal consolidation. Incidentally, the imaging demonstrated a filling defect within the apex of LV, transcending into further cardiac workup. Initial troponin was elevated at 0.04 ng/mL, and electrocardiogram showed sinus rhythm without any acute ST-T wave changes. Transthoracic echocardiography confirmed the presence of large, sessile, mobile, 1.3 x 2.1 cm LV thrombus but normal LV systolic function, ejection fraction, and no evidence of regional wall motion abnormalities. However, due to ongoing chest heaviness, the decision was made to perform a diagnostic left heart catheterization, which showed insignificant CAD. The patient received treatment with convalescent plasma, Remdesivir, and dexamethasone as per our institutional protocol and started on unfractionated heparin for anticoagulation. She was discharged on enoxaparin as per the patient's preference on a stable condition with close cardiology follow up. DiscussionLV thrombosis is a well-known complication of LV dysfunction associated with ischemic cardiomyopathy. While PE is an established phenomenon of COVID- 19 induced hypercoagulability, thrombus formation within the cardiac chamber is rarely reported. As cardiovascular complications such as acute myocardial injury, myocarditis, and cardiomyopathy are substantially reported in COVID-19, through this case report, we highlight the rare presentation of COVID 19 hypercoagulability with LV thrombus in the absence of predisposing cardiac conditions such as myocardial infarction or atrial fibrillation. Although the mechanism remains unclear, endothelial dysfunction eliciting local myocardial inflammation and blood stasis is a plausible explanation. Early recognition of LV thrombus and treatment with anticoagulation is of paramount importance to reducing stroke risk and systemic embolization. The detection of LV thrombus mandates anticoagulation with warfarin or heparin due to insufficient evidence to support the use of direct oral anticoagulants.
一例以肺栓塞和左心室尖血栓为表现的新型冠状病毒引起的高凝
最近的数据表明,COVID-19和高凝性与血栓栓塞表现谱(包括深静脉血栓形成和肺栓塞(PE))有很强的相关性。在这里,我们报告了一个独特的COVID-19相关高凝性病例,在没有潜在冠状动脉疾病(CAD)的情况下,表现为PE和根尖左心室(LV)血栓形成。病例:一名71岁女性,诊断为轻度COVID-19肺炎,在发病的第13天出现日益加重的疲劳、咳嗽、呼吸急促和胸重。患者入院时缺氧,需补充3l氧气。实验室分析显示d -二聚体含量极高(大于20,000 ng/mL)。因此,进行了胸部计算机断层血管造影,显示右下叶节段性和亚节段性PE,并伴有双侧多灶实变。顺便提一下,影像学显示左室心尖处充盈缺损,进一步的心脏检查。初始肌钙蛋白升高0.04 ng/mL,心电图显示窦性心律,未见急性ST-T波改变。经胸超声心动图证实存在大的、无梗的、可移动的、1.3 x 2.1 cm的左室血栓,但左室收缩功能、射血分数正常,无区域壁运动异常的证据。然而,由于持续的胸部沉重,决定进行诊断性左心导管插入术,显示不明显的CAD。患者接受恢复期血浆、瑞德西韦和地塞米松治疗,并开始使用无分离肝素抗凝治疗。她出院依诺肝素根据病人的喜好,病情稳定,密切的心脏科随访。左室血栓形成是众所周知的与缺血性心肌病相关的左室功能障碍并发症。虽然PE是COVID- 19诱导的高凝现象,但心腔内血栓形成的报道很少。由于在COVID-19中大量报道了急性心肌损伤、心肌炎和心肌病等心血管并发症,因此,通过本病例报告,我们强调了在没有心肌梗死或房颤等易感心脏疾病的情况下,罕见的COVID-19高凝伴左室血栓的表现。虽然机制尚不清楚,内皮功能障碍引起局部心肌炎症和血瘀是一个合理的解释。早期识别左室血栓并进行抗凝治疗对于降低卒中风险和全身栓塞至关重要。由于没有足够的证据支持直接使用口服抗凝剂,左室血栓的检测要求使用华法林或肝素抗凝。
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