title: Mechanisms of diastolic intraventricular regional pressure differences and flow in the inflow and outflow tracts.
abstract: OBJECTIVE
  We sought to investigate the mechanisms of left ventricular (LV) intracavitary early diastolic flow during changes in contractility and loading.
  
  
  BACKGROUND
  There is limited understanding of how intracavitary flow velocities relate to intraventricular driving pressures.
  
  
  METHODS
  In 12 anesthetized dogs, we measured pressures in the left atrium (LA), LV at the mitral tip, apex, and subaortic region; intraventricular velocities by color M-mode Doppler echocardiography (CMD); and volume by sonomicrometry. We also investigated responses to isoprenaline, ischemic failure, and volume loading.
  
  
  RESULTS
  During rapid, early filling, the mitral to apical pressure gradient (LVP(mitral-apex)) correlated with the peak mitral to apical velocity (r = 0.92). The LVP(mitral-apex) increased from 1.4 +/- 0.6 (SD) to 3.2 +/- 1.8 mm Hg during isoprenaline (p < 0.05) and decreased to 0.6 +/- 0.5 during ischemic failure (p < 0.01). The pressure gradient correlated positively with the time constant of isovolumic relaxation (tau) (r = 0.82) and negatively with LV end-systolic volume (ESV) (r = -0.77). Volume loading increased LA pressure, tau, and ESV, but caused no significant change in LVP(mitral-apex). At baseline and during isoprenaline, tau was shorter (p < 0.05) at the apex than at the base. When the mitral to apical gradient approached zero, filling velocities were directed toward the LV outflow tract, and a pressure gradient was established between the apex and subaortic region.
  
  
  CONCLUSIONS
  Changes in LVP(mitral-apex) induced by inotropic stimuli, loading, and ischemia appeared to reflect dependency of the pressure gradient on the rate of relaxation, ESV, and LA pressure. Regional differences in the rate of relaxation may also contribute to intraventricular pressure gradients. These findings have implications for how to interpret intraventricular filling in a clinical context.
authors.affiliation: Medical Department, Aker University Hospital, University of Oslo, Norway. kjetil.steine@ioks.uio.no
authors.forename: Kjetil
authors.initials: K
authors.lastname: Steine
authors.forename: Marie
authors.initials: M
authors.lastname: Stugaard
authors.forename: Otto
authors.initials: O
authors.lastname: Smiseth
mesh_terms: D000818:Animals; D003327:Coronary Disease / Q000503:physiopathology; D003971:Diastole / Q000502:physiology*; D004285:Dogs; D015150:Echocardiography, Doppler; D005260:Female; D007545:Isoproterenol / Q000494:pharmacology; D008297:Male; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology; D016276:Ventricular Function / Q000502:physiology*; D017725:Ventricular Pressure / Q000502:physiology*
chemical_list: D007545:Isoproterenol