title: How to detect early left atrial remodelling and dysfunction in mild-to-moderate hypertension.
abstract: OBJECTIVE
  Early changes in left atrial function in hypertension are difficult to assess quantitatively. Measuring atrial reversal flow into the pulmonary veins and regional left atrial deformation parameters assessed by Tissue Doppler-derived strain/rate (S/SR) imaging could provide quantitative assessment of left atrial deformation. We aimed to quantify changes in left atrial volume and deformation and pulmonary flow reversal (PVREVERS) in hypertension to detect subclinical left atrial dysfunction.
  
  
  METHODS
  In 74 hypertensive and 34 age-matched normotensive patients (mean age 49 +/- 1.4 vs. 44.2 +/- 2.1 years) echo studies were performed, including measurements of LAV during reservoir, conduit and pump phases and standard indices reflecting left ventricular filling. S/SR was measured in the lateral left atrial wall. Total deformation (STOTAL) and the contribution to early (SE-index) and late (SA-index) filling were calculated.
  
  
  RESULTS
  Hypertensive patients had significantly impaired diastolic function and increased left atrial volume during all phases. Only LAVCONDUIT significantly correlated with both ventricular hypertrophy and parameters of diastolic function. Velocity time integral of PVREVERS correlated with blood pressure and LAVCONDUIT. In hypertensive patients STOTAL was significantly higher (54.9 +/- 2.6 vs. 45.5 +/- 2.7%, P < 0.03) and SE-index was lower (P < 0.0001). This was compensated for by an increased SA-index (P < 0.0001) and SR during atrial contraction (-4.9 +/- 0.2 vs. -2.9 +/- 0.3 1/s, P < 0.0001). SA-index correlated significantly with blood pressure (R = 0.4; P < 0.0001) and PVREVERS (R = 0.3; P < 0.001).
  
  
  CONCLUSIONS
  Changes in left atrial function due to hypertensive diastolic impairment are best reflected by LAVCONDUIT expansion. Hypertensive atrial dilatation is related to increase in PVREVERS. Left atrial S/SR offers a clinically valuable approach to detecting subclinical atrial dysfunction.
authors.affiliation: Blood Pressure Unit, Department of Cardiac and Vascular Sciences, St. George's, University of London, Blackshaw Road, London SW17 0QT, UK. abaltaba@sgul.ac.uk
authors.forename: Aigul
authors.initials: A
authors.lastname: Baltabaeva
authors.forename: Maciej
authors.initials: M
authors.lastname: Marciniak
authors.forename: Bart
authors.initials: B
authors.lastname: Bijnens
authors.forename: Chirine
authors.initials: C
authors.lastname: Parsai
authors.forename: James
authors.initials: J
authors.lastname: Moggridge
authors.forename: Tarek F
authors.initials: TF
authors.lastname: Antonios
authors.forename: Graham A
authors.initials: GA
authors.lastname: Macgregor
authors.forename: George R
authors.initials: GR
authors.lastname: Sutherland
mesh_terms: D000328:Adult; D016279:Atrial Function, Left / Q000502:physiology*; D001794:Blood Pressure / Q000502:physiology; D006332:Cardiomegaly / Q000000981:diagnostic imaging* / Q000209:etiology*; D003971:Diastole / Q000502:physiology; D015150:Echocardiography, Doppler / Q000379:methods* / Q000592:standards; D005260:Female; D006801:Humans; D006973:Hypertension / Q000150:complications* / Q000000981:diagnostic imaging*; D008297:Male; D008875:Middle Aged; D015203:Reproducibility of Results; D012720:Severity of Illness Index