title: Physical Properties of Blood Are Altered in Young and Lean Women with Polycystic Ovary Syndrome.
abstract: Classic features of polycystic ovary syndrome (PCOS) include derangement of metabolic and cardiovascular health, and vascular dysfunction is commonly reported. These comorbidities indicate impaired blood flow; however, other than limited reports of increased plasma viscosity, surprisingly little is known regarding the physical properties of blood in PCOS. We aimed to investigate whether haemorheology was impaired in women with PCOS. We thus measured a comprehensive haemorheological profile, in a case-control design, of lean women with PCOS and age-matched healthy controls. A clinical examination determined similar cardiovascular risk for the two groups. Whole blood and plasma viscosity was measured using a cone-plate viscometer. The magnitude and rate of red blood cell (RBC) aggregation was determined using a light-transmission aggregometer, and the degree of RBC deformability was measured via laser-diffraction ektacytometry. Plasma viscosity was significantly increased in women with PCOS. Blood viscosity was also increased for PCOS at lower-to-moderate shear rates in both native and standardised haematocrit samples. The magnitude of RBC aggregation-a primary determinant of low-shear blood viscosity-was significantly increased in PCOS at native and 0.4 L·L-1 haematocrit. No difference was detected between PCOS and CON groups for RBC deformability measurements. A novel measure indicating the effectiveness of oxygen transport by RBC (i.e., the haematocrit-to-viscosity ratio; HVR) was decreased at all shear rates in women with PCOS. In a group of young and lean women with PCOS with an unremarkable cardiovascular risk profile based on clinical data, significant haemorheological impairment was observed. The degree of haemorheological derangement observed in the present study reflects that of overt chronic disease, and provides an avenue for future therapeutic intervention in PCOS.
authors.affiliation: Menzies Health Institute Queensland, Griffith University, Gold Coast, Queensland, Australia.
authors.forename: Michael J
authors.initials: MJ
authors.lastname: Simmonds
authors.affiliation: Bond Institute of Health and Sport, Faculty of Health Sciences and Medicine, Bond University, Gold Coast, Queensland, Australia.
authors.forename: Nikki
authors.initials: N
authors.lastname: Milne
authors.affiliation: Monash IVF, Southport, Queensland, Australia.
authors.forename: Kee
authors.initials: K
authors.lastname: Ong
authors.affiliation: Menzies Health Institute Queensland, Griffith University, Gold Coast, Queensland, Australia.
authors.forename: Emily
authors.initials: E
authors.lastname: Brotherton
authors.affiliation: Menzies Health Institute Queensland, Griffith University, Gold Coast, Queensland, Australia.
authors.forename: Antony P
authors.initials: AP
authors.lastname: McNamee
authors.affiliation: Menzies Health Institute Queensland, Griffith University, Gold Coast, Queensland, Australia.
authors.forename: Jarod
authors.initials: J
authors.lastname: Horobin
authors.affiliation: Menzies Health Institute Queensland, Griffith University, Gold Coast, Queensland, Australia.
authors.forename: Surendran
authors.initials: S
authors.lastname: Sabapathy
mesh_terms: D000328:Adult; D001835:Body Weight; D016022:Case-Control Studies; D005260:Female; D018056:Hemorheology; D006801:Humans; D011085:Polycystic Ovary Syndrome / Q000503:physiopathology*