Texas Heart Institute journal
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Heparin-induced thrombocytopenia is an immunologically mediated syndrome that is associated with potentially life-threatening arterial and venous thrombosis. Re-exposing patients who have heparin-induced thrombocytopenia to heparin during cardiopulmonary bypass may be hazardous. We describe the re-exposure to unfractionated heparin of a patient with a left ventricular assist device and evidence of heparin-induced thrombocytopenia who needed cardiac transplantation, which was accomplished without complications.
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Comment Letter Historical Article
History of streptokinase use in acute myocardial infarction.
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Acute fulminant myocarditis commonly manifests itself as severe, rapidly progressive hemodynamic deterioration and circulatory collapse that may be resistant to high doses of inotropic agents and steroids and to mechanical support by intra-aortic balloon pump. Acute myocarditis has a high mortality rate and may necessitate heart transplantation. ⋯ Two of our patients who experienced profound, therapy-resistant heart failure arising from acute myocarditis were successfully supported by the TandemHeart. To the best of our knowledge, these are the 1st reported cases in which the TandemHeart percutaneous ventricular assist device served as a bridge to recovery from acute fulminant myocarditis.
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Inherited arrhythmic disorders comprise a group of syndromes with unique genetic abnormalities and presentations but with very similar clinical outcomes and complications, the most terrifying of which are life-threatening arrhythmias and sudden cardiac death. Advances in molecular biology have enabled us to define and pinpoint many such disorders, which were previously labeled as idiopathic, to specific genes on various chromosomes. The current trend in the management of these potentially deadly disorders is to use pharmacotherapy (antiarrhythmic agents) and defibrillators for the prevention of sudden death; however, targeted therapy at a molecular level appears to be the path of the future. Herein, we review long QT and Brugada syndromes and focus on the genetics, pathophysiology, and clinical manifestations of these inherited arrhythmogenic disorders that affect patients with structurally normal hearts.