Left ventricular diastolic function
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Chapter 1: Left ventricular diastolic function
Diastolic function and echocardiographic assessment
The importance of systolic function can be understood on an intuitive basis. Consider the fact that the left ventricle contracts and ejects blood into the aorta roughly 100,000 times daily, each time overcoming the aortic resistance, which is typically 110 mmHg or more. It is straightforward to understand why systolic function is fundamental to global cardiac function. Systole is a complicated process involving three distinct ventricular contractions, namely longitudinal, radial and circumferential contraction (refer to Myocardial Mechanics and Figure 1).
Diastole starts immediately after systole. The entire ventricular myocardium must relax rapidly during diastole, such that the ventricle can expand (relax) and refill with blood. Although diastole may appear as a simple and passive process, it is actually a complicated and fundamental aspect of ventricular function. Impaired diastolic function (i.e diastolic dysfunction) may lead to diastolic heart failure (i.e heart failure with preserved ejection fraction, HFPEF). Diastolic heart failure is presumably at least as common as systolic heart failure (heart failure with reduced ejection fraction, HFREF). Diastolic heart failure is particularly common among people with diabetes, hypertension, overweight/obesity, and the elderly (Pieske et al).
Figure 1. Myocardial motion during (A) systole and (B) diastole.
Physiology and phases of diastole
Diastole is divided into the following four phases (Table 1):
| TABLE 1 | |
|---|---|
| PHASE | EVENT |
| IVRT (Isovolumetric Relaxation Time) | No ventricular filling |
| Rapid filling (rapid passive filling) | Passive emptying of the left atrium |
| Diastasis | No ventricular filling |
| Atrial contraction | Active emptying (contraction) of the left atrium |
Figure 2, a modified Wiggers diagram, provides a comprehensive view of the phases and events during the cardiac cycle. As illustrated in Figure 2, diastole begins when the aortic valve closes and it ends when the mitral valve closes. Systole occurs between mitral valve closure and aortic valve closure. On ECG, the R-wave apex coincides with the onset of systole, and diastole starts at the end of the T wave.
Figure 2. Wiggers diagram showing pressure, volume, Doppler signal, ECG and AV valves during the cardiac cycle. Doppler recording of mitral valve flow during diastole. (a) = active atrial filling; (b) = increased atrial pressure due to bulging of mitral valve into the left atrium, when valve closes; (c) = passive atrial filling.
When the aortic valve closes, the left ventricular myocardium begins to relax and ventricular pressure drops rapidly (Figure 2). The initial relaxation is isovolumetric, meaning that relaxation occurs without changes in ventricular volume. This isovolumetric relaxation lasts for approximately 80 milliseconds and ends when the mitral valve opens. The time interval between aortic valve closure and mitral valve opening is the isovolumetric relaxation time (IVRT). The ability of the myocardium to relax during IVRT is governed by left ventricular compliance. The greater the compliance, the better the ability to relax and stretch out during diastole.
During IVRT the pressure in the left ventricle decreases and when it is lower than left atrial pressure, the mitral valve opens, which results in blood flowing into the left ventricle. The low ventricular pressure causes blood to be drawn into the ventricle. This defines the second phase of diastole–the rapid filling–which can be studied using pulsed Doppler. The sample volume (in apical view) is placed at the tips of the mitral valve leaflets (Figure 2, top right). The rapid blood flow from the left atrium to the left ventricle results in a positive wave called the E wave.
As blood flows into the left ventricle, the pressure gradient between the left atrium and the ventricle diminishes, and the passive filling subsides. The greater the ventricular compliance, the larger the volume of blood that flows from the atrium to the ventricle during this phase. If the ventricle has poor compliance, then the passive filling will cease faster, which is explained by a faster equalization of the pressure gradient. When ventricular and atrial pressure has equalized passive flow ceases. This marks the beginning of the diastasis (Figure 2). Diastasis ends when the left atrium starts to contract, which defines the fourth and final phase of diastole. Atrial contraction contributes to the final emptying of the atrium. This gives rise to an A wave on the spectral (Doppler) curve.
In healthy young individuals, the volume of blood transported during the rapid filling phase (E wave) is greater than the volume transported during atrial contraction (A wave). With age, however, the A wave becomes larger, which is explained by the fact that ventricular compliance diminishes and atrial contraction becomes increasingly important for atrial emptying.
When the atrial contraction is completed, atrial myocardium begins to relax and atrial pressure drops. The mitral valve closes when the atrial pressure is below the ventricular pressure.
Thus, diastole includes two phases when there is no filling (IVRT and diastasis) and two phases with filling (rapid filling and atrial contraction). Rapid filling is a passive process, propelled by the pressure gradient between the atrium and the ventricle. The final emptying of the atrium is achieved by active atrial contraction.
