Giant Left Atrial Thrombus with Double Coronary Vascularization

Serafino, Ciambelli Giuliano; Baptista, Mariana Lins; Rosa, Vitor Emer Egypto; Lopes, Antonio Sérgio de Santis Andrade; Accorsi, Tarso Augusto Duenhas; Tarasoutchi, Flávio

doi:10.5935/abc.20140128

Cited by 1 publication

(1 citation statement)

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“…Alternatively, arterial thrombosis usually occurs as a result of rupture of chronic atherosclerotic plaque and is characterized by inflammation and activation of cell adhesion molecules (25,30). Left atrial thrombus (LAT) is a complication secondary to severe mitral stenosis (26 -33% of cases) (22,42), atrial fibrillation (AF, 10 -30%) (14), and congestive heart failure (CHF) (~30%) (19) with most cardiac valvular disease and AF causally related with CHF (20).…”

Section: Introductionmentioning

confidence: 99%

Animal model of left atrial thrombus in congestive heart failure in rats

Chen

Strauss

Liang

et al. 2019

American Journal of Physiology-Heart and Circulatory Physiology

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The aim of the present study was to develop and study a new model of left atrial thrombus (LAT) in rat with congestive heart failure (CHF). CHF was induced by aortic banding for 2 mo, followed by ischemia-reperfusion (I/R) and subsequent aortic debanding for 1 mo. Cardiac function and the presence of LAT were assessed by echocardiography. Masson’s staining was performed for histological analysis. All CHF rats presented with significantly decreased cardiac function, fibrosis in remote myocardium, and pulmonary edema. The incidence rate of LAT was 18.8% in the rats. LAT was associated with severity of aortic constriction, aortic pressure gradient, aortic blood flow velocity, and pulmonary edema but not myocardial infarction or a degree of left ventricular depression. The progressive process of thrombogenesis was characterized by myocyte hypertrophy, fibrosis, and inflammation in the left atrial wall. Fibrin adhesion and clot formation were observed, whereas most LAT presented as a relatively hard “mass,” likely attributable to significant fibrosis in the middle and outer layers. Some LAT mass showed focal necrosis as well as fibrin bulging. Most LAT occurred at the upper anterior wall of the left atrial appendage. Aortic debanding had no significant impact on large LATs (>5 mm2) that had formed, whereas small LATs (<5 mm2) regressed 1 mo after aortic release. LAT is found in a rat model of aortic banding plus I/R followed by aortic debanding. The model provides a platform to study molecular mechanisms and potential new pathways for LAT treatment. NEW & NOTEWORTHY It is critically important to have a rodent model to study the molecular mechanism of thrombogenesis in the left atrium. Left atrial thrombus (LAT) is not a simple fibrin clot like those seen in peripheral veins or arteries. Rather, LAT is a cellular mass that likely develops in conjunction with blood clotting. Studying this phenomenon will help us understand congestive heart failure and promote new therapies for LAT.

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