title: Paradoxical low-flow aortic stenosis is defined by increased ventricular hydraulic load and reduced longitudinal strain.
abstract: OBJECTIVE
  Patients with paradoxical low-flow severe aortic stenosis (PLF-AS) reportedly have higher left ventricular hydraulic load and more systolic strain dysfunction than patients with normal-flow aortic stenosis. This study investigates the relationship of systolic loading and strain to PLF-AS to further define its pathophysiology.
  
  
  METHODS
  One hundred and twenty patients (age 79 ± 12 years, 37% men) with an indexed aortic valve area (AVAi) of 0.6 cm/m or less and an ejection fraction of 50% or higher were divided into two groups based on indexed stroke volume (SVi): PLF-AS, SVi ≤ 35 ml/m, N = 46; normal-flow aortic stenosis, SVi > 35 ml/m, N = 74). Valvular and arterial load were assessed using multiple measurements, and strain was assessed using speckle-tracking echocardiography.
  
  
  RESULTS
  Patients with PLF-AS were found to have more valvular load (lower AVAi, P = 0.028; lower energy loss coefficient, P = 0.001), more arterial load [decreased arterial compliance and increased systemic vascular resistance (SVR), both P < 0.001] and more total hydraulic load [increased valvuloarterial impedance (Zva), P < 0.001]. Transvalvular gradients and arterial pressures were similar. Longitudinal strain was lower in PLF-AS (P < 0.001), but circumferential and rotation strains were similar. On adjusted regression, AVAi, SVR and longitudinal strain were associated with PLF-AS [odds ratio (OR) = 1.34, P = 0.043; OR = 1.31, P = 0.004; OR = 1.34, P = 0.011, respectively]. When SVR and AVAi were replaced with Zva, longitudinal strain and Zva (OR = 1.38, P = 0.015; OR = 1.33, P < 0.001 for both, respectively) were associated with PLF-AS.
  
  
  CONCLUSIONS
  Increased hydraulic load, from more severe valvular stenosis and increased vascular resistance, and longitudinal strain impairment are associated with PLF-AS and their interplay is likely fundamental to its pathophysiology.
authors.affiliation: aDepartment of Medicine bDivision of Cardiology cDepartment of Cardiovascular and Thoracic Surgery, Montefiore Medical Center, Bronx, New York, USA.
authors.forename: Anthony A
authors.initials: AA
authors.lastname: Holmes
authors.forename: Cynthia C
authors.initials: CC
authors.lastname: Taub
authors.forename: Mario J
authors.initials: MJ
authors.lastname: Garcia
authors.forename: Jian
authors.initials: J
authors.lastname: Shan
authors.forename: David P
authors.initials: DP
authors.lastname: Slovut
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D001021:Aortic Valve / Q000000981:diagnostic imaging*; D001024:Aortic Valve Stenosis / Q000601:surgery*; D062186:Arterial Pressure; D001783:Blood Flow Velocity; D015897:Comorbidity; D004452:Echocardiography; D005260:Female; D006352:Heart Ventricles / Q000503:physiopathology*; D006801:Humans; D016015:Logistic Models; D008297:Male; D015999:Multivariate Analysis; D012189:Retrospective Studies; D012720:Severity of Illness Index; D065467:Transcatheter Aortic Valve Replacement / Q000379:methods*; D014655:Vascular Resistance; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging*; D020257:Ventricular Remodeling