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.

The impact of time and day on the presentation of acute coronary syndromes

“…Circadian changes in catecholamines, cortisol, blood pressure, and pulse have been described, potentially altering coronary artery wall shear stress. 16 An increase in platelet aggregation has been described in the morning, 17 and the fibrinolytic system has marked circadian variation. 18 The mechanisms underlying the increase in STEMI, which is more often associated with an occlusive, fibrin-rich thrombus than NSTEMI and UA, may also underpin the resistance to thrombolytic therapy that has been observed in the early morning and late evening hours.…”

Platelet Glycoprotein IIIa Pl A Polymorphism, Fibrinogen, and Platelet Aggregability

“…19 Blood was drawn in 3.8% sodium citrate solution (9:1 vol/vol). Platelet-rich plasma was separated by centrifugation for 10 minutes at 160g.…”

Circadian pattern of acute variceal bleeding among cirrhotic Egyptian patients

“…For instance, in the mid 1980s, it was proved that events potentially favouring vascular occlusion, namely hypercoagulability and hypofi brinolysis, show their peaks at the time of the maximal incidence of myocardial infarction both in normal subjects and in patients with ischemic heart diseases [17][18][19][20][21] . A chronoriskbased evidence for the determination of the acute events was thereby produced.…”

“…Interestingly, platelet adhesiveness and aggregation are relatively lower in the late evening, theoretically making primary hemostasis less effective [18,21], although the extent of variation of all these parameters in healthy subjects is much more limited than that of fi brinolysis. The confi rmation of these rhythms in cirrhosis would further detail and strengthen the hypothesis of a contribution of the hemostatic and clotting systems in facilitating the evening peak of hemorrhage.…”