Circulation Journal
Online ISSN : 1347-4820
Print ISSN : 1346-9843
ISSN-L : 1346-9843

This article has now been updated. Please use the final version.

Echocardiographic Measurement of Left Atrial Strain ― A Key Requirement in Clinical Practice ―
Byung Joo SunJae-Hyeong Park
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Article ID: CJ-21-0373

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Abstract

Unlike the left ventricle (LV), the left atrium (LA) has a thin-walled structure and has been regarded as a simple conduit chamber. However, the unique function of the LA to modulate LV filling has recently drawn much attention. Because LA structure and function are directly influenced by the LV filling pressure, LA assessment is an essential step in the diagnosis of diastolic dysfunction that can help predict new-onset atrial fibrillation, assess the risk of further embolic events, and identify high-risk patients for adverse cardiovascular events. Even in the recent era of multimodality imaging, 2-dimensional (2D) echocardiography is the most common imaging method and the central modality for evaluation of LA function. LA strain derived from 2D echocardiography can help assess LA function objectively and demonstrates the 3 distinct phasic motions of the LA cycle. Further, LA strain provides invaluable pathophysiologic information and helps to predict clinical prognosis in various cardiovascular diseases. In this review article, we focus on LA strain: basic concepts, advantages over conventional parameters, and some unresolved issues. Additionally, we present a brief history of the clinical evidence for LA strain. Through this review, we suggest echocardiography for LA strain assessment in clinical practice.

Structure and Function of the Left Atrium (LA)

In current cardiology clinical practice, the LA is no longer regarded as a simple conduit to the left ventricle (LV). It has a complex structure composed of 3 parts, each derived from different embryologic origin: the anterior LA, the posterior (venous) LA, and the LA appendage (LAA).1 The LA actively coordinates with the LV during the whole cardiac cycle.2 LA function has 3 phases: reservoir, conduit, and contraction (Figure 1). The reservoir function accommodates pulmonary venous blood return until the LA reaches maximal volume. During the LA reservoir phase, the LV is in the systolic phase, performing isovolumic contraction, ejection, and isovolumic relaxation.3 The LV coordinates LA expansion by mitral annulus motion (downward to the cardiac apex), a motion very similar to the ‘unfolding of a tent’. Therefore, the determining factors of the LA reservoir function include LA compliance (or stiffness), mitral annular movement, and end-systolic LV volume.2 The conduit phase begins with LV diastole and continues up to the active LA contraction.3 During the early- and mid-conduit phase, most blood volume (∼75%) shifts to the LV while LA volume shrinks. There is a close interplay between the conduit function of the LA and LV relaxation, manifested as a reciprocal relationship with LA reservoir function.2 During LA contraction, the LA myocardial wall actively contracts and pumps the remaining blood (∼25%). Finally, the LA cycle returns to the starting point with minimal LA volume. However, as there is no effective atrial contraction in the case of atrial fibrillation (AF), LV usually loses ∼25% of the stroke volume.

Figure 1.

The left atrial cycle with three phasic functions. LA, left atrium; LV, left ventricle.

LA Remodeling

Intact LA function is a harmony of LA wall compliance, preload (pulmonary venous flow), afterload (LV filling pressure), and electromechanical synchrony.4 In contrast, a diseased LA, as observed in ‘LA remodeling’, represents structural and functional alterations. It is a result of cumulative hemodynamic stress to the LA, and the intensity and duration of the stress determines the phenotype of LA remodeling.5 Substrate changes are usually present inside the LA wall, including cardiomyocyte atrophy and replacement by fibrotic tissue. These changes are ongoing and eventually cause thinning of the LA wall.6,7 Such pathologies, accumulated over a long period, cause LA deterioration, stiffening, and dilation.4 LA dilation is a visual representation of LA remodeling. As the LA is directly exposed to LV filling pressure during diastole, LA dilation is the most potent evidence of LV diastolic dysfunction (LVDD).2 Moreover, LA dilation is a prognostic marker in a variety of cardiovascular diseases such as heart failure (HF), AF, coronary disease, and stroke.810

Conventional Assessment of LA Remodeling With Echocardiography

Since the advent of cardiac catheterization as a classical diagnostic modality for LA pressure measurement, a variety of non-invasive imaging modalities, including echocardiography, have been developed, focusing on LA morphology and hemodynamics, and have mostly replaced cardiac catheterization (Figure 2).

