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O R I G I N A L R E S E A R C H

Influence of Atrial Function and MechanicalSynchrony on LV Hemodynamic Status in HeartFailure Patients on Resynchronization Therapy

Hsin-Yueh Liang, MD,*† Alan Cheng, MD,* Kuan-Cheng Chang, MD,†Ronald D. Berger, MD,* Kunal Agarwal,* Patrick Eulitt,* Mary Corretti, MD,*Gordon Tomaselli, MD,* Hugh Calkins, MD,* David A. Kass, MD,*Theodore P. Abraham, MD*

Baltimore, Maryland; and Taichung, Taiwan

O B J E C T I V E S The aim of this study was to evaluate atrial and ventricular function in patients

undergoing cardiac resynchronization therapy (CRT).

B A C K G R O U N D Right atrial pacing (AP) in CRT induces delays in electrical and mechanical

activation of the left atrium. The influence of atrial sensing (AS) versus AP on ventricular performance in

CRT and the mechanisms underlying the differences between AS and AP in CRT have not been fully

elucidated.

M E T H O D S Fifty-five patients with heart failure undergoing CRT for 9 � 12.5 months and 22 control

subjects without heart failure were enrolled. Conventional and tissue Doppler echocardiography was

performed to examine atrial and ventricular mechanics and hemodynamic status.

R E S U L T S The optimal atrioventricular interval was shorter in AS compared with AP mode (126 � 19

ms vs. 155 � 20 ms, p � 0.0001). Left ventricular (LV) outflow tract time-velocity integral (22 � 7 cm vs.

20 � 7 cm, p � 0.001), diastolic filling period (468 � 124 ms vs. 380 � 93 ms, p � 0.001), and global

strain (�32 � 24% vs. �27 � 22%, p � 0.001) were greater in AS compared with AP mode. Atrial strain

was higher in AS compared with AP mode in the right atrium (�28.2 � 8.6% vs. �22.6 � 7.6%, p � 0.0007),

interatrial septum (�17.1 � 6.5% vs. �13.2 � 5.4%, p � 0.002), and left atrium (�16.4 � 11.0% vs. �13.6 �

8.5%, p � 0.02). There was no difference in intraventricular dyssynchrony but significantly lower atrial

dyssynchrony in AS compared with AP mode (31 � 19 ms vs. 42 � 24 ms, p � 0.0002).

C O N C L U S I O N S AS is associated with preserved atrial contractility and atrial synchrony, resulting

in optimal LV diastolic filling, stroke volume, and LV systolic mechanics. This pacing mode maximizes LV

performance and the hemodynamic benefit of CRT in patients with heart failure. (J Am Coll Cardiol Img

2011;4:691–8) © 2011 by the American College of Cardiology Foundation

From the *Division of Cardiology, Johns Hopkins University School of Medicine, Baltimore, Maryland; and the †GraduateInstitute of Clinical Medical Science, China Medical University, Taichung, Taiwan. This work was supported in part by grantAG22554 from the National Institutes of Health. Dr. Abraham has received a research grant from GE Ultrasound. All otherauthors have reported that they have no relationships to disclose.

Manuscript received January 14, 2011; revised manuscript received February 16, 2011, accepted February 24, 2011.

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ardiac resynchronization therapy (CRT)alleviates symptoms, improves functionalcapacity, induces reverse remodeling, andextends survival in patients with heart

ailure with electrocardiographic evidence of con-uction abnormalities, low ejection fractions, anddvanced symptoms despite optimal medical ther-py (1,2). In CRT, both ventricles are paced at aertain atrioventricular (AV) interval after atrialensing (AS) or atrial pacing (AP). Hemodynamictudies in patients with conduction disease, with

See page 699

and without CRT, have demonstrated that there isa finite range of AV delays during which cardiacoutput and left ventricular (LV) performance isoptimal (3,4). Although differences in interventric-

ular (VV) activation can be modifiedthrough device programming, interatrialmechanical delays are not adjustable andcan significantly affect left-sided AV fill-ing and consequentially LV stroke volume.Right atrial (RA) pacing in CRT inducesdelays in electrical and mechanical activa-tion of the left atrium (5–9). However, theinfluence of AS versus AP on ventricularperformance in CRT remains unclear.Furthermore, the mechanisms underlyingthe differences between AS and AP inCRT have not been fully elucidated. Rightventricular pacing induces LV dyssyn-chrony and dysfunction, but it is plausiblethat a similar mechanism exists in the atria(10). To better clarify the implications of

AS versus AP in CRT, we prospectively examinedatrial and ventricular mechanics and hemodynamicstatus, and AV coupling, using standard Dopplerindexes and tissue Doppler strain Z in patientsundergoing CRT after the optimization of AV andVV delays. We hypothesized that AS allows supe-rior LV hemodynamic status and performance by atleast affecting atrial mechanics.

