Clin Cardiol. 1997 Mar;20(3):265-8. Tanabe K, Osada N, Suzuki N, Nakayama M, Yokoyama Y, Yamamoto A, Oya M, Murabayashi T, Yamamoto M, Omiya K, Itoh H, Murayama M. Second Department of Internal Medicine, St. Marianna University School of Medicine, Kawasaki, Japan.
BACKGROUND AND HYPOTHESIS: The mechanism of sudden cardiac death occurring in patients with chronic fatigue is controversial. This study was designed to define a hypothesis that coronary arterial spasm and thrombus formation can occur during chronic fatigue.
METHODS: For evaluating the feasibility of coronary arterial spasm, erythrocyte magnesium (Mg) was measured. Blood coagulability was evaluated by the change of prostaglandin concentration. Subjects included 16 healthy male volunteers (mean age 21.6 +/- 2.5 years).
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Test conditions were as follows: (A) control state: a day following a night of good sleep; (B) temporary sleep deprivation: a day preceded by < 3 h of sleep; (C) chronic sleep deprivation: a day preceded by a month during which sleep lasted < 60% of that in condition (A) above.
The erythrocyte Mg concentration was measured by the atomic absorption method. The plasma concentration of thromboxane B2 and 6-keto-prostaglandin F1 alpha were measured in eight subjects by radioimmunoassay method.
RESULTS: (1) Mean erythrocyte Mg concentration was significantly less in chronic sleep deprivation (1.1 +/- 0.4 mg/dl) than in the control state (1.8 +/- 0.4 mg/dl, p < 0.01) or in temporary sleep deprivation (1.6 +/- 0.4, p < 0.01). (2) The level of thromboxane B2 was significantly higher during chronic sleep deprivation than under control conditions (104.4 +/- 78.0 vs. 20.4 +/- 9.0 pg/ml, p < 0.05). (3) There were no significant intergroup differences in 6-keto-prostaglandin F1 alpha level.
CONCLUSION: These findings could support the hypothesis that coronary arterial spasm and thrombus formation occur in chronic sleep deprivation.
PMID: 9068914 [PubMed – indexed for MEDLINE]