References
Pieske et al – How to diagnose heart failure with preserved ejection fraction: the HFA–PEFF diagnostic algorithm: a consensus recommendation from the Heart Failure Association (HFA) of the European Society of Cardiology (ESC).
Chapter 2: Relaxation of the left ventricle
Myocardial relaxation and left ventricular diastolic function
Diastolic function is determined by the efficiency of myocardial relaxation. The degree and velocity of relaxation are the key parameters. Ideally, relaxation should proceed rapidly and the ventricle should expand substantially. This requires that the myocardium has high compliance, a term used to describe myocardial elasticity. The greater the compliance, the more rapid and pronounced the relaxation (i.e the stretching of myocardial fibers). The opposite is also true; the stiffer the myocardium, the slower and less pronounced the relaxation.
Left ventricular compliance
Multiple factors affect ventricular compliance. These factors include age, afterload, myocardial synchronization and intracellular processes (e.g intracellular calcium signaling, the sodium–potassium pump, mitochondrial function, actin-myosin interactions, etc.).
Afterload
Afterload is the resistance that the left ventricle must overcome to eject blood into the aorta. Afterload affects myocardial muscle fibers during systole and diastole. Afterload is a function of the following three variables:
Aortic resistance (pressure).Left ventricular volume.Ventricular wall thickness (myocardial thickness).
The left ventricle must generate sufficient contractile force to overcome the pressure in the aorta. The greater the pressure in the aorta, the greater the load on individual muscle fibers. Also, the load on individual fibers is positively correlated with left ventricular volume, meaning that load on the muscle fibers increases as ventricular volume increases. However, there is an inverse relationship between wall thickness and load, such that greater wall thickness reduces the load on muscle fibers.
The exact mathematical relationship between aortic pressure, ventricular volume, and wall thickness is rather complicated and not within the scope of this discussion. The bottom line, however, is of direct clinical relevance and states that increased afterload results in a slower relaxation. Any condition leading to increased afterload will, therefore, lead to impaired diastolic function.
Increased afterload causes impaired diastolic function.
Myocardial synchronization
Myocardial synchronization refers to the sequence of activation of the ventricular myocardium. The ventricles should be depolarized (activated) by impulses spreading through the left and right bundle branch, which branches out into the Purkinje network (refer to Cardiac Electrophysiology: The Action Potential). Impulse conduction through the Purkinje network is rapid and coordinated, enabling synchronization of left and right ventricular contraction. Rapid impulse conduction is crucial; slow spread of the impulse results in temporal dissociation of cellular activation, and thus desynchronization of contraction. Importantly, the desynchronization of myocardial activation results in disturbed ventricular relaxation.
Desynchronization of myocardial activation causes impaired ventricular relaxation.
Impaired relaxation causes increased diastolic pressure in the left ventricle.
Disturbance in ventricular relaxation results in the disruption of pressure conditions in the left ventricle. Ventricular pressure should drop rapidly and substantially during diastole, but if relaxation is impaired, the drop in pressure will be slower and less pronounced. This ultimately leads to increased diastolic pressure in the left ventricle.
Impaired relaxation results in increased ventricular diastolic pressure.
Myocardial stiffness
Myocardial stiffness is inversely related to compliance; the stiffer the myocardium, the lower the compliance. Stiffness is determined by several factors, e.g ventricular geometry (a large ventricle yields greater afterload and consequently increasing diastolic pressure), sarcomere structure, the composition of extracellular matrix (extracellular fibrosis reduces compliance), pericardial status, etc.
Diastolic Dysfunction and Diastolic Heart Failure
Heart failure with preserved ejection fraction (HFPEF)
Diastolic heart failure accounts for approximately half of all cases of heart failure. The condition is characterized by diastolic dysfunction and normal systolic function. Ejection fraction–which is a measure of systolic function–should be 50% or higher. Diastolic heart failure is also referred to as heart failure with preserved ejection fraction (HFPEF). Echocardiography is the preferred modality for diagnosing diastolic dysfunction and heart failure.
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Chapter 3: Assessment of diastolic function by echocardiography
Echocardiographic assessment of left ventricular diastolic function
Methods for evaluating left ventricular diastolic function have evolved considerably in the past two decades. Currently recommended methods evaluate left atrial and left ventricular function, geometry, and various Doppler parameters. Blod flow velocities across the mitral valve and mitral annular plane velocity are standard assessments. Mitral flow velocities are measured using Pulsed Doppler. Tissue Doppler is used to measuring mitral annular plane velocity. The American Society for Echocardiography (ASE) and the European Association of Cardiovascular Imaging (EACVI) stress that the following parameters are of particular importance for the evaluation of diastolic function:
The ratio between E-wave and A-wave (E/A ratio). The E/A ratio is derived by measuring flow velocities across the mitral valve using pulsed Doppler.Estimating left ventricular filling pressure via e’.Measurement of deceleration time (DT).
