A has been available as an antipyretic for approximately 100 years, and it has been known to have antiplatelet activity for .30 years.1 During the 1980s, several well-controlled trials unequivocally established aspirin as an effective agent for primary and secondary prevention of cardiac events.2,3 Despite the available data, the use of aspirin in acute coronary syndromes is inappropriately low.4 We undertook a retrospective, 1-year analysis of the antecedent use of aspirin for primary prevention by patients presenting with a primary diagnosis of acute myocardial infarction (AMI). • • • We performed a retrospective chart review of the 291 patients admitted to Stanford University Medical Center from June 1, 1996, to May 30, 1997, with a primary diagnosis of AMI. Patients were defined as having had an AMI by creatine phosphokinase elevation .2 times the normal range with either consistent clinical history, pathologic Q waves, or dynamic electrocardiographic repolarization abnormalities. We included only patients who had sufficiently detailed information available to ascertain aspirin use and other key study variables. We tabulated established cardiac risk factors that included male gender, age .55 years for men, or .65 years for women, previously diagnosed diabetes mellitus or systemic hypertension, current or previous tobacco use .20 packyears, a family history of coronary disease diagnosed before age 50, hypercholesterolemia as defined by National Cholesterol Education Program guidelines, and absence of estrogen replacement therapy in postmenopausal women. Individual patient data were obtained from both the admitting cardiologist and house staff notes. The emergency room attending’s note was reviewed as the deciding factor if there were discrepancies between recorded history of both medication use and the presence or absence of a certain risk factor. Lack of specific mention of a risk factor in a detailed history was taken as that factor being absent. Out-of-hospital transfers for cardiac catheterization were included if there was a full dictated admission note from an attending cardiologist addressing all of the relevant data points. Exclusion criteria included patients admitted with a different primary diagnosis, in-hospital transfers from other services, and transferred patients with an inadequate history. Of the 291 patient charts meeting the criteria for AMI, 123 were found to have sufficiently detailed information regarding the key variables to be included in the study population. The clinical profile of these patients was similar to patients for whom inadequate information was available. The average age of included patients was 69 years, versus 70 years for excluded patients (p 5 NS). Sixty-six percent of included patients were men versus 70% for those excluded. However, the ratio of patients admitted through the emergency department to those transferred from other hospitals was significantly higher in the study population (2.45/1) than the admission ratio for excluded patients (1.04/1, p 5 0.006), reflecting more complete histories for direct admissions. Of the 123 patients with complete information, 33 (27%) were taking some form of aspirin at the time of their AMI. Of the patients who were taking aspirin, 82% took a dose of 325 mg/day. With the exception of those with specified aspirin allergy (,3%), all patients received aspirin on admission. The average creatine phosphokinase elevation in the study population was 1,593 IU, with 53 patients (43%) with AMIs defined as transmural. Ninety-seven of the 123 study patients (76%) had diagnostic catherization for further evaluation and treatment. The distribution of known risk factors for coronary disease among the study population is summarized in Table I, with systemic hypertension and hypercholesterolemia occurring most often. By quantitative risk factor assessment, there were essentially equivalent numbers of highand low-risk patients. Categorization of patients based on whether they had .3 or ,3 risk factors demonstrated no significant differential use of aspirin therapy. We hypothesized that the proportion of patients From Stanford University Medical Center, Stanford, California. Dr. Alderman’s address is: Stanford University Medical Center CVRC261, Stanford, California 94305. E-mail: alderman@leland. stanford.ed. Manuscript received October 13, 1999; revised manuscript received and accepted January 31, 2000. TABLE I Baseline Characteristics of Patients
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Oct 20, 2023
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