Figure 2.

Development of diagnostic modalities for the LA. 2D, two-dimensional; 3D, three-dimensional; LA, left atrium; LAA, LA appendage. Thickness of arrows represent volume of clinical evidence.

LA Diameter The anterior-posterior (AP) LA diameter derived by M-mode or 2-dimensional (2D) echocardiography is the simplest marker of LA remodeling. Owing to its simplicity and reproducibility, this diameter has been widely used in many patients. Normal reference values are 27–38 mm in women and 30–40 mm in men.11 We can define LA remodeling as LA AP diameter >38 mm in women and >40 mm in men. However, this simple measurement has some fundamental limitations. The LA diameter does not represent global LA geometry and can be distorted according to angle alignment. Especially in the case of a dilated LA, the increase in diameter is disproportionate to the increase in total LA volume and is a critical source of error.11,12 To overcome these limitations, some researchers have measured the LA diameter on multiple planes (AP, superior-inferior, and medial-lateral) and developed an integrative parameter – the LA eccentricity index.13 In one study, a decrease in the LA eccentricity index reflected spherical remodeling in patients with chronic mitral regurgitation.14 However, LA diameter is currently not recommended as the sole parameter for assessing LA remodeling because of its definite limitations.11

LA Area and Volume LA area and volume can be derived by disc summation or area-length methods using 2D echocardiography.11 The LA volume index (LAVI), calculated by dividing the LA volume by body surface area, is currently used as a representative marker of LA remodeling (LAVI >34 mL/m2 is considered to be LA remodeling). The LAVI is simple, reproducible and can approximate the 3-dimensional (3D) geometric changes in the LA. Compared with LA diameter, the LAVI has shown better prognostic correlations in many cardiovascular diseases in large-sized clinical studies.8,10,15,16 Using similar volumetric methods, LA dynamicity can be assessed by the LA ejection fraction, which is calculated using the maximal, minimal, and pre-atrial systolic LA volumes.2

As with other 2D echocardiography-derived parameters, LA volume and related parameters have inherent limitations. It can underestimate the LA geometry due to foreshortening. Therefore, the 2D echocardiographic LA volume generally appears smaller than the volumes from computed tomography (CT) and cardiac magnetic resonance imaging (CMR).2,17 In addition, all the 2D echocardiography-derived LA volumes are based on geometric assumptions, which is also a fundamental source of error. In contrast, the 3D echocardiography-derived LAVI is free from geometric assumptions and shows excellent correlation with the LAVI values derived from CT and CMR18,19 and better prognostic correlations than the 2D echocardiographic LAVI.18 Both the 3D echocardiographic LA volume and the time-volume curve have been shown to be effective in distinguishing between LVDD grades.20 Despite these advantages of 3D echocardiographic measurements, LA assessment using 3D echocardiography is currently not standardized, and the lack of data from large-sized clinical studies has been a major limitation.

Assessment of LA Deformation: LA Strain

Echocardiographic assessment of LA deformation is a relatively new modality for the assessment of LA remodeling. There are 2 methods of assessment: tissue Doppler imaging and speckle-tracking.

