Successful surgical transmitral removal of left ventricular thrombus after acute anterior myocardial infarction without left ventriculotomy

Abstract

Left ventricular thrombus (LVT) is known as a life-threatening complication of acute myocardial infarction, in terms of sequential systemic embolization. When an LVT is found to be sufficiently large or mobile, not only anticoagulation therapy but also surgical thrombectomy should be administered immediately to prevent embolic events. Generally, since infarcted myocardium is comparatively fragile, ventriculotomy may result in anastomotic failure or further deterioration of LV function. We report herein a case of transmitral removal of LVT by which we successfully avoided ventriculotomy. A 50-year-old Japanese man was hospitalized due to ST-segment elevation myocardial infarction and emergency coronary angiography revealed total occlusion at the proximal left anterior descending artery. On hospital day 9, transthoracic echocardiography detected a massive LVT at the apex, protruding into the left ventricle. Considering the risk of embolization, urgent thrombectomy via a transmitral approach was performed. The LVT was easily removed through the mitral valve under endoscopic support, without any embolic events or postoperative complications.

<Learning objective: Left ventricular thrombus following acute myocardial infarction may result in fatal embolization. Although surgical removal should be considered to prevent embolic events, some previous reports state that surgical approaches such as left ventriculotomy can lead to further cardiac dysfunction and ruptured sutures. Thus, transmitral approach may be useful for avoiding embolic events without left ventriculotomy and sequential complications.>

Introduction

Left ventricular thrombus (LVT) is a relatively common complication following acute myocardial infarction (AMI). While its frequency has been decreasing due to early revascularization and anticoagulation, this pathology is still a life-threatening problem, in terms of arterial embolic complications. When a large and mobile LVT is found in AMI patients on echocardiography, surgical removal should be considered to prevent embolic events. However, because LVT is often associated with poor left ventricular (LV) function, surgical approaches such as left ventriculotomy may lead to further LV dysfunction and ruptured sutures. We report a case of transmitral removal of a large mobile LVT following AMI, in which left ventriculotomy was avoided to preserve remnant LV function.

Case report

A 50-year-old man presented with chest pain and cold sweats at rest, and was transported to the emergency department of our hospital. He complained of persistent chest discomfort on arrival, but vital signs were largely preserved. We performed electrocardiography and identified ST-segment elevation in leads I, aVL, and V2–V6. ST-segment elevation myocardial infarction was suspected and emergency coronary angiography showed total occlusion at the proximal left anterior descending artery. Primary percutaneous coronary intervention was performed successfully, and he was admitted to the coronary care unit. Serum creatine kinase (CK) level peaked at 7450 U/L at 3 h after admission, and serum troponin T level was increased to 16.76 ng/mL (normal: <0.014 ng/mL). Serum low-density lipoprotein cholesterol and hemoglobin A1c were 179 mg/dL and 9.8%, respectively. He had never been treated for dyslipidemia or diabetes mellitus. Transthoracic echocardiography (TTE) showed anteroseptal and apical akinesis, moderate impairment of LV function with an ejection fraction (EF) of 44%. Although the clinical course seemed good without any complications, electrocardiography for daily follow-up revealed unexpected ST-segment elevation remaining in leads V3–V5 (Fig. 1).

Fig. 1.

Continued ST-segment elevation in precordial leads. Electrocardiography on hospital day 9 shows unnatural ST-segment elevation remaining in the precordial leads (V3–V5).

TTE performed on hospital day 9 for follow-up revealed a large, mobile LVT at the apex (Fig. 2). The LVT had a major diameter of 29 mm and protruded into the LV, and was so mobile that the risk of systemic embolism was considered very high. We thus immediately administered anticoagulation using unfractionated heparin, achieving activated partial thromboplastin time twice as much as control. However, LVT size did not change in 2 days. Therefore, we finally decided to perform surgical removal of the thrombus to avoid acute embolic events.

Fig. 2.

LVT visualized by transthoracic echocardiogram. On hospital day 9, LVT is found on transthoracic echocardiography for daily follow-up. LVT is adherent to the apical wall and protruded into the ventricle. This thrombus is mobile and large, with a diameter of 28.7 × 12.9 mm.

LVT, left ventricular thrombus.

On hospital day 11, thrombectomy was performed via a transmitral approach. Thoracotomy was performed in the right lateral fourth intercostal space, and the left atrium was opened without ventriculotomy under cardioplegic cardiac arrest and cardiopulmonary support. The LVT was visualized using an endoscope inserted through the mitral valve, and was located at the apex (Fig. 3). The LVT was easily extracted using forceps and suctions, without any residual thrombi (Fig. 4). The left atrium was closed and no difficulty was encountered in weaning from cardiopulmonary support. As postoperative follow-up, TTE revealed no residual thrombus in the left ventricle, although oral vitamin K antagonist was administered to prevent recurrence of LVT. After the operation, CK level rerose to 2588 U/L, and the patient was discharged from our hospital on postoperative day 28 without any further complications.

Fig. 3.

LVT visualized by an endoscope. White arrow indicates LVT which is located at the apex, visualized by an endoscope inserted from left atrium.

LVT, left ventricular thrombus.

Fig. 4.

LVT extracted from the apex. Maximum diameter of the LVT is >30 mm macroscopically. All thrombi were easily extracted and no residual thrombi were apparent in the heart.

LVT, left ventricular thrombus.

Discussion

LVT is known as one of the most critical complications of AMI, in terms of the risk of thromboembolic events, particularly cerebrovascular accidents. In this era of primary percutaneous coronary intervention, frequency of LVT was lower than before, but two studies found that LVT formation was seen in 5.4% and 7.1% of patients with acute anterior MI [1], [2]. Another study showed that the incidence of LVT was higher in patients with EF < 40% (10.5%) than in those with EF ≥ 40% (4%, p < 0.0001) [3]. Risk factors for the creation of LVT are considered to be large infarction size, severe apical asynergy, LV aneurysm, and anterior MI, and embolic complications reportedly occur in 2–3% of patients with LVT [4]. One study suggested that LV thrombi protruding into the ventricular cavity and exhibiting independent mobility are associated with a higher rate of embolization. Patient age >68 years is also one of the key predictors of peripheral embolus, and the long axis of the thrombus was significantly greater in patients with emboli than in those without emboli [5]. According to recent reports, both the European Society of Cardiology and the American College of Cardiology/American Heart Association guidelines recommend vitamin K antagonist therapy in patients with LVT after AMI [6], [7].

In this case, as the LVT was comparatively mobile and large enough (long axis, 29 mm) to incur embolic complications, not only anticoagulation but also surgical removal of the thrombus was warranted in the early phase. However, in general, because ischemic myocardium is comparatively vulnerable, left ventriculotomy after MI tends to result in ruptured sutures and further LV dysfunction. That is the reason why we first wished that the LVT would be dissolved only by anticoagulant. The timing of operation is still a controversial issue. Finally, since anticoagulation therapy seemed no longer effective, we decided to perform LV thrombectomy under a transmitral approach using endoscopy and succeeded in preserving remnant LV function. To sum up, when deciding the treatment of LVT, especially its timing and method, we must ponder the risks and benefits for each patient.

In summary, we encountered a case of LVT created after AMI, and performed successful thrombectomy under a transmitral approach without any postoperative complications.