title: Large artery biomechanics and diastolic dysfunctionin patients with Type 2 diabetes.
abstract: OBJECTIVE
  To comprehensively characterize large artery biomechanical properties and examine their relationship to cardiac function in patients with Type 2 diabetes mellitus (DM).
  
  
  METHODS
  Fifty-five individuals with Type 2 DM were compared with 66 age- and sex-matched healthy control subjects. Arterial biomechanical properties were assessed by systemic arterial compliance (SAC; two-element Windkessel model), carotid-femoral pulse wave velocity (PWVc-f), femoral-dorsalis pedis pulse wave velocity (PWVf-d) and carotid augmentation index. Cardiac structure and function were assessed by echocardiography.
  
  
  RESULTS
  Individuals with Type 2 DM had lower SAC and higher PWVc-f when compared with the healthy population. The PWVc-f was significantly lower than the PWVf-d in control individuals, but this difference was not evident in individuals with Type 2 DM due to higher PWVc-f. Augmentation index was similar in both groups, but the time to the first systolic inflection (time to reflection) was shorter in the individuals with Type 2 DM. The individuals with Type 2 DM had a greater prevalence of diastolic abnormalities when compared with the control group. Arterial stiffness indices, including SAC and pulse pressure, correlated with left ventricular filling pressure (defined as peak velocity during early diastolic filling divided by the velocity of movement of the mitral valve annulus in early diastole; r = -0.33 and 0.36 respectively.
  
  
  CONCLUSIONS
  Patients with Type 2 DM on standard medication showed preferential stiffening of the large central arteries. However, carotid augmentation index was not different between the two groups and is therefore not a reliable indicator of large artery stiffening in this patient group. Diastolic dysfunction, present in a significant proportion of this population with Type 2 DM, was closely associated with arterial stiffening, suggesting a common aetiology.
authors.affiliation: Diabetes Complications Unit, Vascular Division, Baker IDI Heart and Diabetes Institute, Melbourne, Australia. georgia.soldatos@bakeridi.edu.au
authors.forename: G
authors.initials: G
authors.lastname: Soldatos
authors.forename: K
authors.initials: K
authors.lastname: Jandeleit-Dahm
authors.forename: H
authors.initials: H
authors.lastname: Thomson
authors.forename: M
authors.initials: M
authors.lastname: Formosa
authors.forename: K
authors.initials: K
authors.lastname: D'orsa
authors.forename: A C
authors.initials: AC
authors.lastname: Calkin
authors.forename: M E
authors.initials: ME
authors.lastname: Cooper
authors.forename: A A
authors.initials: AA
authors.lastname: Ahimastos
authors.forename: B A
authors.initials: BA
authors.lastname: Kingwell
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D050197:Atherosclerosis / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology*; D001783:Blood Flow Velocity / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology; D001916:Brachial Artery / Q000378:metabolism / Q000503:physiopathology*; D003430:Cross-Sectional Studies; D003924:Diabetes Mellitus, Type 2 / Q000150:complications / Q000378:metabolism / Q000503:physiopathology*; D003925:Diabetic Angiopathies / Q000378:metabolism / Q000503:physiopathology*; D003971:Diastole / Q000502:physiology*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D012307:Risk Factors; D014655:Vascular Resistance / Q000502:physiology; D055815:Young Adult