Tissue Doppler Imaging Tissue Doppler is widely available for routine examinations and has the advantage of being simple to interpret. The A′ velocity at the mitral annulus reflects regional atrial systolic motion. Early systolic (S′) and early diastolic (E′) velocities correspond to the LA reservoir and conduit function, respectively. However, these velocities also bear definite limitations related to angle dependency and tethering effect.2 Color Doppler tissue imaging (CDTI) is a modality for LA deformation assessment that uses myocardial tissue velocity, which has the advantage of lower load-dependency.21 Although CDTI has been invaluable in some studies, it has limitations related to angle dependency and is not representative of global LA function, because tissue velocity is measured at a sample volume (2×12 mm) placed at each atrial segment.2

Speckle-Tracking Imaging LA deformation assessed by 2D speckle-tracking imaging is generally known for LA strain. It has several advantages over conventional echocardiographic measurement: it is free from angle alignment and is less influenced by loading conditions.4 It is a modality focused on LA dynamicity for which the software constructs a longitudinal strain and strain rate curve for each segment. The strain curve can provide information about the LA physiology (Figure 3). Currently, the terminology differs and appears as peak LA strain, peak atrial longitudinal strain or LA reservoir strain in various studies. Based on a recent consensus statement, we use the terms LA reservoir strain (LASr), conduit strain (LAScd), and contractile strain (LASct) in this review.3

Figure 3.

LA phasic functions demonstrated on LA strain curve. The maximal height between the top and bottom of the strain curve (A) represents the LA reservoir function. Each height (B) and (C) corresponds to the conduit and contractile strain, respectively. LA, left atrium. (Reproduced with permission from Sun BJ, et al.26)

Current Clinical Evidence for LA Strain

After D’Andrea et al22 published a milestone study in which they showed the changes in LA strain after cardiac resynchronization therapy in patients with idiopathic dilated cardiomyopathy and ischemic cardiomyopathy, there have been a number of studies on LA strain (Table).

