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Although improvements in the treatment of thalassemia with transfusion and chelation therapy have been achieved, iron overload because of repeated red blood cell transfusions continue to cause organ dysfunction. The prognosis is determined by the degree of involvement of heart disease, mortality in these patients is mainly because of heart failure. In this case, cardiac hemosiderosis due to thalassemia and admitted to our Emergency Room with ventricular tachycardia with hemodynamic disrupts, then have implantable cardioverter defibrillator (ICD), 30-year-old male patient is presented. This is the first report among the thalassemia patients, presented with ventricular tachycardia based on literature search.
Balloon expandable stents are an integral part in the catheter treatment of congenital heart disease. In the growing child, stents require dilatation to greater diameters over time. The Cook Formula stent is a recent 316 stainless steel open-cell design licensed for peripheral vascular work. The Cook Formula stent is a premounted balloon-expandable stent that can be significantly overdilated with virtually no shortening allowing for precise placement and minimal protrusion into adjacent vessels. The Formula stent is a very versatile addition to the range of stents for use in the catheter treatment of complex congenital heart disease in children.
The purpose of the prospective, multicenter, nonrandomized CABANA study was to evaluate periprocedural clinical outcomes in high surgical risk patients with carotid artery stenosis treated with the Carotid WALLSTENT plus FilterWire EZ Embolic Protection System by a diverse group of clinicians. CAS with the Carotid WALLSTENT and FilterWire EZ yielded a low 30-day MAE rate that did not differ significantly across operator experience and training levels.
Chemotherapy-induced heart failure is increasingly recognized as a major clinical challenge. Cardiotoxicity of imatinib mesylate, a highly selective and effective anticancer drug belonging to the new class of tyrosine kinase inhibitors, is being reported in patients, some progressing to congestive heart failure. This represents an unanticipated challenge that could limit effective drug use. Understanding the mechanisms and risk factors of imatinib mesylate cardiotoxicity is crucial for prevention of cardiovascular complications in cancer patients. The results indicate that imatinib action on the heart targets cardiomyocytes and involves mitochondrial impairment and cell death that can be further aggravated by oxidative stress. This in turn offers a possible explanation for the current conflicting data regarding imatinib cardiotoxicity in cancer patients and suggests that cardiac monitoring of older patients receiving imatinib therapy may be especially warranted.
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