New Doppler echocardiographic applications for the study of diastolic function
Mario J. Garcia, MD, FACCa,
James D. Thomas, MD, FACCa and
Allan L. Klein, MD, FACCa
a Cardiovascular Imaging Center, Department of Cardiology, Cleveland Clinic Foundation, Cleveland, Ohio, USA
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Figure 1 Parabolic curve representing the changes in pulsed Doppler early-to-atrial (E/A) ratio during transition from normal diastolic function to severe dysfunction. Effect of preload and relaxation. Other indices of transmitral and pulmonary venous flow have similar bimodal distribution (see text for details).
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Figure 2 Diagram representing the relationship between pulsed and color M-mode Doppler of the left ventricular inflow. Flow propagation velocity (Vp) is given by the slope of any isovelocity line. Other index reported in the literature is the time delay (TD) of the peak E velocity from mitral tips to the apex.
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Figure 3 Color M-mode recording of the left ventricular inflow showing the early E and atrial contraction A waves. Vp = flow propagation velocity; TD = time delay (see Figure 2).
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Figure 4 Pulsed and color M-mode Doppler recordings of the left ventricular inflow in a subject with normal diastolic function, a patient with delayed relaxation and a patient with restrictive filling. Notice the delayed apical filling (reduced Vp and prolonged TD in both the delayed relaxation and restrictive cases).
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Figure 5 Two-dimensional color and pulsed tissue Doppler axial velocities of the myocardium recorded from the apical four-chamber view. Systolic (Sm), early diastolic (Em) and atrial contraction (Am) velocities are shown in the pulsed Doppler tracing. The two-dimensional image was obtained during systole.
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Figure 6 Standard pulsed Doppler transmitral inflow (upper panels) and myocardial axial velocities (lower panels) recorded at the basal lateral wall in a healthy volunteer and in a patient with severe aortic stenosis, left ventricular hypertrophy and elevated filling pressures (pseudonormal). Early diastolic myocardial velocity (Em) is significantly reduced as well as the early-to-atrial velocity ratio (Em/Am) in the pseudonormal patient (see text for details).
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Figure 7 Differentiation of restrictive cardiomyopathy from constrictive pericarditis. Representative examples of the mitral annular M-mode, tissue Doppler axial velocities and transmitral Doppler flow velocities in a normal volunteer, a patient with restrictive cardiomyopathy and a patient with constrictive pericarditis. A marked difference in early diastolic velocity (arrows) despite similar transmitral flow velocities is appreciated.
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