Diastolic function can be estimated from E/A ratio, e’ and deceleration time (DT). These three methods, as well as several supplementary methods, will now be discussed in detail.
E/A ratio: Blood flow across the mitral valve
Flow velocity across the mitral valve is examined in the apical four-chamber view (A4C) using pulsed Doppler. The sample volume (SV) should be placed between the leaflet tips (1–3 mm axial length of SV) and sweep speed is set to 50 mm/s to 100 mm/s (Figure 1). Gain and filter should be minimized in order to obtain optimal images. The pulsed Doppler beam can be positioned using color Doppler (to visualize the direction of flow) and continuous Doppler (to locate the maximum flow velocities). As Figure 1B illustrates, the mitral inflow yields 3 phases on the spectral curve: E-wave, diastasis, and A-wave.
Figure 1. Measurement of mitral inflow velocities.
Mitral E-wave velocity
The E-wave represents passive blood flow from the left atrium to the left ventricle. This flow is propelled by the pressure gradient between the left atrium and the left ventricle. This pressure gradient develops immediately after the aortic valve closes (which marks the start of diastole) and the left ventricle starts to relax. The relaxation results in a rapid drop in ventricular pressure. Ventricular pressure drops below atrial pressure, which results in the opening of the mitral valve and passive flow of blood from the atrium to the ventricle. Thus, the initial flow (ventricular filling) is propelled by the pressure gradient between the atrium and the ventricle.
The amplitude and form of the E-wave reflect the velocity and course of the flow. The main factors determining E-wave velocity and form are the following:
The pressure gradient between the left atrium and the left ventricle.Left ventricular compliance (i.e the ability of the ventricle to relax and stretch out during diastole).
Normally, the peak E-wave velocity is between 0.6 and 0.8 m/s and it occurs approximately 100 ms after the start of the E-wave.
Deceleration time (DT)
The normal E-wave displays a rapid acceleration (ascending part) and rapid deceleration (descending part). Deceleration time (DT) is the time interval from the peak of the E-wave to its projected baseline (Figure 2). The E-wave deceleration time is normally between 150 ms and 240 ms.
The deceleration time indicates the duration for equalizing the pressure difference between the left atrium and the left ventricle. The deceleration time is prolonged in conditions leading to a delayed equalization of the pressure gradient. Conversely, the deceleration time is shortened if left ventricular compliance is reduced, or if left atrial pressure is increased.
Figure 2. Deceleration time (DT).
Diastasis
The phase following the E-wave is the diastasis, during which there is no significant flow across the mitral valve. The duration of diastasis is inversely related to heart rate (diastasis is shorter at higher heart rates and vice versa). The diastasis may disappear at very high heart rates.
Mitral A-wave velocity
The mitral A-wave reflects blood flow generated by active atrial contraction. The velocity and form of the A-wave are determined by atrial contractility and left ventricular compliance. The peak A-wave velocity is normally 0.2 ms/s to 0.35 m/s.
Peak A-wave velocity is normally 0.2 ms/s to 0.35 m/s.
Mitral E/A ratio
The ratio between the E-wave and the A-wave is the E/A ratio. Since the E-wave is normally larger than the A-wave, the ratio should be >1. The E/A ratio is age-dependent. The E-wave becomes smaller and the A-wave becomes larger with age. At the age of 60 to 70 years, the E-wave and A-wave display similar amplitudes. Deceleration time and IVRT are also prolonged with age.
Conditions that lead to impaired ventricular relaxation–i.e diastolic dysfunction–will result in a reduced E/A ratio. Impaired relaxation results in reduced passive filling (i.e smaller E-wave), which leaves a larger blood volume for the atrium to eject during contraction (i.e larger A-wave).
Reduced E/A ratio is a hallmark of diastolic dysfunction.
Mitral annular velocity with tissue Doppler imaging (TDI)
The motions of the mitral annulus during systole and diastole can be studied using tissue Doppler. During systole, the mitral annulus travels toward the apex of the heart, and during diastole it recoils back. Mitral annular excursions are measured in apical four-chamber view (A4C), with sample volume (5–6 mm axial length) located 1 cm below the mitral annulus.
Mitral annular plane diastolic motion is of particular interest. Since the mitral plane travels away from the ultrasound transducer during diastole, the velocities are negative. Two dominant waves are observed during diastole, namely e’ and a’. These waves reflect the same events as the E-wave and A-wave, respectively (Figure 3).
Figure 3. The mitral annular velocity during systole and diastole, recorded with tissue Doppler sampling 1 cm below the mitral plane. The sample volume can be placed either medially or laterally.