Table. Summary of Clinical Studies on Left Atrial Strain
Clinical category,
authors, year
Study subjects Parameter Modality and
analysis software
Main findings
Healthy subjects
 Okamatsu et al23
(2009)
Healthy subjects
(n=140)
LA strain (reservoir,
conduit, contraction)
2D speckle-tracking
imaging, QLAB®, Philips
Age was a determining factor for LA conduit
and contractile function
 Morris et al24
(2015)
Healthy subjects
(n=329)
LA reservoir strain
and strain rates
2D speckle-tracking
imaging, EchoPAC®, GE
Normal LA strain was 45.5+11.4% and LA strain
rate was 22.11+0.61 s−1
 Pathan et al27
(2017)
Healthy subjects,
meta-analysis of the
previous 40
researches (n=2,542)
LA strain (reservoir,
conduit, contraction)
2D speckle-tracking
imaging
LA reservoir strain was 39% (95% CI, 38–41%)
LA conduit strain was 23% (95% CI, 21–25%)
LA contractile strain was 17% (95% CI, 16–19%)
 D’Ascenzi et al28
(2019)
Healthy subjects,
meta-analysis of the
previous 326
researches (n=2,087)
LA reservoir strain 2D or 3D speckle-
tracking imaging
LA reservoir strain was 38±3% (95% CI: 32–43%)
 Liao et al25
(2017)
Healthy subjects
(n=2,812)
LA reservoir strain
and strain rates
2D speckle-tracking
imaging, EchoPAC®, GE
Presented age- and sex-stratified normal LA
strain values. Male sex, increasing age and blood
pressure significantly reduced LA reservoir strain
 Sun et al26
(2020)
Healthy subjects
(n=324)
LA strain (reservoir,
conduit, contraction)
2D speckle-tracking
imaging, EchoPAC®, GE
LA reservoir strain was 35.9±10.6%
LA conduit strain was 21.9±9.3%
LA contractile strain was 13.9±3.6%
 Park et al30
(2020)
University athletes
(n=1,073)
LA reservoir strain
and strain rates
2D speckle-tracking
imaging, EchoPAC®, GE
About 19.1% among the university athletes
showed LA enlargement. Reduced LA reservoir
strain was observed only in 5.2%
Heart failure
 D’Andrea et al22
(2007)
Patients with
idiopathic and
ischemic DCM
(n=90)
LA strain at basal
two segments of LA
2D speckle-tracking
imaging, EchoPAC®, GE
First clinical study of LA strain
To assess the changes in LA function after CRT
at 6 months. LA function more impaired in
idiopathic DCM compared with ischemic DCM
 Santos et al31
(2014)
Patients with
HFpEF (n=135)
LA strain (reservoir,
conduit, contraction)
2D speckle-tracking
imaging, a customized
software from TomTec
Imaging Systems
Reduced LA strain was associated with AF and prior HF admission
 Santos et al32
(2016)
Patients with
HFpEF (n=357)
LA strain (reservoir,
conduit, contraction)
2D speckle-tracking
imaging, a customized
software from TomTec
Imaging Systems
During follow-up of 31 months (IQR, 18–43
months), LA strain was associated with a higher
risk of HF admission
 Singh et al36
(2017)
Subjects with and
without LVDD
(n=224)
LA strain (reservoir,
conduit, contraction)
2D speckle-tracking
imaging, EchoInsight,
Epsilon
LA strain demonstrated gradual decrease
between all stages of LVDD
 Freed et al41
(2016)
Patients with
HFpEF (n=308)
LA strain (reservoir,
conduit, contraction)
2D speckle-tracking
imaging, 2D Cardiac
Performance Analysis,
TomTec
During follow-up of 13.8 months (IQR, 4.5–23.9
months), LA reservoir strain was the strongest
predictor of adverse cardiac events
 Morris et al33
(2018)
Subjects at risk for
LVDD (n=517)
LA reservoir strain 2D speckle-tracking
imaging, EchoPAC®, GE
LA reservoir strain had additional value to LAVI
for detection of LVDD
 Park et al40
(2021)
Patients with acute
HF (n=3,818)
LA reservoir strain 2D speckle-tracking
imaging, TomTec-
Arena®, TomTec
LA reservoir strain tertile groups showed
significant differences in the clinical event rate
(death and HF hospitalization)
 Park et al46
(2020)
Patients with acute
HF (n=2,461)
2D speckle-tracking
imaging, LA
reservoir strain
2D speckle-tracking
imaging, TomTec-
Arena®, TomTec
LA reservoir strain was shown as a significant
predictor for newly-developed AF
Atrial fibrillation
 Tops et al51
(2011)
Patients with AF
who underwent
RFCA (n=148)
Peak LA strain Color Doppler tissue
imaging, EchoPAC®, GE
During follow-up of 13.2±6.7 months, LA strain
at baseline was a predictor of LA reverse
remodeling after RFCA
 Hirose et al45
(2012)
Patients without
arrhythmia
(n=580)
LA strain (reservoir,
conduit, contraction)
and strain rates
Velocity vector imaging,
Syngo Velocity Vector
Imaging®, Siemens
Reduced LA contractile function was a useful
predictor for newly-developed AF
 Obokata et al47
(2014)
Patients with AF
and acute
embolism (n=82)
LA reservoir strain 2D speckle-tracking
imaging, EchoPAC®, GE
LA strain had incremental diagnostic value over
the CHA2DS2-Vasc score for prediction of future
embolic risk
 Yasuda et al52
(2015)
Patients with AF
who underwent
RFCA (n=100)
LA reservoir strain
and strain rates
2D speckle-tracking
imaging, EchoPAC®, GE
Baseline LA strain could predict recurrent AF
after RFCA

2D, two-dimensional; 3D, three-dimensional; AF, atrial fibrillation; CRT, cardiac resynchronization therapy; DCM, dilated cardiomyopathy; HF, heart failure; HFpEF, HF with preserved ejection fraction; IQR, interquartile range; LA, left atrium; LVDD, left ventricular diastolic dysfunction; RFCA, radiofrequency catheter ablation.

