1. Assessment of Diastolic Function of the Heart: Background and Current Applications of Doppler Echocardiography. Part II. Clinical Studies 
RICK A. NISHIMURA, M.D. 
Mayo Clinic Proceedings 
Volume 64, Issue 2, Pages (February 1989)
DOI: /S (12)
Copyright © 1989 Mayo Foundation for Medical Education and Research Terms and Conditions

2. Fig. 1
Graph of left ventricular volume (top) and first derivative of the volume (bottom) over time. Dotted lines (from left to right) represent the following: (1) end-systole, (2) mitral valve opening, (3) peak diastolic filling, (4) onset of atrial contraction, and (5) end-diastole. (See text for details.)
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3. Fig. 2
Diagram of left ventricular and left atrial pressure contours in normal heart (top), with corresponding mitral flow velocity curve (bottom).
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4. Fig. 3
Diagram of a normal mitral flow velocity curve, demonstrating Doppler-derived determinations. A = velocity at time of atrial contraction; A2 = aortic valve closure; AT = acceleration time; DT = deceleration time; E = initial peak velocity; IVR = isovolumic-relaxation period; phono = phonocardiogram; S1 = first heart sound.
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5. Fig. 4
Diagram of prolongation of myocardial relaxation on left ventricular and left atrial pressure contours (top). There is a slower rate of decline of left ventricular pressure, which continues into middiastole. Resultant mitral flow velocities are shown below, with decrease in initial peak velocity, prolongation of deceleration time, and a low E:A ratio.
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6. Fig. 5
Mitral flow velocity curves in the same patient during various loading conditions. Top Left, Control state. Top Right, During pharmacologic increase in afterload, resulting in decrease in peak velocity and prolongation of deceleration time (DT). Bottom Left, During preload reduction with intravenously administered nitroglycerin (NTG), resulting in decrease in peak velocity and prolongation of deceleration time. Bottom Right, During fluid loading, resulting in increase in peak velocity and shortening of deceleration time. BP = blood pressure; PCW= pulmonary capillary wedge pressure.
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Copyright © 1989 Mayo Foundation for Medical Education and Research Terms and Conditions

7. Fig. 6
Diagram showing left ventricular and left atrial pressure tracings (top) and resultant mitral flow velocities (bottom) at different preload conditions. Center example depicts a patient with normal hemodynamics. Lower preload will result in example on the left. Higher preload will cause changes observed in example on the right. (See text for details.)
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8. Fig. 7
Measurement of isovolumic-relaxation period with use of phonocardiogram. Left, Phonocardiogram superimposed on pulsed-wave Doppler tracing of aortic valve, verifying that the first high-frequency component of the second heart sound (S2) represents aortic valve closure (avc). Right, Phonocardiogram superimposed on pulsed-wave Doppler tracing of mitral flow velocity. Isovolumic-relaxation period is time from aortic valve closure to mitral valve opening (mvo). S1 = first heart sound.
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9. Fig. 8
Continuous-wave Doppler tracing intersecting left ventricular outflow velocity and mitral valve motion. Isovolumic-relaxation period is time from aortic valve closure (avc) to mitral valve opening (mvo).
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Copyright © 1989 Mayo Foundation for Medical Education and Research Terms and Conditions

