title: Lack of inertia force of late systolic aortic flow is a cause of left ventricular isolated diastolic dysfunction in patients with coronary artery disease.
abstract: OBJECTIVE
  We investigated whether a lack of inertia force of late systolic aortic flow and/or apical asynergy provoke early diastolic dysfunction in patients with coronary artery disease (CAD).
  
  
  BACKGROUND
  Left ventricular (LV) isolated diastolic dysfunction is a well-recognized cause of heart failure.
  
  
  METHODS
  We evaluated LV apical wall motion and obtained left ventricular ejection fraction (LVEF) by left ventriculography in 101 patients who underwent cardiac catheterization to assess CAD. We also computed the LV relaxation time constant (Tp) and the inertia force of late systolic aortic flow from the LV pressure (P)-first derivative of left ventricular pressure (dP/dt) relation. Using color Doppler echocardiography, we measured the propagation velocity of LV early diastolic filling flow (Vp). Patients with LVEF > or =50% (preserved systolic function [PSF], n = 83) were divided into 2 subgroups: patients with inertia force (n = 53) and without inertia force (n = 30). No patient with systolic dysfunction (SDF) (LVEF <50%) had inertia force (n = 18).
  
  
  RESULTS
  The Tp was significantly longer in patients with SDF (85.7 +/- 21.0 ms) and with PSF without inertia force (81.1 +/- 23.6 ms) than in those with PSF with inertia force (66.3 +/- 12.8 ms) (p< 0.001). The Vp was significantly less in the former 2 groups than in the last group. In patients with PSF, LV apical wall motion abnormality was less frequently observed in those with inertia force than in those without (p < 0.0001).
  
  
  CONCLUSIONS
  An absence of inertia force in patients with PSF is one of the causes of isolated diastolic dysfunction in patients with CAD. Normal LV apical wall motion is substantial enough to give inertia to late systolic aortic flow.
authors.affiliation: Department of Internal Medicine and Pathophysiology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
authors.forename: Takayuki
authors.initials: T
authors.lastname: Yoshida
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Ohte
authors.forename: Hitomi
authors.initials: H
authors.lastname: Narita
authors.forename: Seiichiro
authors.initials: S
authors.lastname: Sakata
authors.forename: Kazuaki
authors.initials: K
authors.lastname: Wakami
authors.forename: Kaoru
authors.initials: K
authors.lastname: Asada
authors.forename: Hiromichi
authors.initials: H
authors.lastname: Miyabe
authors.forename: Tomoaki
authors.initials: T
authors.lastname: Saeki
authors.forename: Genjiro
authors.initials: G
authors.lastname: Kimura
mesh_terms: D000368:Aged; D001011:Aorta / Q000502:physiology*; D006328:Cardiac Catheterization; D003324:Coronary Artery Disease / Q000503:physiopathology*; D003326:Coronary Circulation; D015150:Echocardiography, Doppler; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D012039:Regional Blood Flow; D013599:Systole / Q000502:physiology; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology*; D016276:Ventricular Function