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C© 2007, the AuthorsJournal compilation C© 2007, Blackwell Publishing, Inc.DOI: 10.1111/j.1540-8175.2007.00542.x

ECHO ROUNDS Section Editor: E. Kenneth Kerut, M.D.

An Approach to Analysis of Left VentricularDiastolic Function and Loading Conditionsin the Echocardiography LaboratoryNabhan Alnabhan, M.D.,∗ Edmund Kenneth Kerut, M.D.,† Stephen A. Geraci, M.D.,∗‡Michael R. McMullan, M.D.,∗ and Ervin Fox, M.D.∗

∗Division of Cardiology, University of Mississippi, School of Medicine, Jackson, Mississippi, †HeartClinic of Louisiana, Marrero, Louisiana, Departments of Physiology and Pharmacology, LSUHealth Sciences Center, New Orleans, Louisiana, and ‡G. V. (Sonny) Montgomery VAMC, Jackson,Mississippi

(ECHOCARDIOGRAPHY, Volume 25, January 2008)

echocardiography, diastolic function

About one-third of patients presenting witha clinical syndrome of heart failure (HF) havenormal left ventricular (LV) systolic function(EF ≥ 45%). This group is described as hav-ing diastolic dysfunction with diastolic HF.1 Inthe evaluation of patients with suspected car-diogenic dyspnea, echocardiography providesinformation about both LV function (systolicand diastolic) and LV loading conditions.2 Ob-taining reliable, reproducible data relative todiastolic ventricular performance can be chal-lenging. This review summarizes the echocar-diographic assessment of diastolic function andLV filling pressures, as well as pitfalls in acqui-sition and interpretation of applicable data.

Diastole is defined clinically as that periodof the cardiac cycle beginning with aortic valveclosure (AVC), and ending with mitral valve clo-sure (MVC).3 Exactly when ventricular relax-ation begins is not clear. At the cellular level,diastole starts with actin–myosin crossbridgeunlinking, allowing sarcomere relaxation inan energy-consuming process requiring ATPhydrolysis. Active relaxation does not beginsimultaneously throughout the heart; the pro-cess of crossbridge unlinking begins in some ar-eas of the myocardium while active contraction

Address for correspondence and reprint requests: ErvinFox, M.D., University of Mississippi Medical Center, 2500 NState Street, Heart Station, Jackson, MS 39056. Fax: 601–984-2631; E-mail: [email protected]

continues in others. When a sufficient numberof myocardial cells enter the active relaxationphase, ventricular pressure begins to fall andthe aortic valve closes.4

There are four clinical phases of diastole(Fig. 1).5,6 The first is isovolumic relaxation,beginning with AVC and ending with mitralvalve opening (MVO). Rapid filling begins atMVO with continued active myocardial relax-ation causing LV pressure to drop below leftatrial (LA) pressure (resulting in diastolic “suc-tion”). The third phase, diastasis, is character-ized by passive LV filling. During this phase, LVand LA pressures are nearly equal and LV fill-ing mostly occurs by pulmonary vein (PV) flowand fluid inertia. The LA acts as a passive con-duit, allowing PV flow to directly enter the LV.The last phase is atrial systole, during whichatrial contraction contributes about 15% of LVfilling in normal patients.6–8

Active relaxation occurs early in diastole,during the isovolumic relaxation and rapid fill-ing phases. Active relaxation is normally com-plete by mid-diastole. Diastasis and atrial con-traction constitute the passive parts of diastole,during which LV passive stiffness is the pre-dominant factor determining compliance. In-terventricular interaction (septal impingementinto the LV cavity) and the pericardium (limit-ing chamber enlargement via extra-ventricularrestriction) also have important roles in late di-astole.9

Vol. 25, No. 1, 2008 ECHOCARDIOGRAPHY: A Jrnl. of CV Ultrasound & Allied Tech. 105

ALNABHAN, ET AL.

Figure 1. Recording of LV pressure, volume, and the changein volume as a function of time (dv/dt). The four phases ofdiastole are illustrated. (Reproduced with permission fromLittle WC, Downs TR. Clinical evaluation of left ventric-ular diastolic performance. Prog Cardiovasc Dis Jan/Feb1990;17(4):274.)

