Embolic Stroke Diagnosed by Elevated D-Dimer in a Patient With Negative TEE for Cardioembolic Source.
Bottom Line: The D-dimer level of this patient was normalized after 3 months of anticoagulation therapy.Although TEE is considered the gold standard for evaluation of cardiac source of embolism, exclusion of intracardiac thrombus with TEE alone does not eliminate the risk of thromboembolic events.This case highlights the utility of D-dimer as a potential adjunct in the decision-making process to guide investigation of thromboembolism, determine subsequent therapy, and hence reduce the risk of embolic stroke recurrence.
Affiliation: Georgia Regents University, Augusta, GA, USA.
We report a case of cerebrovascular accident with thromboembolic stroke etiology in a patient who had atrial flutter and negative transesophageal echocardiography (TEE) results. The increased D-dimer levels (1877 ng/mL) initiated referral for magnetic resonance imaging and magnetic resonance angiography of the brain that showed classic recanalization of an embolic thrombus in the angular branch of the left middle cerebral distribution. The D-dimer level of this patient was normalized after 3 months of anticoagulation therapy. Although TEE is considered the gold standard for evaluation of cardiac source of embolism, exclusion of intracardiac thrombus with TEE alone does not eliminate the risk of thromboembolic events. This case highlights the utility of D-dimer as a potential adjunct in the decision-making process to guide investigation of thromboembolism, determine subsequent therapy, and hence reduce the risk of embolic stroke recurrence.
No MeSH data available.
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Mentions: A 79-year-old female presented for routine follow-up in our cardiology clinic. She had a 20-year history of an ostium secundum atrial septal defect (ASD) for which she refused closure and had a prior cerebrovascular accident without sequel. The patient also had a history of hypertension and dyslipidemia. The patient reported having an episode of right upper limb weakness 6 days previously. The symptoms lasted for 20 minutes before completely resolving. On examination, her heart rate was 52/min, blood pressure 118/60 mm Hg, and the chest was clear to auscultation. The glucose level was 80 mg/dL. The patient did have a hypercoagulability workup as follows: protein C activity (113%), protein S activity (124%), fibrinogen (313 mg/dL), ATIII (85%), APC ratio (3.0). Cardiac exam revealed fixed splitting of the second heart sound. Her neurological exam was normal. A 12-lead electrocardiogram (EKG) showed minor anterolateral T-wave changes, less pronounced than on previous EKG 6 months ago. There was no history or echocardiographic findings to suspect valvular vegetation. Initially the patient was diagnosed with a transient ischemic attack. The computed tomography (CT) of the head without contrast found no evidence of an acute intracranial process (Figure 1A). CT angiography of chest/pelvis/abdomen found no evidence of pulmonary embolus. A TEE was performed and showed no evidence of thrombus in the heart including the left atrial appendage (Figure 1B), no valvular vegetations, normal left ventricular function, and a small secondum ASD (Figure 1C).
No MeSH data available.