Ventricular tachycardia in acute myocardial infarction: the role of hypophosphatemia.

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 hospitalization. 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.

Rapid resolution of hyperkinesis after exercise. Two-dimensional echocardiographic studies in normal subjects.

Abnormal wall motion detected with exercise echocardiography identifies ischemic myocardium, while normal myocardium exhibits hyperkinetic motion. The normal, hyperkinetic response to exercise is transient and is predictive of an excellent prognosis. However, there are few data on the duration of the hyperkinesis after peak exercise. Our purpose was to determine the time course of wall thickening after exercise in eight normal subjects with two-dimensional echocardiography. Percentage of wall thickening increased from 53 +/- 24 percent at baseline to 82 +/- 24 percent at 0 to 2 min postexercise (p < 0.001 vs baseline) and then decreased to 64 +/- 27 percent at 2 to 4 min, and 54 +/- 20 percent at 5 to 7 min (both NS vs baseline). We conclude that (1) systolic wall thickening is maximal within the initial 2 min following peak exercise, and (2) accurate identification of hyperkinetic, normal myocardium with exercise echocardiography requires immediate postexercise imaging.