Self-reported habitual short sleep duration is associated with endothelial fibrinolytic dysfunction in men: a preliminary report.

STUDY OBJECTIVES

Habitual short sleep duration is associated with increased cardiovascular disease morbidity and mortality resulting from atherothrombotic events. The mechanisms responsible for this heightened cardiovascular risk are not fully understood. The capacity of the endothelium to release tissue-type plasminogen activator (t-PA), the primary activator of the fibrinolytic system, is a key endogenous defense mechanism against intravascular fibrin deposition and thrombosis. We tested the hypothesis that endothelial t-PA release is impaired in adults who sleep less than 7 h/night compared with adults who sleep between 7 and 9 h/night.

DESIGN

THIRTY ADULT MEN WERE STRATIFIED BASED ON AVERAGE NIGHTLY HABITUAL SLEEP DURATION: 15 with normal sleep duration (age: 55 ± 2 years; sleep duration: 7.6 h/night) and 15 with short sleep duration (56 ± 2 years; 6.1 h/night). Net endothelial release of t-PA was determined, in vivo, in response to intra-brachial infusions of bradykinin (12.5-50.0 ng/100 mL tissue/min) and sodium nitroprusside (1.0-4.0 μg/100 mL tissue/min).

MEASUREMENTS AND RESULTS

Net endothelial t-PA release to bradykinin was significantly lower (∼25%) in the short (from 0.4 ± 0.8 to 41.5 ± 4.3 ng/100 mL tissue/min) compared with the normal (0.4 ± 0.5 to 64.9 ± 6.7 ng/100 mL/tissue/min) sleep duration group. Furthermore, there was an inverse relation between average nightly sleep duration and peak t-PA release to bradykinin (r = 0.36, P < 0.05).

CONCLUSIONS

Endothelial t-PA release is impaired in adults who report short habitual sleep duration. Impaired endothelial fibrinolytic function may underlie the increased atherothrombotic risk associated with chronic short sleep.