trointestinal bleeding after septal reduction therapy in patients with hypertrophic obstructive cardiomyopathy-associated acquired von Willebrand syndrome. J Thromb Haemost 2015; 13: 191-6.Summary. Background: Gastrointestinal hemorrhage is considered to be a severe complication of von Willebrand disease. The optimal therapy for acquired von Willebrand syndrome and severe gastrointestinal bleeding with hypertrophic cardiomyopathy is undefined. Patients/Methods: Seventy-seven patients (median age, 67 years; interquartile range [IQR], 56-75 years; 49% women) with hypertrophic cardiomyopathy underwent von Willebrand factor multimer testing and acquisition of bleeding history. Bleeding was detected in 27 (36%) (median age, 74 years; IQR 66-76 years; 74% women), 20 with gastrointestinal bleeding, including 11 women with transfusion dependence. In these 11 women, the median duration of transfusion dependency was 36 months (IQR 18-44 months), and the median number of transfusions required was 25 (IQR 20-38). Two patients had undergone bowel resection for bleeding, one of them twice. Seven patients showed angiodysplasia, and the remainder had no endoscopic lesion. Bleeding recurred after bowel surgery or endoscopic intervention and medical therapy for hypertrophic cardiomyopathy in 10 of 11 patients. Two patients had septal myectomy, and six patients underwent alcohol septal ablation. With the exception of one patient in whom a significant gradient persisted after septal ablation, after the periprocedural period, patients after septal reduction therapy remained free of recurrent bleeding and need for transfusions. Conclusion: Acquired von Willebrand syndrome is common in hypertrophic cardiomyopathy. Gastrointestinal bleeding often recurs after endoscopic therapy, but may be relieved by structural cardiac repair.
Absence of an infrarenal inferior vena cava is an infrequent finding on computed tomography scans and is usually an unexpected, incidental finding. This report concerns a young patient with an absent infrarenal inferior vena cava who presented with abdominal and back pain.
Reactive eosinophilia is associated with inflammatory bowel disease, but its association with eosinophilic myocarditis is rare. We report a case of a 42-year-old man who presented with hypovolemic shock secondary to diarrhea and recently diagnosed nonischemic cardiomyopathy (left ventricular ejection fraction, 0.29). Laboratory evaluation revealed marked peripheral eosinophilia. Cardiac magnetic resonance imaging showed evidence of subacute-to-chronic myocarditis, and endomyocardial biopsy results were consistent with eosinophilic myocarditis. Colonic biopsy specimens revealed ulcerative colitis and no eosinophils. Hematologic evaluation was negative for an alternative cause of eosinophilia. The patient was given corticosteroids; his diarrhea resolved, but there was no short-term improvement in his ejection fraction, so an implantable cardioverter-defibrillator was placed. Follow-up at one year showed that the patient's left ventricular ejection fraction had improved to 0.42.
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