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to the editor: Hohnloser et al. (Dec. 9 issue), 1 who conducted the Defibrillator in Acute Myocardial Infarction Trial (DINAMIT), assume that implantable cardioverter–defibrillator (ICD) therapy early after myocardial infarction decreases the rate of death due to arrhythmia but that the patients die of other cardiac disease. We believe alternatives must be considered. First, it should not be assumed that the mechanism of death has been changed by the ICD; rather, the presence of an ICD will affect classification (a doctor or committee member will be less likely to believe a death is due to arrhythmia if a patient has a device). It is more likely that ICD implantation has led to worsening cardiac function. Second, the implantation and testing of a defibrillator may negatively interrupt the adaptive remodeling in the dynamic postinfarction myocardium. Shocks delivered during testing of the device result in myocyte necrosis. 2 Furthermore, the effects of the implantation of the device on hemodynamic variables, including blood pressure and heart rate, predispose the myocardium to further ischemia and infarction. Neurohormonal activation and inflammation could also lead to maladaptive remodeling, hastening the downward spiral of chronic heart failure. 3 All these factors might be particularly detrimental immediately after a myocardial infarction.
implantable; defibrillator; myocardial infarction, Myocardial Infarction, Humans, Arrhythmias, Cardiac, Stroke Volume, Spironolactone, Defibrillators, Implantable, Eplerenone, Mineralocorticoid Receptor Antagonists
implantable; defibrillator; myocardial infarction, Myocardial Infarction, Humans, Arrhythmias, Cardiac, Stroke Volume, Spironolactone, Defibrillators, Implantable, Eplerenone, Mineralocorticoid Receptor Antagonists
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