Diastolic LV dysfunction is the impaired ca-pacity of the LV to fill and maintain its strokevolume without a compensatory increase of LApressure,10 and is considered clinically relevantwhen LV filling becomes impeded, with resul-tant symptoms of low cardiac output (from lossof Starling forces), elevated pulmonary venouspressure, or both.5 Elevated diastolic pressuresare transmitted through the PVs to the prox-imal pulmonary vasculature, causing a hydro-static increase in mean pulmonary artery pres-sure. Over time, secondary changes occur in thepulmonary arterioles, with (first) reactive andeventually fixed pulmonary arterial hyperten-sion.11,12

Almost any form of organic heart diseasecan be associated with LV diastolic dysfunc-tion, with hypertension, diabetes, obesity, coro-nary artery disease, LV systolic dysfunction,stenotic valvular disease, hypertrophic car-diomyopathy, and infiltrative disorders beingmost common.13 In addition, with increasingage, a pattern of diastolic abnormalities is rou-tinely present: by age 65, changes in filling pa-rameters can be seen, while by age 70, a patternof frank impaired relaxation is usually observa-ble.14

Patient Profile

When evaluating a patient for cardiac dys-pnea, in addition to searching for significantvalvular disease, systolic failure, and active is-chemia, the clinician should assess diastolicperformance: echo parameters related to ac-tive relaxation (early diastole) and passive re-laxation (late diastole), and how ventricularloading conditions affect those parameters. Di-astolic pressures estimated in the echo labo-ratory include LA mean pressure (LAP) (esti-mated by the pulmonary artery occlusion pres-sure [PAOP] when pulmonary venous diseaseis absent), and the LV end diastolic pressure(LVEDP).15 It is the resultant elevation in pul-monary venous pressure, by various means,which results in clinical dyspnea.

Historical factors important in interpretingecho findings include patient age, history ofcoronary artery disease and/or myocardial in-farction, diabetes mellitus, and hypertension.Blood pressure at the time of the study, if avail-able, is also useful in interpreting loading condi-tions. Pathological Q-wave and left ventricularhypertrophy (LVH) on electrocardiography arealso suggestive of LV diastolic abnormality.

M-Mode/Two-dimensionalEchocardiography

Several M-mode and two-dimensional (2D)echo findings help the examiner determine thepretest (pre-Doppler) probability of diastolicdysfunction. Therefore, evaluation of LA and LVsize and function is important.

LVH, cavity enlargement, and segmental wallmotion abnormalities are indicative of disor-ders associated with impaired relaxation. In theevaluation of LV volume, mass and function,both quantitative and qualitative assessmentsshould be performed.

Several methods have been validated toobtain linear and volumetric measurementsof the LV. The examiner should be famil-iar with the advantages and disadvantagesof each method. Linear measurements (septalwall thickness, posterior wall thickness, andLV internal dimensions at end diastole andend systole) are obtained from the paraster-nal views using M-mode, 2D images or 2D tar-geted M-mode echocardiography. These valuesare reproducible; however, they can be off axisand not representative in abnormally shapedventricles.16 Volumetric methods correct forshape distortion; however, they require optimal

106 ECHOCARDIOGRAPHY: A Jrnl. of CV Ultrasound & Allied Tech. Vol. 25, No. 1, 2008

ANALYSIS OF DIASTOLIC FUNCTION

Figure 2. Normal M-mode mitral AC slope and prolongedAC slope. A B-bump is evident. (Reproduced with permis-sion from D’Curz IA, Kleinman D, Aboulatta H, Oran-der P, Hand, RC. A reappraisal of the mitral B-bump (B-inflection): its relationship to left ventricular dysfunction.Echocardiography 1990;7(1):70.)

visualization of endocardial and epicardial bor-ders. In addition, there are a few accumulateddata from normal populations. Volumetric mea-surements are obtained from the mid-papillaryshort axis view and the apical two-chamberand four-chamber views using mathematicalformulas or biplane Simpson’s method (see Ref.16 for calculations).

In the absence of mitral valve (MV) regurgi-tation or stenosis, left atrial enlargement (LAE)reflects chronic elevation of LV filling pressureand thus suggests diastolic dysfunction.18 Leftatrial diameter (LAD) is measured from theparasternal long axis view using M-mode, oftenwith 2D guidance, and is specific but not verysensitive for LAE. Left atrial volume (LAV),however, is a better measure of LA size. An el-lipse formula may be used to calculate LAV:

Figure 3. Mitral valve (MV) inflowas recorded in the 2D apical four-chamber view. Normally MV inflow is∼20˚ laterally directed, but increasesas the LV enlarges. The transducershould be laterally placed with re-spect to the LV apex, so that MV in-flow is directed straight toward thetransducer. Color flow Doppler super-imposed on the 2D image helps trans-ducer and PW cursor positioning. (Re-produced with permission from Ap-pleton CP, Jensen JL, Hatle LK, OhJK. Doppler evaluation of left andright ventricular diastolic function:A technical guide for obtaining op-timal flow velocity recordings. J AmSoc Echocardiogr 1997;10(3):272.)

