Concurrent Morning Increase in Platelet Aggregability and the Risk of Myocardial Infarction and Sudden Cardiac Death
Abstract
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 microM (P less than 0.01) for ADP and from 3.7 +/- 0.8 to 1.8 +/- 0.5 microM (P less than 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.
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Highest platelet aggregability and highest concentration of plasminogen activator inhibitor-1 (PAI-1) occur in the morning.
“For instance, highest platelet aggregability and highest concentration of plasminogen activator inhibitor-1 (PAI-1) occur in the morning (109, 110).”
From Role of the circadian system in cardiovascular disease (2018) · cites this paper as [109]
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Self-citation
- Authors
- Tofler, G. H., Brezinski, D., Schafer, A. I., Czeisler, C. A., Rutherford, J. D., Willich, S. N., Gleason, R. E., Williams, G. H., & Muller, J. E.
- Affiliations
- Brigham and Women's Hospital (US)
- Venue
- New England Journal of Medicine
- Publisher
- Massachusetts Medical Society
- Published
- 1987-06-11
- Volume
- 316
- Issue
- 24
- Pages
- 1514-1518
- ISSN
- 0028-4793 (ISSN-L)
- 1533-4406
- OpenAlex
- W1974742589
- Cited by
- 1,072
- References
- 35
- Citations by year
- 2026: 7 · 2025: 14 · 2024: 8 · 2023: 13 · 2022: 22 · 2021: 18 · 2020: 11 · 2019: 18 · 2018: 16 · 2017: 22 · 2016: 18 · 2015: 21 · 2014: 28 · 2013: 27 · 2012: 29
- FWCI
- 21.71
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- New England Journal of Medicine (publishedVersion)
- PubMed (publishedVersion)
- Funders
- U.S. Public Health Service (9535 A607606)
- National Heart, Lung, and Blood Institute (HL-27465, HL-705861)
- Topics
- Health Sciences › Medicine › Hematology › Platelet Disorders and Treatments
- Health Sciences › Medicine › Hematology › Blood Coagulation and Thrombosis Mechanisms
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Antiplatelet Therapy and Cardiovascular Diseases
- Keywords
- platelet aggregability, circadian rhythm, myocardial infarction, sudden cardiac death, adenosine diphosphate, epinephrine, supine rest, platelet function
- MeSH terms
- Adenosine Diphosphate, Adult, Death, Sudden, Epinephrine, Hematocrit, Humans, Male, Myocardial Infarction, Platelet Aggregation, Platelet Count, Posture, Time, In Vitro Techniques
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