M E T H O D S

All participants provided informed consent for thisstudy, which was approved by the institutionalreview board. Seventy-two consecutive patientswho had undergone the implantation of a CRTdevice and been referred for echocardiography-based optimization were enrolled. We excluded

tion

ow

patients with permanent atrial fibrillation or poor g

image quality (n � 17), and analysis was performedn 55 subjects. We also enrolled 21 patients withual-chamber pacemakers but without heart failures a control group.Echocardiography. A Vivid 7 cardiac ultrasound

achine (GE Healthcare, Milwaukee, Wisconsin)ith a 3.5-MHz transducer was used. Echocardio-raphic examinations were performed with patientsn the left lateral decubitus position. At each pro-rammed AV interval of the optimization proce-ure (described in the following), an apical-chamber view with tissue Doppler imaging anditral pulsed-wave Doppler examination using a

ample volume at the mitral leaflet tip and annulusevel was obtained. Pulsed Doppler of the LVutflow tract (LVOT) was acquired from an apical-chamber view.

Optimization protocol. All subjects underwent opti-mization of the AV delay and VV delay. TheLVOT time-velocity integral (TVI) was used as theprimary end point for optimization. For sensed AVoptimization (AS mode), the AV delay was initiallyprogrammed to 250 ms and reduced by 30 ms untiltruncation of mitral Doppler inflow A-wave wasnoted. At each stage, LVOT TVI, total transmitralinflow TVI, and the mitral late diastolic inflowvelocity A-wave TVI were measured. The optimalAV delay was defined as that which yielded com-pletely paced beats (i.e., without evidence of ven-tricular fusion) and the maximal LVOT TVI. Forpaced AV optimization (AP mode), the AP ratewas set 10 beats/min higher than the intrinsic atrialrate, and the AV delay was initially programmed to300 ms. The optimization process was repeated asdescribed earlier. The pacemaker settings were thenadjusted to the optimal AS and AP settings. Wethen performed VV optimization at the optimalsensed and paced AV intervals. The imaging se-quence was repeated with the following VV set-tings: simultaneous (offset 0 ms), right ventriclepre-activated by 30 and 60 ms, and left ventriclepre-activated by 30 and 60 ms. The ideal VV delaywas that which yielded the maximal LVOT TVI.All parameters were measured after 2 min of pacingat each programmed VV interval.Hemodynamic status. We assumed that the mitralnnular and LVOT diameters were unchangeduring the study. Thus, changes in LVOT TVIere considered reflective of changes in strokeolume. The total transmitral inflow TVI at thennulus was used to assess LV diastolic filling. Inddition to LVOT TVI, LV ejection fraction and

A B B R E V I A T I O N S

A N D A C R O N YM S

AP � atrial pacing

AS � atrial sensing

AV � atrioventricular

CRT � cardiac resynchroniza

therapy

LA � left atrial

LV � left ventricular

LVOT � left ventricular outfl

tract

RA � right atrial

TVI � time-velocity integral

lobal longitudinal strain were used to assess LV

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global systolic function. The diastolic filling periodwas defined from the onset of transmitral inflow tothe subsequent R-wave in this study and wasexpressed as a percent of the entire cardiac cycle.Cardiac mechanics. Tissue Doppler and strain echo-ardiography have been extensively validated asccurately depicting regional myocardial motionnd deformation, respectively. Strain has been dem-nstrated as being superior to tissue velocity in thessessment of regional and global function1,11–13). Absolute strain values were used tossess regional and global ventricular function (14).or the purposes of this study, global strain wasefined as the sum of systolic strain in the lateralnd septal walls in the apical 4-chamber view andsed to assess LV global function (13).We have previously shown that strain echocardi-

graphy can be used to evaluate atrial systolicunction (15). Atrial strain and strain rate wereeasured in the RA free wall, atrial septum, and left

trial (LA) free wall. The atrial strain rate tracingFig. 1) comprises 3 waves. The systolic waveoincides with ventricular systole, the early diastolicave coincides with passive atrial filling, and the

ate diastolic wave is produced by active atrialontraction. Late diastolic atrial strain rate reflectstrial contractility. The atrial mechanical activationime was defined as the time from the peak of thetrial contraction wave to the subsequent R-wave.

