title: Myocardial velocity gradient as a noninvasively determined index of left ventricular diastolic dysfunction in patients with hypertrophic cardiomyopathy.
abstract: OBJECTIVE
  We investigated the utility of the peak negative myocardial velocity gradient (MVG) derived from tissue Doppler imaging (TDI) for evaluation of diastolic dysfunction in patients with hypertrophic cardiomyopathy (HCM).
  
  
  BACKGROUND
  Hypertrophic cardiomyopathy is characterized by impaired diastolic function with abnormal stiffness and prolonged relaxation. However, it remains difficult to evaluate these defects noninvasively.
  
  
  METHODS
  Both TDI and conventional echocardiography were performed in 36 patients with HCM and in 47 control subjects. Left ventricular (LV) pressure was measured simultaneously in all HCM patients and in 26 controls.
  
  
  RESULTS
  The peak negative MVG occurred soon after the isovolumic relaxation period during the initial phase of rapid filling (auxotonic relaxation). It was significantly smaller in HCM patients than in control subjects (2.32 +/- 0.52/s vs. 4.82 +/- 1.15/s, p < 0.0001); the cutoff value for differentiation between all HCM patients and 47 normal individuals was determined as 3.2/s. Both the left ventricular end-diastolic pressure (LVEDP) (19.6 +/- 6.1 mm Hg vs. 6.5 +/- 1.7 mm Hg, p < 0.0001) and the time constant of LV pressure decay during isovolumic diastole (tau) (44.0 +/- 6.7 ms vs. 32.1 +/- 5.5 ms, p < 0.0001) were increased in HCM patients compared with controls. The peak negative MVG was negatively correlated with both LVEDP (r = -0.75, p < 0.0001) and tau (r = -0.58, p < 0.0001).
  
  
  CONCLUSIONS
  A reduced peak negative MVG reflects both prolonged relaxation and elevated LVEDP. The peak negative MVG might thus provide a noninvasive index of diastolic function, yielding unique information about auxotonic relaxation in patients with HCM.
authors.affiliation: Cardiovascular Division, Department of Clinical Pathophysiology, Nagoya University, Graduate School of Medicine, Nagoya, Japan.
authors.forename: Tomoko
authors.initials: T
authors.lastname: Kato
authors.forename: Akiko
authors.initials: A
authors.lastname: Noda
authors.forename: Hideo
authors.initials: H
authors.lastname: Izawa
authors.forename: Takao
authors.initials: T
authors.lastname: Nishizawa
authors.forename: Fuji
authors.initials: F
authors.lastname: Somura
authors.forename: Akira
authors.initials: A
authors.lastname: Yamada
authors.forename: Kohzo
authors.initials: K
authors.lastname: Nagata
authors.forename: Mitsunori
authors.initials: M
authors.lastname: Iwase
authors.forename: Akimasa
authors.initials: A
authors.lastname: Nakao
authors.forename: Mitsuhiro
authors.initials: M
authors.lastname: Yokota
mesh_terms: D000328:Adult; D000368:Aged; D001696:Biomechanical Phenomena; D001783:Blood Flow Velocity; D006328:Cardiac Catheterization; D002312:Cardiomyopathy, Hypertrophic / Q000150:complications*; D016022:Case-Control Studies; D003971:Diastole; D015150:Echocardiography, Doppler / Q000379:methods* / Q000592:standards; D004548:Elasticity; D005260:Female; D006439:Hemodynamics; D006801:Humans; D016014:Linear Models; D008297:Male; D008875:Middle Aged; D009200:Myocardial Contraction; D012680:Sensitivity and Specificity; D012720:Severity of Illness Index; D013318:Stroke Volume; D018487:Ventricular Dysfunction, Left / Q000145:classification / Q000000981:diagnostic imaging* / Q000209:etiology* / Q000503:physiopathology; D017725:Ventricular Pressure