Advancing clinical management of left ventricular thrombosis: prevention, detection and treatment modalities in the modern era

Abstract

Heightened interest in left ventricular thrombus (LVT) stems from the consistent association of subsequent stroke and systemic embolism after LVT, and many aspects of its management still exist in a grey area of evidence. The current delay in intervention is likely related to a limited understanding of the disease pathophysiology, along with an underestimation of LVT by standard imaging modalities. With the rapid development of antithrombotic regimens consisting of direct oral anticoagulants (OACs), which have shown early safety and efficacy, there is a growing need to understand and accurately diagnose the LVT process in order to determine appropriate management solutions. This educational review will oversee LVT pathophysiology, current status of the guidelines-recommended echocardiographic approach and the role of multimodality imaging, as well as prevention and treatment modalities in the modern era. Meanwhile, the review proposes an algorithm for the prevention and treatment of LVT based on current guidelines and expert consensus, and highlights the need for more investigations to identify risk stratification methods for individual patients, and lastly, discusses the potential of direct OACs in the management of LVT.

Keywords: Cardiovascular Diseases.

Figure 1. Virchow’s Triad: pathophysiological basis. LV, left ventricular.

Figure 2. Visual representation of left ventricular thrombosis. CMR, cardiovascular MR; DE-CMR, delayed enhancement cardiovascular MR; LV, left ventricular.

Figure 3. Proposed diagnostic modalities for left ventricular thrombosis. AMI, Acute myocardial infarction; CMR, cardiovascular MR; ICM, ischaemic cardiomyopathies; LV, left ventricular; LVEF, left ventricular ejection fraction; NICM, non-ischaemic cardiomyopathies; TTE, transthoracic echocardiography. *Dilated cardiomyopathy, Takotsubo syndrome, left ventricular myocardial densification insufficiency, eosinophilic myocarditis, perinatal cardiomyopathy, or cardiac amyloidosis. #C reactive protein, fibrinogen and the neutrophil-lymphocyte ratio. †Reduced ejection fraction and/or large apical or anterior LV akinesis or dyskinesis (ie, aneurysm) and reduced contractile function facilitating stasis caused by an abnormal vortex.

Figure 4. Proposed prevention modalities for LVT. AMI, acute myocardial infarction; ICM, ischaemic cardiomyopathies; LVT, left ventricular thrombus; MDT, multidisciplinary team; NICM, non-ischaemic cardiomyopathies; OAC, oral anticoagulants. *CT was chosen when cardiovascular MR was unavailable or not tolerated.