e used the electrocardiographic R-wave as theeference point of electric activity, because the-wave is more easily recognized than the P-wave.trial synchrony was defined as the time differenceetween atrial mechanical activation times at theA and LA free walls and the interatrial septum.entricular synchrony was assessed by tissue Dopp-

er imaging and strain echocardiography. Intra-trial and interatrial, AV, and intraventricular me-hanical synchrony were defined as the timeifference between atrial walls, atrial and ventricularalls, and ventricular walls, respectively.Strain echocardiography was analyzed using

train (offset) distances of 8 mm in the ventriclesnd 6 mm in the atria. Mean temporal resolutionas 10 ms. Only tracings with clear systolic andiastolic peaks were analyzed.All time delays were corrected for heart rate using

he Bazett formula (time delay in millisecondsormalized to the square root of the RR interval ineconds).Statistical analysis. Data are expressed as mean �

SD or as frequencies. Paired t tests or Wilcoxon fi

signed rank tests, depending on distribution, wereused to compare data between AS and AP modes.A p value �0.05 was considered statisticallysignificant.

R E S U L T S

We analyzed 55 of 72 enrolled patients with heartfailure who had adequate-quality images and werenot in atrial fibrillation (mean age 63.8 � 13.3years; 35 men). The mean duration of CRT was9.0 � 12.5 months at the time of enrollment.

Table 1 details the baseline echocardiographiccharacteristics of CRT patients in the AS and APsettings. The mitral late diastolic inflow velocityA-wave TVIs were comparable between the twomodes. The optimal AV interval was significantlyshorter in AS compared with AP mode (126 � 19

s vs. 155 � 20 ms) (mean difference 29 � 17 ms,� 0.0001). The optimal AV delay observed withP was �30 ms longer than optimal AV delay withS in 65% of the patients. Almost all Doppler-ased measures of ventricular hemodynamic perfor-ance were better in AS compared with AP mode.he total transmitral inflow TVI (20.6 � 6.5 cm vs.7.5 � 5.1 cm, p � 0.001), LVOT TVI (21.9 �.0 cm vs. 20.0 � 6.7 cm, p � 0.001), diastolic

Figure 1. Atrial Strain Echocardiography

Representative atrial strain rate tracing obtained from the left atrial(A, yellow arrow) depicting ventricular systole (VS), passive atrial fil(PAF), and atrial contraction (AC) (B, white arrow). Integration of thcontraction wave in strain rate yields atrial strain (C, yellow arrow).strain rate and strain reflect atrial contractility.

free walllinge atrialAtrial

lling period (468 � 124 ms vs. 380 � 93 ms, p �

�cf

s

MV-R time � onset of mit

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0.001), and global strain (�32.3 � 24.2% vs.26.8 � 22.2%, p � 0.001) were greater in AS

ompared with AP mode. Differences in LV ejectionraction (0.27 � 0.1 vs. 0.26 � 0.1, p � 0.02) were

statistically significant but numerically very close.To further investigate potential mechanisms un-

derlying these hemodynamic differences, we evalu-ated atrial mechanics, including atrial contractilityand synchrony. Active atrial strain (reflecting atrialcontractility) was significantly higher in AS com-pared with AP mode in the right atrium (�28.2 �8.6% vs. �22.6 � 7.6%, p � 0.0007), interatrialeptum (�17.1 � 6.5% vs. �13.2 � 5.4%, p �

0.002), and left atrium (�16.4 � 11.0% vs. �13.6 �8.5%, p � 0.02). In the control group, active atrialstrain was significantly higher in AS mode as well(Table 2).