Reference Values of LA Strain in Healthy Subjects

The first study to report the reference value of LA strain was by Okamatsu et al from Japan.23 They reported that, out of 140 healthy subjects, the older subjects presented a higher active emptying index; hence, they concluded that age was a determining factor for LA conduit and booster function. Morris et al conducted an international multicenter study including 329 healthy subjects in which they reported the normal LASr value as 45.5±11.4%.24 Liao et al25 conducted a large-sized study on 2,812 healthy individuals from Taiwan and presented age- and sex-stratified normal LA strain values. They reported that females showed higher LASr values than males (39.3±8.0% vs. 38.0±8.0%; P<0.001), and that LASr decreased with increasing age and blood pressure. Sun et al26 performed a multicenter study on 324 healthy Korean subjects and presented the normal LASr, LAScd, and LASct values as 35.9±10.6%, 21.9±9.3%, and 13.9±3.6%, respectively. In that study, age was a determinant for the LA strain values. Further, those authors showed that LV diastolic strain rates and LV global longitudinal strain (LVGLS) significantly influenced LA strain. There are 2 large-sized meta-analyses of normal LASr values. One study analyzed 2,542 healthy subjects and reported the mean LASr as 39.4% (95% confidence interval [CI]=38.0‒40.8%),27 while the other study reported the normal LASr as 38±3% (95% CI=32‒43%) from 2,087 subjects.28 There were substantial differences among the reported LASr values in the 2 meta-analyses27,28 and the study by Morris et al,24 which could be attributed to heterogeneous subject characteristics and differences in algorithms used for strain measurement (these are discussed separately in this review).

LA Strain in Elite Athletes LA remodeling can be observed in athletes after intensive and repetitive exercise.29 The prevalence of LA remodeling (defined by LA diameter >38 mm in females, >40 mm in males, or LAVI >34 mL/m2) was reported as 19.1% among 1,073 university athletes.30 Non-African descent, body muscle mass, heart rate, and sport-type with the highest cardiovascular demand were documented as determinants of LA remodeling. However, the prevalence of abnormal LASr (<27.6%) was only 5.2% and appeared similar between subjects with LA remodeling and healthy controls.30

LA Strain in HF LA strain was shown to be useful in the detection and stratification of HF with preserved ejection fraction (HFpEF). In the PARAMOUNT (Prospective comparison of ARNI with ARB on Management Of heart failUre with preserved ejectioN fracTion) trial, a substudy reported a patient group with HFpEF and significantly decreased LASr (48.4±1.2% vs. 58.4±2.1%, P<0.001) and LASct (29.6±1.5% vs. 42.5±1.8%, P<0.001) compared with controls.31 In the TOPCAT (Treatment Of Preserved Cardiac Function Heart Failure With an Aldosterone Antagonist Trial) trial, decreased LASr (<26.0%) was observed in 52% of patients with HFpEF.32 Reduced LASr (<23.0%) can be detected earlier than increased LAVI in patients with LVDD.33 Furthermore, in diabetic or hypertensive patients with normal LAVI, the LASr, LAScd, and LASct values were significantly lower than those in controls.34 In a study that analyzed 473 women from the general population (BErlin Female RIsk evaluation [BEFRI] study), subjects with LVDD presented significantly reduced LASr values than normal subjects.35 These findings are consistent with the findings of another study by Singh et al.36 They classified 224 patients with HFpEF into 4 groups according to the degree of LVDD (grade 0–3). They showed a grade-dependent difference in LASr values among all groups and concluded that LASr was the only useful tool for the detection of more advanced LVDD.36 LASr has shown significant correlations with other hemodynamic parameters in HFpEF. LASr was associated with age, LVGLS, mitral E/e’ ratio, and LAVI.31,33 Furthermore, it showed significant correlation with invasively measured LV end-diastolic pressure (LVEDP). Therefore, reduced LASr (<18.0%) showed the highest diagnostic accuracy (sensitivity of 96%, specificity of 92%) in the prediction of elevated LVEDP (>12 mmHg).37 Additionally, LASr showed a significant correlation with exercise capacity in 486 patients with HFpEF.38

