Potential interference between implanted cardiac devices such as pacemakers and implantable cardioverter-defibrillators and electromagnetic fields is an important concern for physicians taking care of patients with pacemakers and implantable cardioverter-defibrillators. There are many sources of electromagnetic interference (EMI); however, only a small number of these cause significant problems that need attention. Regardless of its source, EMI is of greater concern for a patient who is dependent on paced rhythm because inhibition of the pacemaker by EMI may produce ventricular standstill. It is important that cardiologists, internists, emergency medicine, critical care physicians, and anesthesiologists be aware of how EMI can affect the function of implanted cardiac devices so that appropriate treatment can be rendered and preventive measures instituted.
This study was designed to determine whether red-cell oxidative stress status and antioxidant enzyme levels can serve as markers in patients predisposed to in-stent stenosis. Blood was collected from patient groups undergoing coronary angiography for chest pain evaluation, namely, group A (without coronary artery disease), group B (previous coronary stents without in-stent stenosis), and group C (previous coronary stents with in-stent stenosis). Thiobarbituric acid reactive substances (measure of lipid peroxidation), glutathione-linked detoxification enzymes, catalase, and superoxide dismutase were determined. Compared with group A, patients in group C showed increased lipid peroxidation products and glutathione-S-transferase but decreased glutathione peroxidase and glutathione reductase activities. Results in group B patients were intermediate between those of groups A and C with significant decreases in glutathione peroxidase versus controls. In-stent stenosis is associated with significant increase in lipid peroxidation and attenuated glutathione-linked detoxification enzymes, consistent with oxidative stress.
Four patients with arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) are described. Two patients presented with sustained ventricular tachycardia and two with cardiac arrest from which they were successfully resuscitated. All four patients had typical electrocardiographic and echocardiographic features and fulfilled the task force criteria for diagnosis of ARVD/C. All four patients had T wave inversion in chest leads V1 to V4, and two had epsilon waves, and all four had premature ventricular complexes of left bundle branch block and left axis deviation pattern. All patients showed a markedly enlarged, thin and hypokinetic right ventricle. Three patients had implantable cardioverter defibrillator (ICD) implanted and are doing well. One patient who refused an ICD died suddenly 6 months after his initial presentation. Three surviving patients are on sotalol for suppression of ventricular tachycardia episodes triggering ICD shocks. A review of the existing literature on diagnosis of ARVD/C, its clinical presentation and natural history, its genetic basis, risk stratification, treatment, and prognosis is presented.
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