LAV = (π /6) (LAD)(Lx)(Sx)where Lx is the apical four-chamber long axisdimension and Sx is the apical four-chambershort axis dimension, both measured at end sys-tole.16,19 Simpson’s method is another way tocalculate LAV, but it is more cumbersome as itrequires tracing the LA endocardium.

The American Society of Echocardiographyrecommends using the area–length methodwith the following equation:

LAV = (8/3π ) (A1A2/D)where A1 and A2 are LA areas traced at ven-tricular end systole (maximum LA size) fromthe apical four and two-chamber views respec-tively, and D is the length from the LA posteriorwall to the line joining the MV hinge points fromeither the two- or four-chamber apical views(whichever is shorter).16 The LAV is often in-dexed to body surface area to obtain the LAV in-dex (LAVI), which does not change significantlywith age and remains at 22 ± 6 ml/m2 through-out life in healthy subjects.16,17

A B-bump (Fig. 2) on the MV M-mode tracingdemonstrates delayed MVC and suggests an el-evated LVEDP, usually ≥ 15 mmHg in patientswith LV systolic dysfunction.20

Doppler Echocardiography

Doppler-derived parameters of diastolic func-tion appear to be most accurate in the setting ofLV systolic dysfunction (EF < 0.45), with some-what less accuracy when LV systolic function isnormal.4,21

Pulsed-wave (PW) Doppler of mitral inflowis obtained from an apical four-chamber view,with the PW sample box placed at the tipsof the MV leaflets. A small sample box (1–2 mm) and wall filter ∼200 Hz result in sharper


ALNABHAN, ET AL.

Figure 4. A. Pulse-wave Doppler mitral inflow and pul-monary vein patterns. Isovolumic relaxation time (IVRT)is the time from aortic valve closure (AVC) to mitral valveopening (MVO). Atrial contraction and mitral valve closure(MVC) are illustrated. Deceleration time (DT) is the time forthe peak E velocity to decline to the zero baseline. Pulmonaryvein systolic (S) and diastolic (D) flows are illustrated. (Re-produced with permission from Ref. 21.) B. The pulmonarysystolic flow could appear biphasic with an early (S1) andlate (S2) waves. (Reproduced with permission from Ref. 22.)

velocity waveforms. The sonographer should po-sition the transducer lateral to the cardiac apexto facilitate mitral inflow directly toward thetransducer (Fig. 3). Color Doppler helps guidesample box placement parallel to flow andwithin the maximum flow profile.

The mitral Doppler early diastolic velocityprofile, or E-wave, reflects rapid filling (Fig. 4A).As LV pressure rises, transmitral velocity de-creases progressively. The fall in velocity is rep-resented by the deceleration time (DT), definedas the time interval between the peak of theE-wave and a point in time where the descend-ing limb of the E-wave crosses the baseline. Fol-

lowing the E-wave is a period of diastasis withlow transmitral velocities. Atrial systole followsmanifesting as an A-wave. Normally, the ratioof E and A peak velocities is greater than 1.7,8

Isovolumic relaxation time (IVRT) is mea-sured from an apical five-chamber view. EitherPW or continuous wave (CW) Doppler can beused. With PW Doppler, the sample gate shouldbe placed close between the aortic and MVsand set wide to facilitate recording the AVCclick followed by MVO.22 M-mode echocardio-graphy can also be used to measure the IVRT,when both AVC and MVO are obtained. How-ever, Doppler-derived IVRT values are 10–25millisecond longer than those obtained using M-mode echo, as mitral inflow is slightly delayedafter MVO.22

PV flow Doppler is usually recorded from anapical four-chamber view, using PW Doppler.The sample volume is placed within the PV 1–2 cm from its orifice. Color Doppler helps lo-calize PV flow for optimal positioning of thePW Doppler sample box.22 Normal PV record-ing has a systolic profile, S-wave, which canbe monophasic or biphasic (Fig. 4B). The firstS-wave (S1) results from atrial diastole (LA re-laxation) and the second S-wave (S2) is thoughtto result from forward flow from the right ven-tricle or from mitral annular descent, causing a“suction” effect accelerating flow into the LA.23

