Stroke Post Myocardial Infarction
Abstract & Commentary
By Michael H. Crawford, MD, Professor of Medicine, Chief of Clinical Cardiology, University of California, San Francisco. Dr. Crawford is on the speaker's bureau for Pfizer.
Source: Witt BJ, et al. A Community-Based Study of Stroke Incidence After Myocardial Infarction. Ann Intern Med. 2005;143:785-792.
The relationship of stroke to myocardial infarction (MI) remains controversial. Thus, Witt and colleagues from the Mayo Clinic in Rochester, MN, evaluated a community-based cohort of 2160 patients with acute MI hospitalized between 1979 and 1998 to determine the incidence of stroke after MI and its influence on survival. Ischemic and hemorrhagic strokes were included. Follow-up averaged 5.6 years (range, 0-22 years). There were 273 strokes, of which 95% were ischemic and 18% occurred within 30 days of MI (2.3% of MI patients). The stroke rate was 22.6 per 1000 person-months during the first 30 days post MI (hazard ratio 44 vs the no MI control population). Thereafter, the stroke risk declined to 2-3 times the non-MI population's rate for 3 years. After 3 years, it was no different than the control population rate. These rates did not differ between the first and second decades of the study despite the advances in MI treatment. The risk of stroke was higher in those with diabetes and previous stroke, and increased with advancing age. The occurrence of stroke increased mortality (hazard ratio 2.89) independent of other risk factors. Witt et al concluded that the risk of stroke is increased post-MI and increases the risk of death.
Commentary
The absolute 30-day stroke risk in this trial of 2% is similar to that observed in other studies, and is virtually unchanged over the last 30 years. Since there have been major improvements in the management of acute MI patients, this suggests that strokes are not directly related to the MI. Although there was a small increase in early stroke risk demonstrated in larger MIs, this implies that embolic stroke could be reduced by earlier reperfusion. The fear that thrombolysis and aggressive platelet inhibition could contribute to hemorrhagic strokes is not supported by this study.
It has been suggested that perhaps the general inflammatory state surrounding an MI increases the stoke risk. If so, current therapy for MI is not addressing this issue adequately. Whether oral anticoagulant therapy would reduce stroke rates is unknown. On the other hand, perhaps embolic strokes observed in earlier decades are now replaced by thrombotic strokes because older individuals now survive acute MI. Why the increased risk persists for 3 years is also not understood. It is difficult to believe the myocardial inflammatory state lasts that long. Until we know more about the pathophysiology of post-MI stroke, we should maximize therapy for the known stroke risk factors in post-MI patients.
There are some limitations to this study. The results may not apply to people of non-European origin, since there were few such people in this part of Minnesota. Also, this was a retrospective chart review. In addition, subtyping ischemic strokes into cardioembolic and others was not available. Finally, drug therapy and its impact could not be determined.
The relationship of stroke to myocardial infarction (MI) remains controversial. Thus, Witt and colleagues from the Mayo Clinic in Rochester, MN, evaluated a community-based cohort of 2160 patients with acute MI hospitalized between 1979 and 1998 to determine the incidence of stroke after MI and its influence on survival. Ischemic and hemorrhagic strokes were included. Follow-up averaged 5.6 years (range, 0-22 years).You have reached your article limit for the month. Subscribe now to access this article plus other member-only content.
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