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Summary: Although the pathophysiological significance of resistant hypertension in postâmyocardial infarction (MI) patients is established, the mechanisms by which increased afterload in that setting worsens outcome are unclear. With regard to sudden cardiac death, whether increased afterload alters the electrophysiological substrate after MI is unknown. We established a new large animal model of chronic post-MI remodeling with increased afterload that exhibits widespread deposition of fibrosis in remote areas from the anterior MI, mimicking the disease phenotype of patients with advanced ischemic heart disease. We identified the mode of initiation and mechanism of arrhythmias that were consistently unmasked by hypokalemia in this clinically relevant model. Key Words: arrhythmias, conduction, hypokalemia, increased afterload, myocardial infarction