Mitral annular velocities can be measured medially (i.e in the septum; Figure 3) or laterally. Medial velocity is normally <8 cm/s and lateral velocity is normally <10 cm/s. Young healthy people may display higher velocities. If medial and lateral velocities are measured, the mean value is used. The sweep speed should be set to 50 mm/s to 100 mm/s.
E/e’ ratio and LVEDP
By dividing the peak E-wave velocity by the peak e’ velocity, left ventricular end-diastolic pressure (LVEDP) can be estimated. This is the E/e’ ratio and it is normally <15. Values greater than 15 suggest that LVEDP is elevated. Diastolic dysfunction leads to larger E/e’ ratio, which is explained by the fact that diastolic dysfunction leads to impaired ventricular relaxation, and thus a smaller e’ wave. Conversely, the E-wave tends to become larger at elevated LVEDP.
Currently, the ASE recommends measuring the E/e’ ratio both medially (septal) and laterally, and calculate the mean value. An E/e’ ratio (mean value) ≥13 suggests elevated ventricular filling pressure (LVEDP). Note that the E/e’ ratio is less reliable in the following situations:
Healthy individualsLeft ventricular dysfunctionConstrictive pericarditisMitral valve disease (mitral valve regurgitation, mitral valve stenosis)Mitral valve surgeryAcute heart failureCRT treatmentHypertrophic obstructive cardiomyopathy (HOCM)
IVRT (isovolumetric relaxation time)
IVRT is the period from aortic valve closure to mitral valve opening. IVRT is measured in apical five-chamber view (A5C), using pulsed Doppler. Sample volume is placed between the aortic valve and the mitral valve, which allows it to record both the closure of the aortic valve and the opening of the mitral valve. IVRT can be measured according to Figure 4 below.
Figure 4. Measurement of IVRT (isovolumetric relaxation time).
Pulmonary vein flow
The pulmonary veins transport oxygen-rich blood from the lungs to the left atrium. The pulmonary veins have no valves. Flow through the pulmonary veins can be used as a supplementary method to examine diastolic function. The pulmonary veins are visualized in apical four-chamber view (A4C). The upper right pulmonary vein is often easiest to visualize. Pulmonary vein velocities are recorded using pulsed Doppler, with sample volume (3–4 mm axial length) located approximately 1 cm into the pulmonary vein. The sweep speed should be set to 50 to 100 mm/s (Figure 5).
Figure 5. Measurement of pulmonary vein velocities with pulsed Doppler.
During systole, two positive waves may be seen, namely PVs1 and PVs2. PVs1 and PVs2 may be fused, making them difficult to distinguish. PVs1 and PVs2 represent flows into the left atrium during systole. The force behind PVs1 is atrial relaxation, which leads to lower atrial pressure. PVs2 is due to an increase in pressure in the pulmonary circulation, caused by right ventricular contraction. PVd occurs during diastole and coincides with the mitral E-wave. For simplicity, PVs1 and PVs2 are henceforth referred to as PVs.
The final wave, PVa (or PV AR) is negative, which implies that the flow is reversed (blood flows from the left atrium back into the pulmonary vein). This reversal of flow is caused by atrial contraction, which squeezes blood back into the pulmonary veins.
PVs is normally larger than PVd, leading to a PVs/PVd ratio >1. Diastolic dysfunction results in increased atrial pressure, which affects left atrial filling. This leads to characteristic changes in PVs and PVd, such that PVs become smaller and PVd becomes larger, leading to a PVs/PVd ratio <1. It should also be noted that young people may display a PVs/PVd ratio <1 as a normal finding.
If left ventricular compliance decreases, the atrium will encounter a higher resistance to atrial contraction, resulting in increased reversed flow in the pulmonary vein. This yields a larger and wider PVa wave. PVa velocity greater than >35 cm/s suggests increased left ventricular end-diastolic filling pressure. PVa duration becomes longer than mitral A-wave duration. If the difference between the PVa duration and the A-wave duration is >30 ms, end-diastolic filling pressure is likely >20 mmHg.
Pulmonary vein velocitites are difficult to perform and they should be considered as supplementary methods.
Grading of diastolic dysfunction
Diastolic dysfunction is graded from 1 to 4.
Grade 1 diastolic dysfunction (abnormal relaxation) – this condition is characterized by a E/A ratio is <1. The deceleration time is prolonged (usually >240 ms) and IVRT is >90 ms.Grade 2 diastolic dysfunction (pseudonormal pattern) — Mitral inflow displays normal appearance, with E/A ratio between 1 and 1.5. The deceleration time is between 150 and 200 ms and IVRT >90 ms.Grade 3 diastolic dysfunction (restrictive filling) — This condition is characterized by high E-wave amplitude and low A-wave amplitude, with reduced deceleration time (<150 ms). E/A ratio is >2. IVRT is >70 ms. Restrictive filling is defined as either irreversible or reversible, depending on whether the pattern disappears during Valsalva maneuver. If the pattern is normalized during Valsalva maneuver, it is classified as reversible restrictive filling.If a grade 3 pattern persists despite Valsalva maneuver, then it is classified as irreversible restrictive filling, which also defines grade 4 diastolic dysfunction.