We subsequently assessed AV mechanical syn-chrony using atrial and ventricular strain signals. Nosignificant differences were noted in the mechanicaldelay between the right atrium and right ventricle

ocardiographic Characteristics in CRT

AS Mode AP Mode p Value

126 � 19 155 � 20 �0.0001

ow velocity 8.6 � 3.0 8.6 � 3.1 0.98

TVI (cm) 20.6 � 6.5 17.5 � 5.1 �0.001

21.9 � 7.0 20.0 � 6.7 �0.001

468 � 124 380 � 93 �0.001

) 49 � 9 43 � 9 �0.0001

52 � 17 50 � 16 0.19

27 � 10 26 � 10 0.02

�32.3 � 24.2 �26.8 � 22.2 0.001

(%) �37.0 � 23.2 �32.4 � 21.3 0.0013

atrial sensing; AV � atrioventricular; CRT � cardiac resynchronization therapy;� left atrial; LV � left ventricular; LVOT � left ventricular outflow tract;ral inflow to the subsequent R-wave; TVI � time-velocity integral.

Table 2. Atrial Mechanics: Regional Active Atrial Strain

Region AS Mode AP Mode p Value

CRT

Right atrium (%) �28.2 � 8.6 �22.6 � 7.6 0.0007

Interatrial septum (%) �17.1 � 6.5 �13.2 � 5.4 0.002

Left atrium (%) �16.4 � 11 �13.6 � 8.5 0.02

Control group

Right atrium (%) �29.0 � 6.4 �25.6 � 6.3 �0.0001

Interatrial septum (%) �16.0 � 4.8 �13.6 � 4.2 0.0025

Left atrium (%) �15.2 � 6.1 �13.6 � 5.4 0.0258

Values are mean � SD.

Abbreviations as in Table 1.

(p � 0.85), the interatrial septum and interventric-ular septum (p � 0.62), and the left atrium and leftventricle (p � 0.70). Similarly, there was no differ-ence in the degree of intraventricular dyssynchronyusing either time to peak strain (p � 0.80) or timeto peak systolic velocity (p � 0.39) (Table 3).

In contrast, there were significant differences inintra-atrial mechanical synchrony, measured usingthe atrial strain rate signal, between AS and APmodes. In the right atrium, the time delay from theRA free wall to the interatrial septum was shorter inAS compared with AP mode (27 � 18 vs. 41 � 26ms, p � 0.001). Similarly, in the left atrium, thetime delay from the interatrial septum to the LAfree wall was shorter in AS compared with APmode (31 � 19 ms vs. 42 � 24 ms, p � 0.0002).The time delay from the RA to the LA free wall(interatrial synchrony) was shorter in AS comparedwith AP mode (56 � 34 ms vs. 80 � 45 ms, p �0.0001). In the control group, there were significantdifferences in intra-atrial and interatrial mechanicalsynchrony in AP mode as well (Table 4).

Interobserver and intraobserver variability showedgood agreement (Fig. 2) in the measurement of timedelay (93% and 92%, respectively) and strain (97%and 96%, respectively). The limits of agreement forinterobserver and intraobserver variability in timedelay ranged from 14.9 to �18.3 ms and from 11.4to �12.6 ms, respectively. The limits of agreementfor interobserver and intraobserver variability instrain ranged from 7.9% to �9.7% and from 6.2%to �6.2%, respectively.

D I S C U S S I O N

Our study clarifies multiple mechanical and he-modynamic issues that have a direct impact onthe management of CRT device programming.First, we demonstrate that most patients (65%)have a difference of �30 ms in the optimal AVinterval between AS and AP modes. We alsodemonstrate, for the first time, the presence ofatrial mechanical dysfunction and dyssynchronyin AP mode in CRT patients, using strain echo-cardiography. Last, we present hemodynamic andmechanical evidence indicating that these atrialmechanical abnormalities result in reduced trans-mitral filling and consequentially lower ventricu-lar stroke volume and global ventricular systolicstrain in AP mode. These multiple lines ofevidence suggest that AS-based pacing in CRTprovides a more favorable mechanical and hemo-

Table 1. Baseline Ech

Variable

AV delay (ms)

Mitral late diastolic inflA-wave TVI (cm)

Total transmitral inflow

LVOT TVI (cm)

MV-R time (ms)

Diastolic filling time (%

LA EF (%)

LV EF (%)

Global LV strain (%)

LV post-systolic strain

Values are mean � SD.AP � atrial pacing; AS �EF � ejection fraction; LA

dynamic profile compared with AP.

