title: Impact of systemic hypertension on the assessment of aortic stenosis.
abstract: OBJECTIVE
  To determine the effect of systemic arterial hypertension on the indices of aortic stenosis (AS) severity.
  
  
  METHODS
  A severe supravalvar AS was created in 24 pigs. The maximum and mean pressure gradients across the stenosis were measured by Doppler echocardiography and by catheterisation. Both echocardiography and catheter data were used to calculate stenosis effective orifice area, energy loss coefficient, and peak systolic left ventricular wall stress. Measurements were taken both at normal aortic pressures and during hypertension induced by banding of the distal thoracic aorta in 14 pigs and by intravenous administration of phenylephrine in 10 pigs.
  
  
  RESULTS
  During hypertension, systemic arterial resistance downstream from the stenosis increased greatly (all animals: 71 (40)%), whereas total systemic arterial compliance decreased significantly (-38 (21)%). Hypertension resulted in a moderate increase in effective orifice area (29 (14)%) and energy loss coefficient (25 (17)%) and substantial decreases in catheter gradients (maximum: -40 (20)%; mean: -43 (20)%; peak to peak: -70 (23)%) and Doppler gradients (maximum: -35 (17)%; mean: -37 (16)%). In multivariate analysis, peak to peak gradient was significantly (p < 0.001) related to the energy loss coefficient, mean flow rate, and arterial compliance, whereas maximum and mean catheter gradients were related only to the energy loss coefficient and flow rate. Of major importance, maximum systolic left ventricular wall stress increased greatly during hypertension (43 (23)%).
  
  
  CONCLUSIONS
  The severity of AS may be partially masked by the presence of coexisting hypertension. The markers of AS severity should thus be interpreted with caution in hypertensive patients and be re-evaluated when the patient is in a normotensive state.
authors.affiliation: Research Centre of Laval Hospital, Quebec Heart Institute, Laval University, Sainte-Foy, Quebec, Canada.
authors.forename: L
authors.initials: L
authors.lastname: Kadem
authors.forename: J G
authors.initials: JG
authors.lastname: Dumesnil
authors.forename: R
authors.initials: R
authors.lastname: Rieu
authors.forename: L-G
authors.initials: LG
authors.lastname: Durand
authors.forename: D
authors.initials: D
authors.lastname: Garcia
authors.forename: P
authors.initials: P
authors.lastname: Pibarot
mesh_terms: D000818:Animals; D001013:Aorta, Thoracic / Q000503:physiopathology; D001021:Aortic Valve / Q000503:physiopathology; D001024:Aortic Valve Stenosis / Q000150:complications / Q000503:physiopathology*; D001783:Blood Flow Velocity / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology; D015150:Echocardiography, Doppler / Q000379:methods; D006973:Hypertension / Q000150:complications / Q000503:physiopathology*; D007262:Infusions, Intravenous; D010656:Phenylephrine / Q000008:administration & dosage; D012720:Severity of Illness Index; D013552:Swine; D014655:Vascular Resistance / Q000502:physiology; D014662:Vasoconstrictor Agents / Q000008:administration & dosage; D018487:Ventricular Dysfunction, Left / Q000150:complications / Q000503:physiopathology
chemical_list: D014662:Vasoconstrictor Agents; D010656:Phenylephrine