Figure 6. Grading of diastolic dysfunction.
Valsalva maneuver and assessment of diastolic function
Valsalva maneuver can be performed to further evaluate diastolic dysfunction. The Valsalva maneuver is performed by moderately forceful attempted exhalation against a closed airway, usually done by closing one’s mouth, pinching one’s nose shut while expelling air out as if blowing up a balloon. This leads to decreased preload and reduced left atrial pressure. The peak E-wave and A-wave velocities decrease by roughly 20%.
The Valsalva maneuver is useful because the reduction in preload and left atrial pressure affects the E/A ratio in a characteristic way, depending on the degree of diastolic dysfunction. Individuals with pseudonormal pattern (grade 2 diastolic dysfunction) will exhibit grade 1 dysfunction (abnormal relaxation) when performing the maneuver. Individuals with grade 3 dysfunction (restrictive filling) may exhibit grade 1 dysfunction (abnormal relaxation) or grade 2 dysfunction (pseudonormal pattern). If a grade 3 dysfunction is not affected by the maneuver, the condition is classified as grade 4 diastolic dysfunction (irreversible restrictive filling).
Table 1. Two-dimensional and Doppler methods for assessment of LV diastolic function (Nagueh et al)
A, atrial filling; AR, Atrial reversal; BSA, body surface area; CW, continuous wave; D, diastole; e′, early diastolic; E, early filling; ECG, electrocardiographic; IVRT, isovolumic relaxation time; LA, left atrium; MV, mitral valve; PV, pulmonary vein; PW, pulsed-wave; S, systole; TDI, tissue Doppler imaging; TR, tricuspid regurgitation. All Doppler and M-mode recordings are preferably acquired at a sweep speed of 100 mm/sec.
| Variable | Acquisition | Analysis |
|---|---|---|
| Peak E-wave velocity (cm/sec) | 1. Apical four-chamber with color flow imaging for optimal alignment of PW Doppler with blood flow.2. PW Doppler sample volume (1–3 mm axial size) between mitral leaflet tips.3. Use low wall filter setting (100–200 MHz) and low signal gain.4.Optimal spectral waveforms should not display spikes or feathering. | Peak modal velocity in early diastole (after ECG T wave) at the leading edge of spectral waveform |
| Peak A-wave velocity (cm/sec) | 1. Apical four-chamber with color flow imaging for optimal alignment of PW Doppler with blood flow. 2. PW Doppler sample volume (1–3 mm axial size) between mitral leaflet tips.3. Use low wall filter setting (100–200 MHz) and low signal gain.4. Optimal spectral waveforms should not display spikes or feathering. | Peak modal velocity in late diastole (after ECG P wave) at the leading edge of spectral waveform |
| MV A duration (msec) | 1.Apical four-chamber with color flow imaging for optimal alignment of PW Doppler with blood flow.2. PW Doppler sample volume (1–3 mm axial size) at level of mitral annulus (limited data on how duration compares between annulus and leaflet tips).3. Use low wall filter setting (100–200 MHz) and low signal gain.4. Optimal spectral waveforms should not display spikes or feathering. | Time interval from A-wave onset to end of A wave at zero baseline. If E and A are fused (E velocity > 20 cm/sec when A velocity starts), A-wave duration will often be longer because of increased atrial filling stroke volume. |
| MV E/A ratio | See above for proper technique of acquisition of E and A velocities. | MV E velocity divided by A-wave velocity |
| MV DT (msec) | Apical four-chamber: pulsed Doppler sample volume between mitral leaflet tips | Time interval from peak E-wave along the slope of LV filling extrapolated to the zero-velocity baseline. |
| Pulsed-wave TDI e′ velocity (cm/sec) | 1. Apical four-chamber view: PW Doppler sample volume (usually 5–10 mm axial size) at lateral and septal basal regions so average e′ velocity can be computed.2. Use ultrasound system presets for wall filter and lowest signal gain.3. Optimal spectral waveforms should be sharp and not display signal spikes, feathering or ghosting. | Peak modal velocity in early diastole at the leading edge of spectral waveform |
| Mitral E/e′ | See above for acquisition of E and e′ velocities | MV E velocity divided by mitral annular e′ velocity |
| LA maximum volume index (mL/BSA) | 1. Apical four- and two-chamber: acquire freeze frames 1–2 frames before MV opening.2. LA volume should be measured in dedicated views in which LA length and transverse diameters are maximized. | Method of disks or area-length method and correct for BSA. Do not include LA appendage or pulmonary veins in LA tracings from apical four- and apical two-chamber views. |
| PV S wave (cm/sec) | 1.Apical four-chamber with color flow imaging to help position pulsed Doppler sample volume (1–3 mm axial size).2. Sample volume placed at 1–2 cm depth into right (or left) upper PV.3. Use low wall filter setting (100–200 MHz) and low signal gain.4. Optimized spectral waveforms should not display signal spikes or feathering. | Peak modal velocity in early systole at the leading edge of spectral waveform |
