299 LEFT VENTRICULAR APICAL THROMBUS

Abstract

Abstract LV thrombus is a complication of AMI. It is estimated that 40-60% of patients with large anterior wall MI will develop a LV thrombus. The risk is highest during the first 3 months following AMI. Accurate and timely detection is important as it poses a high risk for thromboembolic events. Advances in technology have improved the detection rate of intracardiac thrombi, but several uncertainties still remain regarding the optimal treatment strategy within daily clinical practice. We report a case of large LV thrombus in a 61-year-old male with extensive anterior wall MI. A 61-year-old man, hypertension, former smoker, subjected to epatic orthotopic transplant for HCC and treated with immunosuppressive therapy (Everolimus), following development of lymphocytic leukemia in fu. He underwent thoracic ct, wich showed a hypodense imaging in the left ventricular apex referable to thrombotic formation large 2cm, with endocardial rim hypointense like ischemic outcomes. The ECG demonstrated Q waves in anterior leads and biphasic T waves in the same leads. The patient was absolutely asyntomatic. A transthoracic echocardiography, showed the apical mass (2×0,9cm) very mobile and akinesia and thinning of the left ventricol middle-apical wall with apical aneurysmatic evolution. A CMR, confirmed the presence of the thrombus and showed defects at the subendocardial layer of the anterior wall and interventricular septal with also involvement of all the apex; the burden of late gadolinium enhancement (ischemic pattern) extended to the same segment. Coronary angiography showed subocclusion involving the second tract of the left anterior descending (99%) and critical coronary stenosis of the third tract of the right coronary (70%). The thrombus was completely removed surgically through left atriotomy, in prevention of embolization due to the thrombus dimension, the motility and the labile docking station. The histological examination confirmed the thrombotic nature of the mass. International guidelines agree on recommending anticoagulation therapy for patients affected by left ventricular thrombosis. OAC with vitamin K antagonists should be started as soon as LVT is identified, as first-line therapy and parenteral anticoagulation should be discontinued when effective therapeutic range with warfarin has been achieved (INR of 2–3). European and American guidelines stressing the efficacy of parenteral therapy with heparin; there are no randomized trials that have examined the efficacy of VKA anticoagulation compared with parenteral therapy. DOACs are attractive alternatives because of their potential efficacy and safety even though there is no trial that proves the effect of DOACs in LVT. Oral anticoagulation should be discontinued as soon as thrombus resolution has been established. Surgical removal of the LVT is an option for patients with high embolic risk, as in our patient. The high morbidity and mortality of this approach outweigh the benefits of performing surgery solely for the indication of LVT.