The PV diastolic profile, D-wave, occurs concur-rently and varies in a similar pattern and tim-ing to the mitral E-wave. Normally, the S-wavewill have the same or slightly higher velocitythan the D-wave. Reversed flow occurs withinthe PV during atrial systole manifesting as theAC wave. Both width and amplitude of the ACcomponent are significant in estimating LV fill-ing pressure.23,24

Based on recordings of mitral and PV flow,diastolic function is semiquantitatively catego-rized, ranging from normal through four gradesof progressive diastolic dysfunction (Fig. 5). Ab-normal relaxation (grade I) (Fig. 6) occurs withabnormal diastolic function and normal LV fill-ing pressures. Early mitral inflow is reduced(lower E-wave peak) with increased contribu-tion of atrial contraction to LV filling (promi-nent A-wave peak). As a result, the E–A ratiois less than 1. Also, the IVRT and DT are pro-longed. The S–D ratio of the PV flow remains≥1 (Table 1).

When LV filling pressure increases, a mi-tral inflow pattern develops that resembles nor-mal flow. This is termed pseudonormalization(grade II diastolic dysfunction). The S velocity



Figure 5. Patterns of mitral inflow by pulse-wave Doppler, recorded at the tips of the mitral valve in the apical four-chamberview. (Reproduced with permission from Ref. 22.)

of PV flow is blunted, and generally the S–D ra-tio is below 1. Also, the PV AC amplitude andwidth are increased (Fig. 7). As patients tran-sition from grade I to grade II, elevated fillingpressures can be noticed in association with anabnormal relaxation pattern.

As LV filling pressure continues to increase,a pattern of restrictive filling (grade III) (Fig. 8)becomes apparent. A large increase in pressure

Figure 6. Abnormal relaxation pattern in a 54-year-old male with history of hypertension and left ventricular hypertrophy.DT is prolonged; E/A is < 1.

occurs for a relatively small increase in volume.Therefore, early mitral flow is rapid. There isthen a small contribution from atrial contrac-tion; hence, the E–A ratio exceeds 2. The IVRTand DT are shortened. By definition, patientswith grade III diastolic dysfunction will tran-siently manifest a pattern of abnormal relax-ation (or pseudonormalization) with the strainphase of the Valsalva maneuver (reversible


ALNABHAN, ET AL.

TABLE I

Parameters of Transmitral Doppler

Normal Abnormal relaxation Restrictive

IVRT 55–90 ms >110 ms <60 msDT 160–240 ms >240 ms <150 msE-wave 0.8–1.5 m/s ↓ ↔↑A-wave 0.4–0.7 m/s ↑ ↓E/A >1 <1 >2

restrictive filling) as LV preload transientlydecreases. Finally, with grade IV diastolicdysfunction no change in mitral inflow patternoccurs with Valsalva (irreversible restrictive fill-ing).25,26

Mitral E- and A-waves, and PV S and D-waves, reflect diastolic function, and in patientswith depressed LV systolic function, MV inflowcorrelates well with LV filling pressure. In thesepatients the PAOP is predictably greater than20 mm Hg, when E/A exceeds 2 and DT is lessthan 150 ms (Table 2).27,28 PV Doppler helpsidentify a pseudonormal pattern in hearts withboth normal and depressed LV systolic func-tion. When the PR interval on EKG is normal,if the AC velocity is greater than 25 cm/s or

Figure 7. Pulmonary vein Doppler pattern in a patient with pseudonormalization. While the patient has normal mitral flowpattern, prominent AC-wave and S/D < 1 indicate elevated left ventricular filling pressure.

its duration is 30 ms longer than the A-wave,the LVEDP is likely higher than 20 mm Hg(Fig. 7).24,26

When measuring A-wave duration, oneshould keep in mind that a sharper A-wave canbe obtained by moving the sample volume a fewmillimeters closer to the mitral annulus. How-ever, relocating the sample volume all the wayto the level of the annulus should be avoidedbecause the mitral A-wave duration at this sitecan be shorter than that measured more towardthe leaflet tips.29

Occasionally, low velocity flow (L-wave) willbe noticed during diastasis (Fig. 9). It is oftenfound in normal patients with a relatively slowheart rate. The L-wave can also be noted in pa-tients with LVH and normal systolic functionif abnormal relaxation and elevated LV fillingpressures are present.22