| PV D wave (cm/sec) | Same as for PV S wave. | Peak modal velocity in early diastole after MV opening at leading edge of spectral waveform |
| PV AR duration (msec) | Apical four-chamber: sample volume placed at 1–2 cm depth into right (or left) upper PV with attention to presence of LA wall motion artifacts | Time interval from AR-wave onset to end of AR at zero baseline |
| PV S/D ratio | See above for acquisition of pulmonary vein S and D velocities. | PV S wave divided by D-wave velocity or PV S wave time-velocity integral/PV D wave time-velocity integral. |
| CW Doppler: TR systolic jet velocity (m/sec) | 1. Parasternal and apical four-chamber view with color flow imaging to obtain highest Doppler velocity aligned with CW.2. Adjust gain and contrast to display complete spectral envelope without signal spikes or feathering | Peak modal velocity during systole at leading edge of spectral waveform |
| Valsalva maneuver | Recording obtained continuously through peak inspiration and as patient performs forced expiration for 10 sec with mouth and nose closed. | Change in MV E velocity and E/A ratio during peak strain and following release |
| Secondary measures | ||
| Color M-mode Vp (cm/sec) | Apical four-chamber with color flow imaging for M-mode cursor position, shift color baseline in direction of mitral valve inflow to lower velocity scale for red/yellow inflow velocity profile | Slope of inflow from MV plane into LV chamber during early diastole at 4-cm distance |
| IVRT | Apical long-axis or five-chamber view, using CW Doppler and placing sample volume in LV outflow tract to simultaneously display end of aortic ejection and onset of mitral inflow. | Time between aortic valve closure and MV opening. For IVRT, sweep speed should be 100 mm/sec. |
| TE-e′ | Apical four-chamber view with proper alignment to acquire mitral inflow at mitral valve tips and using tissue Doppler to acquire septal and lateral mitral annular velocities. | Time interval between peak of R wave in QRS complex and onset of mitral E velocity is subtracted from time interval between QRS complex and onset of e′ velocity. RR intervals should be matched and gain and filter settings should be optimized to avoid high gain and filter settings. For time intervals, sweep speed should be 100 mm/sec. |
Table 2 – Utility, advantages and limitations of variables used to assess LV diastolic function (Nagueh et al).
AR, Atrial reversal velocity in pulmonary veins; PA, pulmonary artery; PN, pseudonormal; PR, pulmonary regurgitation; PV, pulmonary vein; PVR, pulmonary vascular resistance; RA, right atrial; TDI, tissue Doppler imaging.
| Variable | Utility and physiologic background | Advantages | Limitations |
|---|---|---|---|
| Mitral E velocity | E-wave velocity reflects the LA-LV pressure gradient during early diastole and is affected by alterations in the rate of LV relaxation and LAP. | 1. Feasible and reproducible.2. In patients with dilated cardiomyopathy and reduced LVEF, mitral velocities correlate better with LV filling pressures, functional class, and prognosis than LVEF. | 1. In patients with coronary artery disease and patients with HCM in whom LVEF is >50%, mitral velocities correlate poorly with LV filling pressures.2. More challenging to apply in patients with arrhythmias.3. Directly affected by alterations in LV volumes and elastic recoil.4. Age-dependent (decreasing with age). |
| Mitral A velocity | A-wave velocity reflects the LA-LV pressure gradient during late diastole, which is affected by LV compliance and LA contractile function. | Feasible and reproducible. | 1. Sinus tachycardia, first-degree AV block and paced rhythm can result in fusion of the E and A waves. If mitral flow velocity at the start of atrial contraction is >20 cm/sec, A velocity may be increased.2. Not applicable in AF/atrial flutter patients.3. Age dependent (increases with aging). |
| Mitral E/A ratio | Mitral inflow E/A ratio and DT are used to identify the filling patterns: normal, impaired relaxation, PN, and restrictive filling. | 1. Feasible and reproducible.2. Provides diagnostic and prognostic information.3. In patients with dilated cardiomyopathy, filling patterns correlate better with filling pressures, functional class, and prognosis than LVEF.4. A restrictive filling pattern in combination with LA dilation in patients with normal EFs is associated with a poor prognosis similar to a restrictive pattern in dilated cardiomyopathy. | 1.The U-shaped relation with LV diastolic function makes it difficult to differentiate normal from PN filling, particularly with normal LVEF, without additional variables.2. If mitral flow velocity at the start of atrial contraction is >20 cm/sec, E/A ratio will be reduced due to fusion.3. Not applicable in AF/atrial flutter patients.4. Age dependent (decreases with aging). |
