Alyacoub Ramez, Elkattawy Sherif, Jesani Shruti, Perez Hernandez Carlos, Fichadiya Hardik, Noori Muhammad Atif Masood, Elkattawy Omar, Williams Edward
Department of Internal Medicine, Rutgers NJMS/Trinitas Regional Medical Center, Elizabeth, NJ, USA.
Department of Internal Medicine, Rutgers NJMS, Elizabeth, NJ, USA.
Eur J Case Rep Intern Med. 2022 Jun 23;9(6):003327. doi: 10.12890/2022_003327. eCollection 2022.
Left ventricular thrombus (LVT) formation is a serious clinical complication of low-flow states that may be seen in an ischaemic, arrhythmic heart. While LVT formation has a poor prognosis, in the setting of myocardial infarction it is usually a result of post-infarct sequelae such as left ventricle aneurysms, and inflammatory changes from damaged tissue, with the LVT taking several days to form. Arrythmias such as ventricular tachycardia (VT) or ventricular fibrillation (VF) may also lead to thrombus formation, as they contribute to stasis due to decreased cardiac output. Large anterolateral myocardial infarctions can cause electrical or arrhythmic storm, characterized by more than three episodes of VT or VF in a 24-hour period. This prolonged state of dyskinesis further increases the risk of thrombosis, creating a compounding effect. Here, we report the case of a patient who had a VF cardiac arrest with electrical storm secondary to anterolateral myocardial infarction complicated with LVT formation found on echocardiogram after the cardiac arrest, which was absent on presentation. This thrombus formation occurred particularly early during the course of the patient's arrest, possibly due to the compounding factors increasing the risk of thrombosis. Herein, we discuss in detail the risk factors for LVT formation, its mechanism and management options. A review of the literature also shows that LVT formation in the acute phase of arrest, as seen in our patient, is rare.
Left ventricular thrombus (LVT) formation occurs 3-14 days after myocardial infarction, but in the setting of concomitant ventricular fibrillation arrest, may occur within the first 24 hours.Risk factors for LVT formation include a large infarct, anterior/anterior apical infarction, decreased ejection fraction (particularly <30-35%), left ventricular aneurysm, and delayed time to revascularization.Although diagnosis is generally made on transthoracic echocardiography with intravenous contrast, cardiac MRI with contrast has better sensitivity and specificity.Treatment consists of anticoagulation with a vitamin K antagonist or heparin for 3-6 months with a repeat echocardiogram to confirm the thrombus has organized or resolved. Further trials are needed to assess the efficacy of direct oral anticoagulants.
左心室血栓(LVT)形成是低血流状态的一种严重临床并发症,在缺血性、心律失常性心脏中可能出现。虽然LVT形成预后不良,但在心肌梗死情况下,它通常是梗死后期后遗症的结果,如左心室动脉瘤,以及受损组织的炎症变化,LVT需要数天时间形成。室性心动过速(VT)或心室颤动(VF)等心律失常也可能导致血栓形成,因为它们会因心输出量减少而导致血流淤滞。大面积前壁心肌梗死可引起电风暴或心律失常风暴,其特征是在24小时内发生超过三次VT或VF发作。这种长期的运动障碍状态进一步增加了血栓形成的风险,产生了复合效应。在此,我们报告一例患者,其因前壁心肌梗死继发VF心脏骤停并伴有电风暴,心脏骤停后经超声心动图检查发现合并LVT形成,而在就诊时未发现。这种血栓形成在患者心脏骤停过程中特别早地发生,可能是由于多种因素增加了血栓形成的风险。在此,我们详细讨论LVT形成的危险因素、其机制和管理选择。文献综述还表明,如我们患者所见,在心脏骤停急性期发生LVT形成是罕见的。
左心室血栓(LVT)形成通常发生在心肌梗死后3 - 14天,但在伴有心室颤动心脏骤停的情况下,可能在最初24小时内发生。LVT形成的危险因素包括大面积梗死、前壁/前壁心尖梗死、射血分数降低(特别是<30 - 35%)、左心室动脉瘤以及再灌注延迟时间。虽然一般通过经胸超声心动图加静脉造影进行诊断,但心脏磁共振成像加造影具有更好的敏感性和特异性。治疗包括使用维生素K拮抗剂或肝素进行抗凝3 - 6个月,并重复超声心动图以确认血栓已机化或溶解。需要进一步的试验来评估直接口服抗凝剂的疗效。