LASr has been shown to be a useful predictor of clinical outcome in HF. Recently, in a large-sized acute HF registry including 4,312 patients,39 our group reported that decreased LASr was a significant determinant of composite clinical events combining death, hospitalization, and new-onset AF.40 These findings were shown to be consistent in all HF phenotypes (HF with reduced EF [HFrEF], HF with mid-range EF, and HFpEF). However, the LASr value did not show any association with events in the AF subgroup. In the TOPCAT trial, decreased LASr was a significant determinant of HF hospitalization after the adjustment of other confounders (hazard ratio (HR)=0.95, 95% CI=0.91–0.99, P=0.009).32 Freed et al41 reported that LASr was the strongest predictor for adverse clinical outcomes (HR=1.43, 95% CI=1.05–1.95, P=0.02) in 308 HFpEF patients with a longitudinal follow-up of ∼14 months. Torii et al42 reported that the baseline LASr of 10.8% was a cutoff value for predicting the recovery of LV function, cardiac death, and readmission in a patient group with HFrEF on optimal medical treatment. In addition, in the patient group including various underlying etiologies (coronary disease, hypertensive heart disease, dilated and hypertrophic cardiomyopathy), the 3D echocardiography-derived LASr and LA emptying fraction showed significant associations with adverse cardiovascular events during the follow-up that indicated the prognostic value of LA strain.43

Based on currently available data, LASr would be a more effective tool than LAVI for assessing LVDD, because LASr has the advantages of closer correlation with pulmonary capillary wedge pressure and earlier response on treatment and is a sensitive marker of LA fibrosis and a strong prognostic indicator.44

LA Strain for the Onset of AF Because LA strain can detect functional abnormality even without visual LA dilation, it has been tested as a predictor for new-onset of AF. Hirose et al measured LA strain rate using velocity vector imaging in 580 patients without any previous history of arrhythmia, and reported that reduced booster pump function by strain rate was a predictor for newly-developed AF (odds ratio [OR]=4.33, 95% CI=1.02–18.38, P=0.047).45 In another substudy of our group’s acute HF registry, 16.1% of the patients presented newly-developed AF during the follow-up, and the decreased LASr (<18.0%) was a significant predictor for developing AF (HR=1.60, 95% CI=1.18–2.17, P=0.003).46 LASr in patients with AF can provide additional prognostic information. LASr was independently associated with embolic events in patients with AF (OR=0.74, 95% CI=0.67–0.82, P<0.001), which showed an incremental predictive value over the CHA2DS2-VASc score.47 Thus, decreased LASr (<12.0%) could be a predictor of death after embolic events.47 In a patient group with cryptogenic stroke, reduced LASr and booster pump strain rate were shown to be associated with occult AF, which was masked at the initial diagnosis of stroke but revealed during the follow-up.48,49 And the stroke patients, even without documentation of AF (embolic stroke of undetermined source, ESUS), presented significantly reduced LASr compared with the control group, thus emphasizing the prognostic significance of LA strain.50 In addition, LA strain in AF can be a predictor of LA reverse remodeling after radiofrequency catheter ablation therapy (RFCA).51 Yasuda et al reported that decreased pre-RFCA basal LASr (<25.27%), along with large LAVI, was associated with the recurrence of AF, even during active AF.52

Unfulfilled Clinical Needs and Technical Issues

As strain imaging was initially developed for measuring LV deformation, robust clinical evidence based on LV strain was reported, and several practice guidelines, especially in the field of cardio-oncology, incorporated LV strain as an important diagnostic tool.53,54 Although the field of LA strain is actively developing, there are several obstacles to the use of LA strain in general clinical practice.

