Elapsed time from symptom onset and acute myocardial infarction in a community hospital.
Creator
Logue EE; Ognibene A; Marquinez C; Jarjoura D
Publisher
Annals of emergency medicine
Date
1991
1991-04
Description
STUDY OBJECTIVE: Previous reports have emphasized that thrombolytic therapy for acute myocardial infarction should be initiated within three or four hours of symptom onset to obtain the best clinical outcomes. However, our clinical impression was that late arrivers, who often do not receive thrombolytic therapy, have a good short-term prognosis. Therefore, we investigated the relationships among the elapsed time from symptom onset, thrombolytic therapy, and short-term prognosis in acute myocardial infarction patients. The research hypothesis was that late arrivers have a better in-hospital prognosis because they have less severe disease that may involve spontaneous thrombolysis. DESIGN: Observational cohort study based on reviewing medical records and emergency department service logs. SETTING: 500-bed teaching hospital with medical school affiliation in northeastern Ohio. TYPE OF PARTICIPANTS: Four hundred consecutive patients with acute infarction confirmed by chest pain and positive ECGs or elevated cardiac enzymes. MEASUREMENTS AND MAIN RESULTS: Patients arriving early (elapsed time less than or equal to 1.5 hours) were more likely to be in Killip class III or IV (P = .04) or to have hypotension (P = .0004); and they experienced twofold increased odds of ventricular tachycardia (P = .007), cardiac arrest (P = .03), or death (P = .01). Patients arriving late (elapsed time greater than 3.5 hours) were more likely to have a history of angina (P = .002) and had a better short-term prognosis. CONCLUSIONS: Time of ED arrival after onset of acute myocardial infarction symptoms distinguishes two patient groups that differ in their risk of in-hospital complications. Late arrivers have better short-term prognoses and less (acutely) severe disease, and may have less need for thrombolytic therapy because of possible spontaneous thrombolysis. Patients with prior angina may need education on seeking care if their symptoms change.
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.