As mentioned above, hemodynamic ma-neuvers performed during echo imaging canhelp evaluate LV loading conditions. Tran-sient reduction of preload is accomplishedwith Valsalva or sublingual nitroglycerinadministration. The Valsalva maneuver is per-formed by having the patient blow into amanometer to maintain 40 mm Hg or more.Practically, in the echo laboratory, the Valsalva



Figure 8. Restrictive pattern in a patient with hypertension and dilated cardiomyopathy.

maneuver is performed by having the patientforcefully exhale against a closed glottis for 10second after a deep inspiration. If this maneu-ver is difficult for a patient to perform effec-tively, the echocardiographer places his handon the patient’s abdomen while the patientstrains will raise intrathoracic pressure andapproximate Valsalva hemodynamics.30 WithValsalva, a pseudonormal pattern will revertto abnormal relaxation, whereas a normal mi-tral filling pattern generally will result inlower flow, but an unchanged E–A ratio.27,31

Increasing preload by augmenting systemicvenous return with passive leg raising willchange a pseudonormal pattern to a restrictiveone.

Tissue Doppler Echocardiography

Tissue Doppler imaging (TDI) helps measuremyocardial motion. Evaluation of diastolic mi-tral annulus motion with this technique canquantify LV relaxation. From an apical view,the PW sample box in placed in the mitral annu-lus. The sample box should be 3–7 mm. Circum-ferential mitral annulus velocities may differwithin the annulus, especially if regional wallmotion abnormalities exist. In clinical practice,septal and lateral measurements are generallysufficient. However, the mean velocity of the

septal, lateral, anterior, and posterior segmentsshould be used in the presence of regional wallmotion abnormalities, although there is no con-sensus on how best to obtain tissue Dopplermeasurements.

The normal TDI pattern (Fig. 10) is composedof a positive systolic velocity wave as the annu-lus moves towards the LV apex. A negative di-astolic wave (E′) occurs during early LV filling,and a late negative diastolic wave (A′) occursduring atrial contraction. In normal individu-als E′ is greater than 8 cm/s.

The diastolic E′-wave is reduced (<8 cm/s)with impaired relaxation, and is fairlyindependent of preload in patients with

TABLE II

Formulas for Estimation of LV Filling Pressure

Depressed EF:17 (5 × E/A) – (0.11 × IVRT)

Normal of depressed EF:−Sinus rhythm:

1.9 + 1.24 (E/E′)4.66 + 5.27 (E/Vp)

−Sinus tachycardia:1.55 + 1.47 (E/E′)

−Atrial fibrillation:6.49 + 0.82 (E/E′)


ALNABHAN, ET AL.

Figure 9. Mitral inflow pattern in a patient with long-standing hypertension and moderate mitral regurgitation. Aprominent low velocity L-wave is noted during diastasis.(Reproduced with permission from Ref. 22.)

depressed systolic function. However, it ap-pears to change somewhat proportionately tochanges in preload in patients with normal sys-tolic function. In addition, E′ varies inverselywith afterload.15,32,33

The ratio of the mitral E to E′ is relatively in-sensitive to changes in preload and is thereforeuseful in differentiating normal from pseudo-normal mitral inflow patterns. This ratio ap-pears to be reliable for estimation of LV fill-ing pressures in patients with both normaland depressed systolic function, including thosewith hypertrophic cardiomyopathy, atrial fibril-lation, and sinus tachycardia (Table 2).34–37 AnE/E′ < 8 is seen with normal filling pressure;an E/E′ > 15 is present when filing pressure iselevated (PAOP >15 mmHg). When E/E′ lies be-tween 8 and 15, other echocardiographic mea-sures should be employed to better predict fill-ing pressures.15,26,28

With impaired myocardial relaxation, the on-set of E′ is delayed relative to the E- wave. Thetime interval between E and E′ onsets appearsto predict filling pressures independent of load-ing conditions. As E and E′ cannot be measuredsimultaneously, the times from the electrocar-

diogram QRS onset to both E and E′ are usedto calculate the E′ delay relative to E (TE′ − E).An IVRT/(TE′ − E) ratio < 2 predicts a PAOPabove 15 mmHg.26,38

Finally, TDI is also helpful in differentiatingbetween restrictive and constrictive physiology.In restrictive cardiomyopathy, E′ is < 8 cm/secwhile constrictive pericarditis typically is asso-ciated with an E′ ≥ 8 cm/sec.39,40

Color M-Mode Flow Propagation

Color M-mode allows for temporal and spa-tial assessment of diastolic flow propagationfrom the LA into the LV. This parameter is de-termined by LV relaxation rate and diastolicsuction, but appears to be somewhat dependentupon loading conditions.41,42

Flow propagation velocity (Vp) is obtainedfrom an apical four-chamber view. With colorDoppler activated, the M-mode cursor is placedwithin the mitral inflow to include the LV andpart of the LA. The color scale should be setto 55–60 cm/s and sweep speed 100–200 mm/sto obtain an aliased edge of uniform color. Theslope at the edge of early diastolic flow fromthe MV tip to the LV apex represents the Vp(Fig. 11). One should be careful not to includeIVRT intracavitary flow. Also, color M-modeflow propagation is limited in small hyperdy-namic ventricles.