ft ve

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Cardiac resynchronization corrects the mechan-ical inefficiency of delayed lateral wall contraction ina remodeled and dyssynchronous heart, therebyincreasing ventricular stroke volume. In heart fail-ure, remodeling develops not only in the ventriclesbut also in the atria (16). Traditional pacing algo-rithms are such that only the right atrium is sensedand paced in CRT. It is well known that pacing theRA appendage significantly worsens interatrial con-duction delay, as reflected by the prolonged P-waveduration on the surface electrocardiogram and in-teratrial conduction time on intracardiac electro-grams (5–8). Camous et al. (17) showed that therewas a close positive correlation between paced andspontaneous interatrial conduction times. Inter-atrial conduction block is thought to be a marker ofLA contractile dysfunction, with a linear relation-ship between the degree of electrical delay and theextent of LA dysfunction (18). Cha et al. (9)recently showed an increased latency period of RAstimulation to LA contraction in the AP pacingmode.

Doppler and M-mode echocardiography havepreviously shown that RA pacing significantly in-creases interatrial mechanical delay (6,19). Giventhat Doppler signals are the result of net pressuregradients between the atrium and the ventricle, thetiming of Doppler signals does not necessarilycorrespond to the timing of mechanical activation.Similarly, M-mode echocardiography also has itslimitations, because it can interrogate only a limitednumber of ventricular and/or atrial walls despite itshigh temporal resolution (19). In contrast, tissueDoppler and strain imaging have high temporal(�200 frames/s) and spatial resolution and depictregional mechanical events in real time in virtuallyany segment of the heart. Tissue velocity imaginghas been used to demonstrate a significant increase

Table 3. AV and Intraventricular Mechanics

Variable AS

Delay in time to peak strain rate (ms)

RA to RV 302

IAS to IVS 301

LA to LV 279

Delay in time to peak strain (ms)

LV, septal to lateral wall 18

Delay in time to peak systolic velocity (ms)

LV, septal to lateral wall �4

Values are mean � SD.IAS � interatrial septum; IVS � interventricular septum; LA � left atrium; LV � le

in intra-atrial and interatrial asynchrony in patients

with heart failure in sinus rhythm, compared withnormal controls (20). Also, a time delay of peakstrain in atrial segments, suggestive of atrial dyssyn-chrony, has been documented during RA append-age pacing (5).

Our study used previously validated and sophis-ticated noninvasive techniques to compare atrialand AV mechanics and hemodynamic parametersin 2 common modes of pacing in CRT. Our dataindicate significant atrial contractile abnormalitiesand intra-atrial and interatrial mechanical delays inAP compared with AS mode. Furthermore, Dopp-ler data indicate that these atrial mechanical abnor-malities result in suboptimal AV filling and strokevolume.

The significance of LA contribution to LV fillingand overall LV performance has been previouslynoted in animal and clinical studies. Goyal andSpodick (18) found an inverse correlation betweenP-wave duration and LA ejection fraction. Further-more, AP reduced LV stroke volume without sig-nificant differences in regional LV strain in ananimal study (21). In our study, AP resulted in areduction of LV filling and stroke volume as re-

de AP Mode p Value

53.8 298.6 � 49.7 0.85

54.4 304.5 � 51.9 0.62

62.9 277.9 � 54.7 0.70

62.5 27.3 � 91.5 0.8

71.2 5.4 � 66.1 0.39

ntricle; RA � right atrium; RV � right ventricle; other abbreviations as in Table 1.

Table 4. Intra-Atrial and Interatrial Mechanics

AS Mode AP Mode

VariableDelay in Time to Atrial Contraction b

Rate (ms)

CRT

RA to IAS 27 � 18 42 � 26

RA to LA 56 � 34 80 � 45

IAS to LA 31 � 19 42 � 24

Control group

RA to IAS 26 � 15 34 � 11

RA to LA 59 � 24 78 � 25

IAS to LA 33 � 14 44 � 21

Values are mean � SD.

