Abstract
BackgroundAcute vigorous exercise, associated with increased release of plasma catecholamines, transiently increases the risk of primary cardiac arrest. We tested the effect of acute submaximal exercise on vasoactive substances and their combined result on platelet function.MethodsHealthy volunteers, hypertensive patients and patients with coronary artery disease (CAD) performed a modified treadmill exercise test. We determined plasma catecholamines, thromboxane A2, prostacyclin, endothelin-1 and platelet aggregation induced by adenosine diphosphate (ADP) and collagen at rest and during exercise.ResultsOur results during exercise showed a) platelet activation (increased thromboxane B2, TXB2), b) increased prostacyclin release from endothelium and c) decreased platelet aggregation in all groups, significantly more in healthy volunteers than in patients with CAD (with hypertensives lying in between these two groups).ConclusionDespite the pronounced activation of Sympathetic Nervous System (SNS) and increased TXB2 levels during acute exercise platelet aggregation decreases, possibly to counterbalance the prothrombotic state. Since this effect seems to be mediated by the normal endothelium (through prostacyclin and nitric oxide), in conditions characterized by endothelial dysfunction (hypertension, CAD) reduced platelet aggregation is attenuated, thus posing such patients in increased risk for thrombotic complications.
Highlights
Acute vigorous exercise, associated with increased release of plasma catecholamines, transiently increases the risk of primary cardiac arrest
The Double Product was determined in all patients at the peak of exercise with no significant differences between the three groups (Table 2)
There was a trend towards higher levels at the end of exercise in patients with coronary artery disease, but there were no significant differences between the three groups (Figure 3B)
Summary
Acute vigorous exercise, associated with increased release of plasma catecholamines, transiently increases the risk of primary cardiac arrest. Platelet aggregation and thrombosis play a central role in the pathogenesis of atherosclerosis, since platelet aggregates and thrombus formation has been found in the coronary arteries at sites of plaque rupture [1]. Platelets, upon their activation, further stimulate thrombus formation and recruit additional platelets by releasing thromboxane A2 (TXA2), adenosine diphosphate (ADP), and cytokines, which produce and promote surface thrombin generation and release vasoconstrictor substances [2]. Endothelin-1 (ET-1, a potent vasoconscrictive substance released by the endothelium) and plasma catecholamines play a major role in the pathogenesis of acute ischemic events, and stimulate platelet aggregation, exerting prothrombotic actions
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