title: Seasonal variations of rheological and hemostatic parameters and acute-phase reactants in young, healthy subjects.
abstract: The incidence of cardiovascular diseases is increased in winter months. Recent studies have shown seasonal changes in plasma viscosity, fibrinogen, and factor VII activity with elevated levels during winter. An increase in these factors generates a "hypercoagulable state," which may lead to a rise in cardiovascular morbidity and mortality. It has been suggested that an increase in upper respiratory infections might be the underlying cause for the raised acute-phase reactants, in particular fibrinogen, during the winter season. We investigated seasonal variations of 26 parameters, determining blood rheology and hemostasis in 16 healthy volunteers (8 men and 8 women) aged 20 to 41 years. They were seen at monthly intervals over a period of 1 year. Seasonal variation with peak fitted values in the winter months was found for plasma viscosity (P < .001 for the seasonal difference), red blood cell deformability (P < .001), whole blood viscosity (P < .001), hemoglobin (P < .001), hematocrit (P < .001), mean corpuscular volume (P = .001), platelet count (P = .01), alpha 1-glycoprotein (P < .001), fibrinogen (measured by immunonephelometry; P < .001), plasminogen activator inhibitor-1 (P = .002), LDL cholesterol (P = .003), and triglyceride levels (P < .001). HDL cholesterol (P < .001) and cortisol (P = .001) showed inverse seasonal patterns, with a maximum during summertime. No statistically significant seasonal variations were seen for red blood cell aggregation, complement factor C4, total cholesterol, ceruloplasmin, haptoglobin, white blood cell count, and plasminogen. These data do not support the hypothesis that increased morbidity and mortality from cardiovascular diseases during winter may be mainly attributable to increased synthesis of acute-phase proteins due to infections. The cause for the seasonal variations in rheological and hemostatic parameters remains unclear and should be studied in more detail.
authors.affiliation: Department of Internal Medicine II, Cardiology, University of Ulm Medical Center, Germany. margit.froehlich@medizin.uni-ulm.de
authors.forename: M
authors.initials: M
authors.lastname: Fröhlich
authors.forename: M
authors.initials: M
authors.lastname: Sund
authors.forename: S
authors.initials: S
authors.lastname: Russ
authors.forename: A
authors.initials: A
authors.lastname: Hoffmeister
authors.forename: H G
authors.initials: HG
authors.lastname: Fischer
authors.forename: V
authors.initials: V
authors.lastname: Hombach
authors.forename: W
authors.initials: W
authors.lastname: Koenig
mesh_terms: D000209:Acute-Phase Proteins / Q000032:analysis*; D000328:Adult; D001798:Blood Proteins / Q000032:analysis*; D001809:Blood Viscosity; D002318:Cardiovascular Diseases / Q000453:epidemiology; D004909:Erythrocyte Indices; D005260:Female; D005340:Fibrinogen / Q000032:analysis; D006487:Hemostasis; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007958:Leukocyte Count; D008055:Lipids / Q000097:blood; D008297:Male; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D012016:Reference Values; D012307:Risk Factors; D012621:Seasons
chemical_list: D000209:Acute-Phase Proteins; D001798:Blood Proteins; D008055:Lipids; D017395:Plasminogen Activator Inhibitor 1; D005340:Fibrinogen; D006854:Hydrocortisone