title: The metabolic syndrome in elderly individuals is associated with greater muscular, but not elastic arterial stiffness, independent of low-grade inflammation, endothelial dysfunction or insulin resistance--The Hoorn Study.
abstract: The metabolic syndrome (MetS) increases cardiovascular disease (CVD) risk. How MetS increases CVD risk is incompletely understood, but increasing arterial stiffness is one candidate link, which in turn could be explained by (low-grade) inflammation, endothelial dysfunction (ED) or insulin resistance (IR). However, MetS-related increases in stiffness may not be uniformly distributed over muscular and elastic arteries. Therefore, the purpose of this study was to determine: (1) the associations between the MetS, and muscular and elastic arterial stiffness, and (2) whether any such associations could be explained by inflammation, ED or IR. These questions were addressed in the Hoorn Study. MetS was defined according to the NCEP (National Cholesterol Education Program) criteria. Arterial stiffness was determined by ultrasound, tonometry and echocardiography. Inflammation, ED and IR were estimated by C-reactive protein, flow-mediated vasodilation and the homoeostatic model for the assessment of IR, respectively. The results showed that MetS was associated with both femoral and brachial arterial stiffness, significantly so for the distensibility coefficients and for the femoral compliance coefficient. In the carotid artery and aorta, no particular pattern emerged. Additional adjustment for either inflammation, ED or IR did not materially alter the results. The results therefore indicate that muscular arteries may stiffen preferentially over elastic arteries and that distensibility is affected to a greater extent than compliance, thus maintaining volume compliance over vessel wall stiffening. Additionally, the increase in stiffness was not explained by inflammation, ED or IR and suggests that stiffening of the muscular arteries in MetS may not be the consequence of these phenomena.
authors.affiliation: Department of Internal Medicine, University Hospital Maastricht, Maastricht, The Netherlands. rma.henry@mumc.nl
authors.forename: R M A
authors.initials: RM
authors.lastname: Henry
authors.forename: I
authors.initials: I
authors.lastname: Ferreira
authors.forename: J M
authors.initials: JM
authors.lastname: Dekker
authors.forename: G
authors.initials: G
authors.lastname: Nijpels
authors.forename: P G
authors.initials: PG
authors.lastname: Scheffer
authors.forename: C D A
authors.initials: CD
authors.lastname: Stehouwer
mesh_terms: D000367:Age Factors; D000368:Aged; D001011:Aorta / Q000503:physiopathology; D001158:Arteries / Q000000981:diagnostic imaging / Q000503:physiopathology*; D015415:Biomarkers / Q000097:blood; D001786:Blood Glucose / Q000378:metabolism; D001794:Blood Pressure; D001916:Brachial Artery / Q000503:physiopathology; D002097:C-Reactive Protein / Q000378:metabolism; D002318:Cardiovascular Diseases / Q000097:blood / Q000209:etiology* / Q000503:physiopathology; D002339:Carotid Arteries / Q000503:physiopathology; D015331:Cohort Studies; D003430:Cross-Sectional Studies; D004548:Elasticity; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D005263:Femoral Artery / Q000503:physiopathology; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000150:complications* / Q000503:physiopathology; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D008055:Lipids / Q000097:blood; D008297:Male; D024821:Metabolic Syndrome / Q000097:blood / Q000150:complications* / Q000503:physiopathology; D008875:Middle Aged; D009426:Netherlands; D011159:Population Surveillance; D018570:Risk Assessment; D012307:Risk Factors; D014463:Ultrasonography; D014664:Vasodilation; D055105:Waist Circumference
chemical_list: D015415:Biomarkers; D001786:Blood Glucose; D007328:Insulin; D008055:Lipids; D002097:C-Reactive Protein