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The objective of this article was to determine whether the presence of left ventricular apical thrombus is a marker of nonviable myocardium. Reduced coronary blood flow secondary to atherosclerosis may result in chronic reversible left ventricular wall-motion abnormalities. Severe regional abnormalities also predispose to formation of left ventricular thrombus. The relationship between left ventricular apical thrombus and myocardial viability has not been previously described. Eighty patients with coronary artery disease and chronic left ventricular dysfunction were studied by dobutamine stress echocardiography. Left ventricular apical thrombus was identified using echocardiographic criteria. Wall-motion analysis was performed using a standard 16-segment model and ejection fraction was calculated. As a result, 48 patients (60%) had definite or highly suspicious findings for left ventricular thrombus (group 1), and 32 patients (40%) had no thrombus (group 2). Group 1 had significantly higher composite (54.0 +/- 5.8 vs 43.3 +/- 6.4) and apical (6.0 +/- 2.7 vs 12.4 +/- 3.4) wall-motion scores compared to those in group 2 (P = 0.01). Thirty-two patients (67%) in group 1 demonstrated no contractile reserve in the apical segments, consistent with lack of viability, versus eight patients (25%) in group 2 (P = 0.0003). The number of viable apical segments per patient was significantly less in group 1 (0.7 +/- 1.2) versus group 2 (1.8 +/- 1.3) (P = 0.01). Left ventricular apical thrombus is more likely to be present when there is absence of myocardial viability in the corresponding segments.

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Introduction: Intramural esophageal hematoma is a rare condition presenting with dysphagia, nausea and mid epigastric or retrosternal chest pain. We present a unique case of spontaneous esophageal hematoma in a patient anticoagulated with apixaban for atrial fibrillation. Case presentation: An 88-year-old woman with history of hypertension, hypothyroidism, persistent atrial fibrillation on apixaban presented to emergency department with sudden onset epigastric pain, dysphagia and nausea without vomiting while having dinner. Physical examination was unremarkable except for mild tenderness in the epigastric region. Initial workup including complete blood count, complete metabolic panel, lipase, troponin was unremarkable. EKG showed atrial fibrillation with no ischemic changes. CT chest showed abnormal hyperdense mass-like thickening approximately 4 x 3 x 12 cm involving the mid/distal thoracic esophagus with possible differentials being food bolus, esophageal hematoma or mass. Prothrombin complex concentrate (Kcentra) was given as patient was on apixaban and gastroenterology was consulted for upper endoscopy which showed a large hematoma occupying most of the esophageal lumen at the entire length of esophagus. After family discussion on stroke-versus-bleeding risk with anticoagulation, cardiology recommended holding anticoagulation for at least a month and future evaluation for WATCHMAN device. With stable hemoglobin and gradual advancement to a soft diet, patient was discharged home with repeat endoscopy planned in two weeks. Conclusion: Spontaneous esophageal hematoma, although rare in incidence, should be identified as a differential diagnosis in a patient on anticoagulation presenting with chest pain. Literature shows a higher incidence of this complication in women. Timely diagnosis and management along with discontinuing anticoagulation can significantly lower morbidity and mortality and overall has favorable prognosis.

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