PLATELET-FUNCTION AND FIBRINOLYTIC-ACTIVITY IN HYPERTENSIVE AND NORMOTENSIVE SLEEP-APNEA

Citation
C. Rangemark et al., PLATELET-FUNCTION AND FIBRINOLYTIC-ACTIVITY IN HYPERTENSIVE AND NORMOTENSIVE SLEEP-APNEA, Sleep, 18(3), 1995, pp. 188-194
Citations number
37
Categorie Soggetti
Behavioral Sciences","Clinical Neurology
Journal title
SleepACNP
ISSN journal
01618105
Volume
18
Issue
3
Year of publication
1995
Pages
188 - 194
Database
ISI
SICI code
0161-8105(1995)18:3<188:PAFIHA>2.0.ZU;2-C
Abstract
Platelet function and fibrinolytic activity was studied during rest an d after ergometric exercise in 13 hypertensive or normotensive patient s with obstructive sleep apnea (OSA) and in 10 sex- and weight-matched controls. All patients had undergone a complete polysomnography for t he diagnosis of OSA. The controls did not undergo any sleep investigat ion but had no history of snoring or witnessed apneas during sleep. On antihypertensive drug wash-out, two of the patients were normotensive , whereas 11 had mild to moderate hypertension. Platelet aggregation m easured by adenosine 5'-diphosphate- or adrenaline-induced aggregation , platelet factor-4 or beta-thromboglobulin did not differ between pat ients and controls. During exercise beta-thromboglobulin decreased sig nificantly in both OSA patients and controls. Plasma tissue plasminoge n activator activity was similar in OSA patients and controls and incr eased significantly in both groups after exercise. Plasminogen activat or inhibitor type 1 (PAI-1) was 18.4 +/- 3.6 IU/ml in OSA patients com pared with 8.2 +/- 1.7 IU/ml in controls (p < 0.029) during rest, indi cating decreased fibrinolytic activity. The difference between groups remained after exercise (p < 0.017). Blood pressure elevation was more common and body mass index (BMI) was higher in patients with OSA, but there was no direct relation between blood pressure level or BMI and PAI-1. Nevertheless, differences between groups were smaller when bloo d pressure and obesity were accounted for. It is concluded that patien ts with OSA may exhibit decreased fibrinolytic activity. Low fibrinoly tic activity may represent a confounding pathophysiological mechanism behind the high incidence of myocardial infarction and stroke in patie nts with OSA.