Ventricular Tachycardia in Acute Myocardial Infarction: The Role of Hypophosphatemia

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The relationship between serum concentration of certain electrolytes and the pathogenesis of ventricular arrhythmia in myocardial infarction has been the subject of frequent review. The role of hypophosphatemia in the pathogenesis of arrhythmia in patients with acute myocardial infarction has not been as well studied. In our study group of 325 consecutive patients admitted to the coronary care unit of a community hospital, 111 were confirmed to have had a myocardial infarction. Patients were continuously monitored for ventricular arrhythmia during the first 24 hours, and the electrocardiographic records were reviewed for documentation of arrhythmia. From an admission blood sample, measurement of electrolytes included serum phosphate, calcium, bicarbonate, potassium, and magnesium. Associations between ventricular tachycardia and serum electrolyte abnormalities including magnesium, potassium, phosphate, calcium, and bicarbonate were studied. Low phosphate (less than 2.6 mg/dL) was a significant predictor of ventricular tachycardia in the myocardial infarction group. In the entire group of 325 patients prior to the confirmation of myocardial infarction, both low bicarbonate and low phosphate were significant predictors of ventricular tachycardia during the first 24 hours of hpspitalization. Although management of acidosis is considered early in the hospital course, phosphate replacement therapy is usually not as often considered. We recommend further study on the effectiveness of replacement therapy in hypophosphatemic patients with chest pain to reduce the risk of ventricular tachycardia.

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