Myocardial infarction location was not related to stroke occurrence
ACP J Club. 1994 Nov-Dec;121:82. doi:10.7326/ACPJC-1994-121-3-082
Bodenheimer MM, Sauer D, Shareef B, et al. Relation between myocardial infarct location and stroke. J Am Coll Cardiol. 1994 Jul;24:61-6.
To determine if an association exists between the site of myocardial infarction (MI) and the incidence of subsequent stroke.
A cohort followed for a mean of 25 months as part of the Multicenter Diltiazem Postinfarction Trial (MDPIT) was retrospectively reviewed for incidence of stroke.
Hospitals in the United States.
2466 patients between the ages of 25 and 75 years who were hospitalized and subsequently documented to have had an acute MI were randomly assigned in the MDPIT and formed the cohort. Exclusion criteria were cardiogenic shock, pulmonary hypertension, high-degree atrioventricular block, or other conditions likely to reduce survival.
Assessment of risk factors
Data pertaining to age, previous MI, New York Heart Association functional class, history of hypertension, insulin-dependent diabetes, cigarette smoking, cardiac findings, ejection fraction, thrombolysis, and drug treatment at hospital discharge were collected at baseline.
Main outcome measures
Any acute focal cerebral disorder resulting in localizing findings characterized as a stroke or transient ischemic attack (TIA). Assessors of outcomes were blinded to the site of the index MI.
91 patients had a stroke or a TIA during the follow-up period. 23 of 724 patients (3%) with an anterior wall MI had a stroke or TIA compared with 68 (4%) of 1742 patients with a nonanterior MI (relative risk [RR] 0.82, 95% CI 0.55 to 1.30). The study had an 86% chance of detecting an RR for stroke of 1.5 in patients with anterior compared with nonanterior MI. Using multivariate Cox analysis, only systolic blood pressure was predictive of stroke or TIA (P < 0.001). Patients with anterior infarction had a stroke rate similar to that of patients with nonanterior infarction (hazard ratio 0.825, CI 0.508 to 1.340).
No association was found between the site of myocardial infarction and the incidence of stroke or transient ischemic attack.
Sources of funding: A consortium grant from Godecke Aktiengesellschaft, Germany; Laboratories Dr. Esteve, SA, Spain; Marion Laboratories, Inc., Missouri; Nordic Laboratories, Inc., Canada; Lars Synthelabo, France; Tanabe Seiyaku Co. Ltd., Japan; Warner-Lambert International, New Jersey.
For article reprint: Dr. M.M. Bodenheimer, Chief of Cardiology, The Harris Chasanoff Heart Institute, Room 2135, Long Island Jewish Medical Center, New Hyde Park, NY 11042, USA. FAX 516-396-1580.
Contrary to the observations made in previous studies, Bodenheimer and colleagues report that strokes occur no more often after anterior myocardial infarctions than those located elsewhere. Recognizing that other differences between patient groups might mask an effect of infarction location (e.g., anticoagulation was used more often in those with anterior infarctions), the authors used multivariable analysis seeking independent risk factors. They found no association between anticoagulation and risk for stroke and, again, exonerated infarction site. In fact, only systolic pressure was a risk factor.
These results from a retrospective secondary analysis of trial data are not as trustworthy as those that would have been obtained had the primary purpose of the trial been to determine the relation between infarction site and risk for stroke. Assuming, however, that a major relation is excluded, the results add to the current uncertainty about appropriate long-term antithrombotic strategy for secondary prevention after MI. They argue that embolism from mural thrombus, which is known to be more common after anterior infarctions, may be only 1 of several potential stroke mechanisms after MI (and a minor one, at that).
These negative findings may not apply in the acute setting, and clots that appear on an echocardiogram may still be important. The results should not be construed as evidence that long-term anticoagulation does not prevent stroke after MI. Randomized studies used in a meta-analysis done by Bodenheimer and colleagues, which is reported in their discussion, show that anticoagulation reduces the risk for stroke, as does aspirin (1). The practical questions are as follows: Does warfarin work better in some patients than aspirin, and, if so, can such patients be identified? This study suggests that infarction site by itself is not helpful and highlights the need for a well-designed, direct comparison of antithrombotic approaches in this setting.
David C. Anderson, MD
Hennepin County Medical CenterMinneapolis, Minnesota, USA
1. Antiplatelet Trialists' Collaboration. Collaborative overview of randomised trials of antiplatelet therapy. I. Prevention of death, myocardial infarction, and stroke by prolonged antiplatelet therapy in various categories of patients. BMJ. 1994;308:81-106.