Mitral E wave propagation as an index of left ventricular diastolic function. I: Its hydrodynamic basis.
OBJECTIVE
Left ventricular (LV) diastolic dysfunction is an early sign of myocardial disease and an important determinant of symptoms and prognosis in patients with various cardiovascular disorders. Evidence suggests the presence and clinical importance of abnormal LV diastolic function in patients with valvular heart diseases, but it is difficult to measure non-invasively. Mitral E wave propagation inside the left ventricle studied by analysis of digitized color M-mode and pulsed wave Doppler technique is a promising technique for the evaluation of LV relaxation. However, the precise mechanism of its transmission is not clearly defined. Understanding the precise hydrodynamic basis of E wave propagation would be helpful for its meaningful application to the evaluation of LV diastolic performance. This study investigates the hydrodynamic determinants of mitral E wave propagation in an in vitro setting.


RESULTS
Thirty-one sets of experiments were conducted in a linear, pulsatile left ventricle model with varying operative diastolic characteristics. The rate of transmission of the onset of the E wave was strongly related to operative LV diastolic stiffness (r = 0.93, p < 0.0001), and weakly to mean left atrial (LA) pressure (r = 0.46, p < 0.01), heart rate (r = 0.57, p < 0.01) and stroke volume (r = -0.58, p < 0.01) through an effect on operative LV diastolic stiffness. The peak of the E wave transmission was influenced not only by operative LV diastolic stiffness (r = 0.87, p < 0.0001), but also by the mean LA pressure, heart rate and stroke volume, in an independent fashion.


CONCLUSIONS
The rate of transmission of the onset of the mitral E wave is determined solely by operative LV diastolic stiffness, whereas that of the peak is also affected by the mean LA pressure, heart rate and stroke volume. Analysis of mitral E wave propagation in patients with valvular heart disease may give clinically useful insights into LV diastolic function.
Pai
R G
RG
Loma Linda University, California, USA.
Yoganathan
A P
AP
Toomes
C
C
Eberhardt
C
C
Shah
P M
PM
D003971:Diastole / Q000502:physiology; D004452:Echocardiography; D018618:Echocardiography, Doppler, Color; D006349:Heart Valve Diseases / Q000503:physiopathology; D006801:Humans; D008943:Mitral Valve / Q000502:physiology*; D008955:Models, Cardiovascular; D011673:Pulsatile Flow / Q000502:physiology; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology; D016277:Ventricular Function, Left / Q000502:physiology*