Normal Vp is greater than 40 cm/s. A reducedVp implies impaired relaxation and helps dis-tinguish pseudo-normal from normal mitral in-flow patterns.41,42 The ratio E/Vp correlates re-liably with PAOP and is independent of preload.The PAOP is greater than 15 mm Hg when E/Vp> 2. This ratio remains accurate in the presenceof atrial fibrillation.26,28,41,42

Physiological Influences

An abnormal relaxation pattern may be seenin patients with normal diastolic function andvolume depletion.43 This pattern may also befound in individuals with a prolonged PR in-terval, after a premature contraction, or in thepresence of a left bundle branch block (LBBB).Pressure overload of the right ventricle (RV)(due to pulmonary embolism or pulmonary hy-pertension) and also RV infarction may causean abnormal LV relaxation pattern due to re-sultant reduced LV preload and decline in rapidfilling.44

In young individuals, atrial contraction con-tributes little to diastolic filling; thus, a



Figure 10. Mitral annulus velocity profiles and associated inflow patterns. (Reproduced with permission from Sohn DW,Chai IH, Lea DJ, et al. Assessment of mitral annulus velocity by Doppler tissue imaging in the evaluation of left ventriculardiastolic function. J Am Coll Cardiol 1997;30:474.)

pattern similar to restrictive filling can beseen. Mitral regurgitation (causing increasedLA pressure) and aortic regurgitation (causingincreased LV diastolic pressure) are also associ-ated with a restrictive filling pattern.45 Severeobesity, chronic obstructive lung disease, and

Figure 11. Color M-mode Dopplerin a patient with normal mitralflow pattern. The propagation ve-locity is decreased which suggestspseudonormalization.

simple labored respirations may result in arestrictive LV filling pattern due to elevatedright ventricular pressures with ventricularinterdependence (bulging of the IVS into theLV cavity, reducing septal contribution tocompliance).22


ALNABHAN, ET AL.

Figures 12: Algorithms for assessment of diastolic function in patients with (A) depressed and (B) normal LV systolicfunction. (Modified from Nagueh SF, Zoghbi WA. Clinical assessment of diastolic filling by Doppler echocardiography. ACCCurr J Rev 2001 Jul/Aug:49.)

Tachycardia causes augmentation of the A-wave, with shortening of the IVRT, but nochange in DT. However, as heart rate increasesthe E- and A-waves will merge, making mitralinflow immeasurable.46 Although no A-wave ispresent in atrial fibrillation, DT and IVRT canbe used to analyze diastolic function.

Summary

Doppler echocardiography offers several pa-rameters for the assessment of diastolic func-tion and loading conditions. The clinicianshould be familiar with these diagnostic meth-

ods and their limitations, and interpret mea-surements within the clinical context in-cluding patient’s history and M-mode and2D findings. A proposed algorithm for anal-ysis of diastole in patients with depressedand normal systolic LV function is provided(Fig 12A and B).

Pearls of Diastolic Function Analysis

• Always assess diastolic function in lightof the patient’s medical history and M-mode/2D echo findings.



• Dyspneic patients without history of car-diovascular disease and by echocardiogra-phy have normal LV size, thickness and sys-tolic function, and also normal LA size areunlikely to have diastolic dysfunction.

• A patient with “normal” transmitral flowpattern, but LA enlargement in the absenceof significant MV disease, likely has ele-vated filling pressures with the mitral pat-tern representing pseudonormalization.

• Patients with depressed LV systolic func-tion and a “normal” transmitral flow pat-tern and E/E′ between 8 and 15 likely haveelevated filling pressures.

• Patients with E/A < 1 without hypovolemiatypically have abnormal active relaxation.

• Younger individuals with LVH can havevery active relaxation leading to very rapidearly filling manifested by diminished DTand IVRT with E/A > 2; this should be dis-tinguished from restrictive filling.

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