| Mitral E-velocity DT | DT is influenced by LV relaxation, LV diastolic pressures following mitral valve opening, and LV stiffness. | 1. Feasible and reproducible.2. A short DT in patients with reduced LVEFs indicates increased LVEDP with high accuracy both in sinus rhythm and in AF. | 1. DT does not relate to LVEDP in normal LVEF.2. Should not be measured with E and A fusion due to potential inaccuracy.3. Age dependent (increases with aging).4. Not applied in atrial flutter. |
| Changes in mitral inflow with Valsalva maneuver | Helps distinguishing normal from PN filling patterns. A decrease of E/A ratio of ≥50% or an increase in A-wave velocity during the maneuver, not caused by E and A fusion, are highly specific for increased LV filling pressures. | When performed adequately under standardized conditions (keeping 40 mm Hg intrathoracic pressure constant for 10 sec) accuracy in diagnosing increased LV filling pressures is good. | 1. Not every patient can perform this maneuver adequately. The patient must generate and sustain a sufficient increase in intrathoracic pressure, and the examiner needs to maintain the correct sample volume location between the mitral leaflet tips during the maneuver.2. It is difficult to assess if it is not standardized. |
| Mitral “L” velocity | Markedly delayed LV relaxation in the setting of elevated LV filling pressures allows for ongoing LV filling in mid diastole and thus L velocity. Patients usually have bradycardia. | When present in patients with known cardiac disease (e.g., LVH, HCM), it is specific for elevated LV filling pressures. However, its sensitivity is overall low. | Rarely seen in normal LV diastolic function when the subject has bradycardia but it is then usually <20 cm/sec. |
| IVRT | IVRT is ≤70 msec in normal subjects and is prolonged in patients with impaired LV relaxation but normal LV filling pressures. When LAP increases, IVRT shortens and its duration is inversely related to LV filling pressures in patients with cardiac disease. | 1. Overall feasible and reproducible.2. IVRT can be combined with other mitral inflow parameters as E/A ratio to estimate LV filling pressures in patients with HFrEF.3. It can be combined with LV end-systolic pressure to estimate the time constant of LV relaxation (τ).4. It can be applied in patients with mitral stenosis in whom the same relation with LV filling pressures described above holds.5. In patients with MR and in those after MV replacement or repair, it can be combined with TE-e′ to estimate LV filling pressures. | 1. IVRT duration is in part affected by heart rate and arterial pressure.2. More challenging to measure and interpret with tachycardia.3. Results differ on the basis of using CW or PW Doppler for acquisition. |
| Pulsed-wave TDI-derived mitral annular early diastolic velocity: e′ | A significant association is present between e′ and the time constant ofLV relaxation (τ) shown in both animals and humans.The hemodynamic determinants of e′ velocity include LV relaxation, restoring forces and filling pressure. | 1. Feasible and reproducible.2. LV filling pressures have a minimal effect on e′ in the presence of impaired LV relaxation.3. Less load dependent than conventional blood-pool Doppler parameters. | 1. Limited accuracy in patients with CAD and regional dysfunction in the sampled segments, significant MAC, surgical rings or prosthetic mitral valves and pericardial disease.2. Need to sample at least two sites with precise location and adequate size of sample volume.3. Different cutoff values depending on the sampling site for measurement.4. Age dependent (decreases with aging). |
| Mitral E/e′ ratio | e′ velocity can be used to correct for the effect of LV relaxation on mitral E velocity, and E/e′ ratio can be used to predict LV filling pressures. | 1. Feasible and reproducible.2. Values for average E/e′ ratio < 8 usually indicate normal LV filling pressures, values > 14 have high specificity for increased LV filling pressures. | 1. E/e′ ratio is not accurate in normal subjects, patients with heavy annular calcification, mitral valve and pericardial disease.2. “Gray zone” of values in which LV filling pressures are indeterminate.3. Accuracy is reduced in patients with CAD and regional dysfunction at the sampled segments.4. Different cutoff values depending on the site used for measurement. |
| TE-e′ time interval | Can identify patients with diastolic dysfunction due to delayed onset of e′ velocity compared with onset of mitral E velocity. | 1. Ratio of IVRT to TE-e′ can be used to estimate LV filling pressures in normal subjects and patients with mitral valve disease.2. TE-e′ can be used to differentiate patients with restrictive cardiomyopathy who have a prolonged time interval from those with pericardial constriction in whom it is not usually prolonged. | More challenging to acquire satisfactory signals with close attention needed to location, gain, filter settings as well as matching RR intervals. |
