title: Evaluation of left ventricular contraction abnormalities in patients with dilated cardiomyopathy with the use of pulsed tissue Doppler imaging.
abstract: The left ventricular (LV) systolic wave, as recorded by pulsed tissue Doppler imaging, usually consists of 2 components (Sw(1) and Sw(2)). However, the clinical significance of these waves has not been studied in patients with dilated cardiomyopathy (DCM) and sinus rhythm. We studied 25 patients with DCM (DCM group) and 22 age-matched normal subjects (control group). The LV posterior wall motion velocities along the short and long axes were recorded by pulsed tissue Doppler imaging, and the peak velocities of the Sw(1) and Sw(2) and the times from the electrocardiographic Q wave to the peak Sw(1) and Sw(2) (Q-Sw(1) and Q-Sw(2), respectively) were determined. In all patients cardiac catheterization was performed immediately after the noninvasive examination, and the LV end-diastolic pressure and peak dP/dt were determined. The LV end-diastolic pressure and peak dP/dt were significantly greater and lower, respectively, in the DCM group. The peak Sw(1) along the long axis was significantly greater than Sw(1) and Sw(2) along the short axis and Sw(2) along the long axis in the control group. The peak Sw(1) and Sw(2) along the long and short axes were all significantly lower in the DCM group than in the control group. The Q-Sw(1) along the long axis was significantly shorter than that along the short axis, whereas no significant difference was seen in the Q-Sw(2) in either axis in any patient. The Q-Sw(1) and Q-Sw(2) along both axes were significantly longer in the DCM group than in the control group. All systolic pulsed tissue Doppler imaging variables, particularly the peak Sw(1) along the long axis, correlated well with the peak dP/dt in all patients. LV contractility along both the short and long axes is commonly impaired in patients with DCM. In particular, peak Sw(1) along the long axis is a useful parameter for evaluating LV myocardial contractility during isovolumic contraction.
authors.affiliation: Second Department of Internal Medicine, School of Medicine, The University of Tokushima.
authors.forename: Y
authors.initials: Y
authors.lastname: Mishiro
authors.forename: T
authors.initials: T
authors.lastname: Oki
authors.forename: H
authors.initials: H
authors.lastname: Yamada
authors.forename: T
authors.initials: T
authors.lastname: Wakatsuki
authors.forename: S
authors.initials: S
authors.lastname: Ito
mesh_terms: D001783:Blood Flow Velocity; D006328:Cardiac Catheterization; D002311:Cardiomyopathy, Dilated / Q000000981:diagnostic imaging* / Q000503:physiopathology*; D016022:Case-Control Studies; D004452:Echocardiography / Q000379:methods*; D018619:Echocardiography, Doppler, Pulsed; D006439:Hemodynamics; D006801:Humans; D016014:Linear Models; D008875:Middle Aged; D009200:Myocardial Contraction; D013599:Systole; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging* / Q000503:physiopathology*; D017725:Ventricular Pressure