Journal Article10.1056/NEJM198706113162405
Concurrent morning increase in platelet aggregability and the risk of myocardial infarction and sudden cardiac death.
Geoffrey H. Tofler,Damian Brezinski,Andrew I. Schafer,Charles A. Czeisler,John D. Rutherford,Stefan N. Willich,Ray E. Gleason,Gordon H. Williams,James E. Muller +8 more
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TL;DR: The period from 6 to 9 a.m. was the only interval in the 24-hour period during which platelet aggregability increased significantly, and in vitro platelet responsiveness to either adenosine diphosphate or epinephrine was lower.
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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 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 increas...
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Circadian variation in the frequency of onset of acute myocardial infarction
James E. Muller,Peter Stone,Zoltan G. Turi,John D. Rutherford,Charles A. Czeisler,Corette B. Parker,W. K. Poole,Eugene R. Passamani,Robert Roberts,Thomas L. Robertson +9 more
TL;DR: If coronary arteries become vulnerable to occlusion when the intima covering an atherosclerotic plaque is disrupted, the circadian timing of myocardial infarction may result from a variation in the tendency to thrombosis.
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