Mo

.2 �

.6 �

.7 �

.0 �

.6 �

p Value

y Strain

�0.001

�0.0001

0.0002

0.0286

0.0003

0.003

Abbreviations as in Tables 1 and 3.

ash

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flected by lower total transmitral inflow TVI andLVOT TVI, respectively. A recent study by Bern-heim et al. (22) involving a small number of patientssuggested that AP is suboptimal in CRT, because itinduces intraventricular dyssynchrony. Althoughour study supports the contention that AS mode issuperior to AP mode, our data are not fully con-cordant with this previous study, especially withregard to the possible mechanisms underlying thesuperiority of AS mode. For example, Bernheim etal. (22) reported intraventricular dyssynchrony withAP. This finding seems counterintuitive given thatall patients were on CRT and that their settingswere optimized before the study. In contrast, ourstudy demonstrated synchronous ventricular con-traction, by tissue Doppler imaging and strainmethods, in AS and AP modes. All patients weretreated with CRT, and AV and VV timings wereoptimized before evaluation. One potential reasonfor this discrepancy could be the difference in themethod of optimization. We determined the opti-mal AV interval in either mode on the basis ofmaximal LVOT TVI, whereas Bernheim et al. (22)used a fixed “pace compensation” of 40 ms plus theoptimal AV interval in AS mode as the optimal AV

Figure 2. Intraobserver and Interobserver Variability

Bland-Altman plots of intraobserver (A, B) and interobserver (C, D)The solid line indicates the mean value of the difference, and the d

delay in AP mode. Therefore, there is a possibility

of fusion activation of the left ventricle betweenintrinsic and biventricular paced rhythms because ofan inappropriately “long” AV interval, resulting in aloss of LV synchronization in AP mode in the studyby Bernheim et al. (22).

Our data are somewhat divergent from those ofGold et al. (23), who reported a mean AS to APoffset of 75 ms, compared with about 30 ms inour study. Also their data suggested that APresulted in superior hemodynamic results com-pared with AS mode in CRT. The use of differ-ent end points (percent change in LV dP/dt intheir study vs. stroke volume by echocardiographyin ours) may partially explain these differences.Others have demonstrated that LV dP/dt andcardiac output measurements do not agree inheart failure models (24). The mean difference inoptimal AV delay in AS and AP modes in ourstudy is concordant with other studies (25). Theadditional mechanistic evaluation in our studysupports our observation that AS mode is supe-rior to AP mode, which agrees with that reportedby Bernheim et al. (22).

Although LV ejection fractions were statisti-cally lower in the AP group, suggesting lower

ability in the measurement of time delay and peak strain.ed line indicates mean � 2 SDs.

vari

global LV systolic function, the absolute mean

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difference of 1% between the 2 pacing modes isnot clinically meaningful. However, the moresensitive strain measurements demonstrate larger,statistically significant differences, indicating thatLV systolic function is indeed lower in AP mode.Our data indicate that this difference in LVfunction is related to significant atrial systolicdysfunction and dyssynchrony, causing decreasedatrial emptying and consequently reduced LVpreload. In a failing human heart, the Frank-Starling mechanism is well preserved in theisolated whole heart and an isolated muscle strip.However, the myocardium is considerably stifferin heart failure compared with the normal heart(26). Thus, the failing heart may be more sensi-tive to small changes in LV preload such as thoseinduced by the atrial mechanical abnormalitiesand dyssynchrony noted in our study, suggestingthat AS is the preferred pacing mode in CRT.Study limitations. This study was performed withpatients at rest, and its findings may not hold trueduring activity. Because of time constraints, globalLV strain was acquired in 6 representative segmentsin the 4-chamber view rather than all 16 segmentsof the left ventricle. Our global strain data, how-ever, closely track changes in stroke volume and

in patients with heart failure second- Difference in mech

data suggest AS as the preferred mode of pacing inCRT patients, sinus node dysfunction in heartfailure may necessitate the use of AP (27). There isa small theoretical possibility that some of thechanges in atrial or ventricular performance can beattributed to the 10 beats/min difference in heartrate between the 2 pacing modes. We used theBazett formula to adjust for any differences in heartrate between the 2 modes, realizing that the heartrate dependence of AV delays may not be welldescribed by this formula.

C O N C L U S I O N S

Intrinsic atrial activation during AS mode in CRTis associated with preserved atrial contractility andatrial synchrony, resulting in better LV diastolicfilling, stroke volume, and LV systolic mechanics.This mode maximizes LV performance and thehemodynamic benefit of CRT in patients withheart failure. Our data suggest that AS is theoptimal mode of pacing in CRT.

Reprint requests and correspondence: Dr. Theodore P.Abraham, Johns Hopkins University, 600 North WolfeStreet, Carnegie 568, Baltimore, Maryland 21287. E-mail:

ejection fraction in our population. Although our tabraha3@jhmi.edu.

1

1

1

1

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Key Words: atrial function ycardiac resynchronization

therapy y strain echocardiography.