Concurrent Morning Increase in Platelet Aggregability and the Risk of Myocardial Infarction and Sudden Cardiac Death

G. H. Tofler, D. Brezinski, A. I. Schafer, C. A. Czeisler, J. D. Rutherford, S. N. Willich, R. E. Gleason, G. H. Williams, J. E. Muller

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We have previously reported that the frequencies of myocardial infarction and of sudden cardiac death are highest during the period from 6 a.m. to noon. Since platelet aggregation may have a role in triggering these disorders, we measured platelet activity at 3-hour intervals for 24 hours in 15 healthy men. In vitro platelet responsiveness to either adenosine diphosphate (ADP) or epinephrine was lower at 6 a.m. (before the subjects arose) than at 9 a.m. (60 minutes after they arose). The lowest concentration of these agents required to produce biphasic platelet aggregation decreased (i.e., aggregability increased) from a mean ±SEM of 4.7±0.6 to 3.7±0.6 μM (P<0.01) for ADP and from 3.7±0.8 to 1.8±0.5 μM (P<0.01) for epinephrine. The period from 6 to 9 a.m. was the only interval in the 24-hour period during which platelet aggregability increased significantly. We subsequently studied 10 subjects on alternate mornings after they arose at the normal time and after delayed arising. The morning increase in platelet aggregability was not observed when the subjects remained supine and inactive. Thus, there is a temporal association between increased platelet aggregability in the morning and an increased frequency of myocardial infarction and of sudden cardiac death. Demonstration of this association does not establish a cause–effect relation, but together with other evidence linking platelets to these disorders, it may provide insight into the mechanisms precipitating myocardial infarction and sudden cardiac death and aid in the design of more effective preventive measures. (N Engl J Med 1987; 316:1514–8.), IT has recently been demonstrated that nonfatal myocardial infarction1 and sudden cardiac death2 are more likely to occur between 6 a.m. and noon than during other times of the day. Since platelets may be involved in the pathogenesis of these conditions, a possible explanation for the similar morning increases in onset of these disorders may be that platelets become more aggregable when people arise from sleep and become active. Such platelets would perhaps be more likely to aggregate at the site of a thrombogenic, atherosclerotic lesion and precipitate arterial occlusion.3 4 5 To determine whether platelet hyperactivity occurs during the morning, we…

Original languageEnglish (US)
Pages (from-to)1514-1518
Number of pages5
JournalNew England Journal of Medicine
Issue number24
StatePublished - Jun 11 1987

ASJC Scopus subject areas

  • Medicine(all)


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