10. Fig. 9
Respirometer tracing superimposed on mitral flow velocity curve, indicating onset of inspiration (insp) and expiration (exp). There is a 200-ms delay inherent in the respiratory tracing. Measurement of deceleration time (DT), initial peak velocity (E), and velocity at time of atrial contraction (A) are shown.
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11. Fig. 10
Mitral flow velocity curve of a patient with abnormal myocardial relaxation. A, Deceleration time (DT) is prolonged, and E:A ratio is low (see text). B, Isovolumic-relaxation period (IVR) is substantially prolonged to 140 ms. avc = aortic valve closure; mvo = mitral valve opening.
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12. Fig. 11
Diagram depicting left atrial and left ventricular pressure tracings and mitral flow velocity curve in a patient who initially demonstrated abnormal myocardial relaxation (solid lines). With increase in preload, left atrial pressure increased relative to left ventricular pressure in early diastole. Thus, driving force across mitral valve will be higher, and “pseudonormalization” pattern will appear (dotted lines).
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13. Fig. 12
Mitral flow velocity curve of a patient with restriction to filling. Note high initial peak velocity, shortened deceleration time (DT), and low velocity at time of atrial contraction.
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14. Fig. 13
Diagram depicting left atrial and left ventricular pressure tracings (top) and mitral flow velocity curve (bottom) in restriction to filling. Initial gradient is high during early diastole, and left ventricular pressure shows “dip-and-plateau” pattern. The result is shortening of deceleration time and high E:A ratio on mitral flow velocity curve (see text).
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15. Fig. 14
Mitral flow velocities in a normal patient when sample volume is placed at mitral valve leaflet tips (top), 5 mm inferior to level of mitral annulus (middle), and into the left atrium (LA) (bottom). Opening click of mitral valve is shown in top panel, and closing click of mitral valve is shown in middle and bottom panels. Changes in E:A ratio and deceleration time are more pronounced in patients with abnormalities of mitral flow velocity curves (see text). MVI = mitral valve inflow.
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16. Fig. 15
Mitral flow velocities, illustrating differences in deceleration time (DT) and E:A ratio (see text) when pulsed-wave Doppler (PW) (left) is used in comparison with continuous-wave Doppler (CW) (right).
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17. Fig. 16
Flow toward left ventricular apex (small arrowheads) occurring during isovolumic relaxation (IVR). This pattern should not be mistaken for true peak filling velocity (large arrowheads) starting at mitral valve opening (MVO).
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18. Fig. 17
Velocity curves of normal superior vena cava (SVC) (A) and hepatic vein (B). Antegrade flow is evident during both systole and diastole (systolic flow is greater than diastolic flow). There is a small reversal at time of atrial contraction; reversal is relatively higher in hepatic vein, where reversal at end-systole may be seen.
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19. Fig. 18
Normal pulmonary vein flow, consisting of both systolic (S) and diastolic (D) antegrade signals and atrial reversal (A).
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20. Fig. 19
A, Hepatic vein velocity curve from a patient with severe tricuspid regurgitation. Because of regurgitation, holosystolic reversal is present. All antegrade flow occurs during diastole. B, Diagram of spectrum of venous inflow patterns occurring with various degrees of tricuspid regurgitation, mod = moderate.
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21. Fig. 20
Diagram of wide spectrum of venous inflow abnormalities occurring in patients with myocardial disease of right side of heart.
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22. Fig. 21
Hepatic vein velocity curve of a normal patient (left), showing characteristic systolic (syst) and diastolic (diast) patterns, and of a patient with right ventricular hypertrophy (right) in whom all forward flow is during systole and diastolic flow is completely absent (vertical arrowhead). Flow reversal is increased (horizontal arrowhead) with onset of atrial contraction (a).
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23. Fig. 22
Hepatic vein velocity curve (HV) of a patient with restriction to filling. There is complete loss of forward systolic flow, and all antegrade flow occurred during diastole. With inspiration, diastolic forward flow increased, and a greater degree of reversal resulted. Simultaneous right atrial (RA) pressure waveform is displayed, which is similar to hepatic vein velocity curve. Note rapid “y” descent, particularly during inspiration. Asc. Ao = ascending aortic pressure; Resp. = respiratory tracing.
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24. Fig. 23
Pulsed-wave Doppler recordings of a patient with constrictive pericarditis. A, Mitral flow velocity curve, demonstrating pronounced decrease in initial velocity during inspiration (arrowheads). B, Tricuspid flow velocity curve, demonstrating appreciable decrease in initial velocity during expiration (arrowheads). C, Hepatic vein velocity curve, demonstrating approximately equal forward flow in systole and diastole. During inspiration, there is an increase in forward flow without an increase in reversal. Notable reversal and loss of diastolic filling occur with expiration (double arrowheads). a = apnea; e = expiration; i = inspiration.
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