EMBOLIC STROKES DUE TO LEFT CARDIAC THROMBI

Abstract

Introduction: Cardio-embolic strokes occur in about 20% of stroke patients. Left ventricular thrombi come second to atrial thrombi from atrial fibrillation as a cause of cardioembolic embolization. Myocardial infarction and dilated cardiomyopathy are most frequently associated with left ventricular thrombi formation. Dyskinetic segments that remodel into aneurysms and left atrial appendage remain chronic foci for thrombosis. Large size infarcts are known to be associated with high risks for hemorrhagic transformation.
Material and methods: In our case we presented a middle-aged patient, 42 years old, male, from the emergency department with acute onset of inability to speak and right sided weakness. Initial CT brain showed a small post ischemic zone in the left parietal lobe. A repeated CT brain after 48 hours showed a large left middle cerebral artery territory infarct with focal areas of hemorrhagic transformation corresponding to the neurological symptoms presented. We used the importance of echocardiography and transoesophageal echocardiography (TOE) in identifying the etiology and clinical evaluation of a ischemic embolic stroke with hemorrhagic transformation. The patient has comorbidities (ischemic cardiomyopathy, hypertension, dyslipidemia) and had a previous cerebral ischemic event. He was on antiplateleted therapy (Clopidogrel 75mg/day) because of previous cardiac ischemic event (myocardial infarction). Initially the patient was observed and treated by a multidisciplinary team consisting of a cardiologist, neurologist and transfusiologist who opted not to initiate full anticoagulation in the beginning. Instead the patient received low molecular weight heparin (enoxiparin) in the acute phase of the illness, the first three weeks and after that was continued with lifelong oral anticoagulation therapy ( according to CHA2DS2-VASc 4 and HAS-BLED score 2). The therapy with antiplateled therapy was discontinued because of high risk of hemorrhagic transformation and reinitiated after 3 months. On discharge from the hospital the patient had mild neurological deficit, hemodynamically compensated, stable, without hemorrhagic event with recommendation for oral anticoagulant and antiplateled therapy.
Conclusion: Early and prompt cardiac evaluation using echocardiography and TOE in the emergency department is necessary in order to detect the etiology of embolic strokes. Multidisciplinary team is extremely important for the evaluation and guidance the patients with this kind comorbites.