title: Associations between cardiac target organ damage and microvascular dysfunction: the role of blood pressure.
abstract: BACKGROUND
  Microvascular dysfunction may be an early precursor of cardiovascular disease (CVD). Increased left ventricular mass (LVM), concentric left ventricular remodelling and increased left atrial size are the factors that could predict future CVD. We investigated whether microvascular dysfunction was associated with these cardiac measures.
  
  
  RESULTS
  Laser Doppler fluximetry of skin vessels was used to study associations with risk factors and echocardiographic measurements of LVM, relative wall thickness (RWT), and left atrial size in 305 people (aged 40-65 years; 117 with type 2 diabetes). Flow in response to a 3-min arterial occlusion was measured. Postischaemic peak flow responses were categorized into three distinct groups: slow rise to peak (normal), nondominant early peak group (mildly abnormal) and a dominant early peak (abnormal). Those with a dominant early peak had higher blood pressure (P = 0.001), weight (P = 0.001), fasting glucose (P = 0.001) and prevalence of diabetes (P = 0.02). LVM (P = 0.01), RWT (P < 0.001) and left atrial size (P < 0.001) were greater with worsening postischaemic peak flow responses. Differences in LVM between postischaemic response groups were accounted for by blood pressure (BP). However, differences in BP and other CVD risk factors did not account for the greater RWT and left atrial size observed in the more adverse peak response groups [geometric mean of RWT [95% confidence interval (CI)] 0.40 (0.38-0.41) vs. 0.41 (0.40-0.42) vs. 0.43 (0.41-0.45), P = 0.007; left atrial size 36.1 (35.4-36.1) vs. 37.4 (36.8-38.0) vs. 38.7 (37.5-40.0), P = 0.002 for normal vs. mildly abnormal vs. abnormal respectively].
  
  
  CONCLUSIONS
  An abnormal microcirculatory cutaneous peak flow response following ischaemia is associated with adverse cardiac remodelling, independent of CVD risk factors including blood pressure.
authors.affiliation: Institute of Biomedical and Clinical Science, Peninsula NIHR Clinical Research Facility, Peninsula Medical School, University of Exeter, Exeter, UK. david.strain@pms.ac.uk
authors.forename: William D
authors.initials: WD
authors.lastname: Strain
authors.forename: Nish
authors.initials: N
authors.lastname: Chaturvedi
authors.forename: Alun
authors.initials: A
authors.lastname: Hughes
authors.forename: Petros
authors.initials: P
authors.lastname: Nihoyannopoulos
authors.forename: Christopher J
authors.initials: CJ
authors.lastname: Bulpitt
authors.forename: Chakravarthi
authors.initials: C
authors.lastname: Rajkumar
authors.forename: Angela C
authors.initials: AC
authors.lastname: Shore
mesh_terms: D000328:Adult; D000368:Aged; D001794:Blood Pressure / Q000502:physiology*; D003924:Diabetes Mellitus, Type 2 / Q000503:physiopathology*; D003925:Diabetic Angiopathies / Q000503:physiopathology*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000503:physiopathology; D017379:Hypertrophy, Left Ventricular / Q000473:pathology / Q000503:physiopathology; D007511:Ischemia / Q000503:physiopathology; D017078:Laser-Doppler Flowmetry; D008297:Male; D008833:Microcirculation / Q000502:physiology*; D008875:Middle Aged; D012307:Risk Factors; D012867:Skin / Q000098:blood supply*; D020257:Ventricular Remodeling / Q000502:physiology