[Thrombocyte activation. A link between stress and myocardial infarction?].
Platelet function is dynamically regulated in vivo, and stress or exercise may have prothrombotic effects due to platelet activation. Platelets are intimately involved in primary hemostasis and it is possible that platelet activation may be a link between stress and myocardial infarction via several mechanisms--neuro-hormonal activation, increased shear stress, and an increased risk for plaque rupture with ensuing platelet activation. Catecholamines and stress may overcome the platelet inhibition afforded by aspirin, which may limit its efficacy in preventing myocardial infarction. Lipid lowering therapy would be expected to attenuate platelet activation, but results to the contrary are presented. New and more efficient platelet inhibitors may antagonize also stress induced platelet activation and be more efficient in the prevention of thrombotic complications, but their greater efficacy also entail a greater risk for bleeding complications.
Wallén
N H
NH
Norrtälje sjukhus, Stockholm.
Larsson
P T
PT
Bröijersén
A
A
Hjemdahl
P
P
D002395:Catecholamines / Q000097:blood; D006801:Humans; D009203:Myocardial Infarction / Q000097:blood / Q000209:etiology* / Q000517:prevention & control; D015539:Platelet Activation / Q000187:drug effects; D013312:Stress, Physiological
D002395:Catecholamines
Trombocytaktivering. en länk mellan stress och hjärtinfarkt?