| LA maximum volume index | LA volume reflects the cumulative effects of increased LV filling pressures over time. Increased LA volume is an independent predictor of death, heart failure, AF, and ischemic stroke. | 1. Feasible and reproducible.2. Provides diagnostic and prognostic information about LV diastolic dysfunction and chronicity of disease.3. Apical four-chamber view provides visual estimate of LA and RA size which confirms LA is enlarged. | 1.LA dilation is seen in bradycardia, high-output states, heart transplants with biatrial technique, atrial flutter/fibrillation, significant mitral valve disease, despite normal LV diastolic function.2. LA dilatation occurs in well-trained athletes who have bradycardia and are well hydrated.3. Suboptimal image quality, including LA foreshortening, in technically challenging studies precludes accurate tracings.4. It can be difficult to measure LA volumes in patients with ascending and descending aortic aneurysms as well as in patients with large interatrial septal aneurysms. |
| Pulmonary veins: systolic (S) velocity, diastolic (D) velocity, and S/D ratio | S-wave velocity (sum of S1 and S2) is influenced by changes in LAP, LA contractility, and LV and RV contractility.D-wave velocity is mainly influenced by early diastolic LV filling and compliance and it changes in parallel with mitral E velocity.Decrease in LA compliance and increase in LAP is associated with decrease in S velocity and increase in D velocity. | 1. Reduced S velocity, S/D ratio < 1, and systolic filling fraction (systolic VTI/total forward flow VTI) < 40% indicate increased mean LAP in patients with reduced LVEFs.2. In patients with AF, DT of diastolic velocity (D) in pulmonary vein flow can be used to estimate mean PCWP. | 1. Feasibility of recording PV inflow can be suboptimal, particularly in ICU patients.2. The relationship between PV systolic filling fraction and LAP has limited accuracy in patients with normal LVEF, AF, mitral valve disease and HCM. |
| Ar-A duration | The time difference between duration of PV flow and mitral inflow during atrial contraction is associated with LV pressure rise because of atrial contraction and LVEDP. The longer the time difference, the higher LVEDP. | 1. PV Ar duration > mitral A duration by 30 msec indicates an increased LVEDP.2. Independent of age and LVEF.3. Accurate in patients with MR and patients with HCM. | 1. Adequate recordings of Ar duration may not be feasible by TTE in several patients.2. Not applicable in AF patients.3. Difficult to interpret in patients with sinus tachycardia or first-degree AV block with E and A fusion. |
| CW Doppler TR systolic jet velocity | A significant correlation exists between systolic PA pressure and noninvasively derived LAP.In the absence of pulmonary disease, increased systolic PA pressure suggests elevated LAP. | Systolic PA pressure can be used as an adjunctive parameter of mean LAP. Evidence of pulmonary hypertension has prognostic implications. | 1. Indirect estimate of LAP.2. Adequate recording of a full envelope is not always possible, though intravenous agitated saline or contrast increases yield.3. With severe TR and low systolic RV-RA pressure gradient, accuracy of calculation is dependent on reliable estimation of RA systolic pressure. |
| CW Doppler PR end-diastolic velocity | A significant correlation exists between diastolic PA pressure and invasively as well as noninvasively derived LAP. In the absence of pulmonary disease, increased diastolic PA pressure is consistent with elevated LAP. | Diastolic PA pressure can be used as an adjunctive parameter of mean LAP. Evidence of pulmonary hypertension has prognostic implications. | 1. Adequate recording of a full PR jet envelope is not always possible though intravenous contrast increases yield.2. Accuracy of calculation is dependent on the reliable estimation of mean RAP.3. If mean PA pressure is >40 mm Hg or PVR >200 dynes·s·cm−5, PA diastolic pressure is higher by >5 mm Hg over mean PCWP. |
| Color M-mode Vp: Vp, and E/Vp ratio | Vp correlates with the time constant of LV relaxation (τ) and can be used as a parameter of LV relaxation.E/Vp ratio correlates with LAP. | 1. Vp is reliable as an index of LV relaxation in patients with depressed LVEFs and dilated left ventricle but not in patients with normal EFs.2. E/Vp ≥ 2.5 predicts PCWP >15 mm Hg with reasonable accuracy in patients with depressed EFs. | 1. There are different methods for measuring mitral-to-apical flow propagation.2. In patients with normal LV volumes and LVEF but elevated LV filling pressures, Vp can be misleadingly normal.3. Lower feasibility and reproducibility.4. Angulation between M-mode cursor and flow results in erroneous measurements. |
References
Nagueh et al – Recommendations for the Evaluation of Left Ventricular Diastolic Function by Echocardiography: An Update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging.