Haeok Lee

Abstract

BACKGROUND: Despite the fact that the effectiveness of thrombolytic therapy for acute myocardial infarction is inversely related to the time between the onset of signs and symptoms and definitive therapy, long delays in seeking treatment have been reported consistently. A variety of reasons for the delays have been suggested. Because such delays are associated with longer hospital stays and higher mortality and morbidity, interventions that reduce delays are especially important. PURPOSE: To examine research on patients with myocardial infarction who delay seeking professional treatment and the factors related to the delay, and to review studies indicating that black patients have premonitory clinical signs and symptoms of myocardial infarction and changes in the structure and function of the cardiovascular system that are different from those in whites. METHODS: Studies were reviewed by using MEDLINE and by doing a manual search of relevant research journals in cardiovascular, nursing, and behavioral medicine published since 1970. Data published by the United States Department of Health and Human Services and the Agency for Health Care Policy and Research were also reviewed. RESULTS: Although the lengths of the delays have varied considerably, blacks have generally experienced longer delays than whites between acute onset of signs and symptoms of myocardial infarction and arrival at the emergency department. Studies show that black patients have a lower incidence of classic chest pain or discomfort but an increased incidence of dyspnea, whereas white patients are much more likely to complain of chest pain. CONCLUSION: Culturally sensitive public education about typical and atypical premonitory clinical signs and symptoms of myocardial infarction and the significance of early treatment of myocardial infarction in blacks is needed.

Abstract

Left ventricular (LV) function is an important predictor of morbidity and mortality after myocardial infarction (MI). Changes in LV function have been examined during the early and late phases after MI, but serial measurements of LV function during the subacute period have not been performed. To assess sequential changes in LV function during the subacute period after MI, we used quantitative two-dimensional echocardiography to examine 22 patients over a 1-year period. Twenty-one of the 22 patients had a Q-wave MI. Eleven had an anterior MI and 10 had an inferior MI; their peak creatine phosphokinase (CPK) was 1213 mlU/ml ± 14. Three weeks after acute MI, LV ejection fraction (LVEF) had increased from 45% to 52%. Seven of 19 patients showed an LVEF <43% at baseline. In five of these patients, LVEF improved, but in two patients, LVEF was still <43% in week 3. There was a significant enlargement of LV end-diastolic volume (LVEDV) (94 ml to 112 ml, p < 0.05) across the four observations but no change in LV end-systolic volume (LVESV; 54 ml to 56 ml, p = n.s.). When two groups (G1 [depressed], LVEF ≤43%; G2 [preserved], LVEF >43%) were compared, the group with depressed LVEF demonstrated a higher probability of improvement in LVEF (34% to 47%, p < 0.001) and stroke volume (38 ml to 65 ml, p < 0.01).