Technical Standardization of LA Strain Measurement The major vendors have provided data for the standardization of LV strain measurements, so the issue has been partially answered.55 However, technical consensus for LA strain is currently insufficient. Different tracing methods have been applied in clinical studies, including speckle-tracking, velocity vector imaging, and edge tracking. As each vendor uses a different software algorithm for LA strain, this is a fundamental source of measurement variance. Moreover, LA strain values substantially differ according to the images used (apical 4-chamber view only vs. both apical 4- and 2-chamber views) and the inclusion of the LA roof in tracing.3,17,27 As the LA is located in the far field of the image, a limited acoustic window is another technical problem. Because the LA is thin-walled, a low signal-to-noise ratio poses problems in analysis, and radial deformation tracing is currently unavailable.3

Thus, in current clinical practice we need to use the same vendor’s system for LA strain measurement in a patient on serial follow-up to avoid measurement variance. In addition, we should reduce the region of interest on the speckle-tracking analysis to fit the thin LA wall and avoid any error arising from including the pericardium.

Lack of Established Reference The lack of an established reference value of LA strain is another barrier for its clinical application. Previously reported normal LASr values vary substantially from 36% to 45%.2427 Such variance might be due to different subject characteristics in each study. For example, the mean age of subjects in the study of Morris et al24 was 36.1±12.7 years, whereas it was 49±16 years in the study of Sun et al.26 Another source of variance could be the non-specific definition of the ‘healthy subject group’, in which there could be substantial heterogeneity. Further, the sample size of a study could affect measurement variability. Pathan et al reported differences in LA strain values among studies, and they found that the size of a study group (n >100 vs. n <100) was a determinant of measurement variability.27 In addition, variance in the measurement of LA strain might be attributable to technical fluency. Acquisition of adequate transthoracic echocardiographic images and the availability of a proficient image specialist are crucial for the quality of the strain analysis.

Currently, the reliability of normal LAScd and LASct values is quite limited. In a large-sized meta-analysis of normal LA strain, only 14 and 18 studies reported LAScd and LASct values, whereas 40 studies reported LASr values.27 Therefore, only LASr would be applicable in real-world clinical settings. More research into LAScd and LASct is needed for the clinical application of these parameters.

Definition of the LA Cycle: R-R Gating vs. P-P Gating Currently, there are 2 definitions of the LA cycle (i.e., R-R gating and P-P gating, Figure 3) for the deformation analysis; each method provides different LA strain values.3 R-R gating is a more generalized method in which the LA cycle is defined from the peak of the R-wave to the same point of the next cycle. The R-R gating method presents LA strain as a monophasic curve in which LASr can be clearly identified. One unique advantage of the R-R gating method is its availability, even during AF, because it is oriented to the R-wave, an actual ventricular event.3 In contrast, in P-P gating, the LA cycle starts just before the atrial contraction, which is oriented to a LA physiologic event.3 The P-P gating method provides a biphasic LA strain curve in which the LASct is demonstrated more clearly. Owing to the different reference frame (this serves as the denominator), R-R gating yields a higher LA strain value than P-P gating.3,56 Hayashi et al measured LA strain with both R-R gating and P-P gating, and they showed that LA strain measured by P-P gating showed better correlation with the 3D echocardiography-derived LA emptying fraction.57 Another clinical study reported that LA strain measured by P-P gating was useful in the prediction of new-onset HF.58 Although these results are meaningful, the number of studies with P-P gating is insufficient. Thus, comparison of the gating methods remains unclear, and more studies are required for better definition of the LA cycle in terms of association with clinical outcomes.

Conclusions

LA strain is a modality that can describe LA function objectively with 3 phasic motions. LA strain allows the assessment of functional alteration, which is more sensitive than conventional parameters confined to structural deterioration. LA strain has been shown to be a reliable marker in a variety of clinical situations. Despite several limitations, LA strain is a powerful modality on the basis of accumulating clinical evidence and developing technologies, and its use in clinical practice will increase. To accelerate the general use of LA strain in cardiovascular diseases, we need standardization of the measurement methods and vendor differences, as well as established normal reference values. Further, we need more clinical data, especially with long-term follow-up, to determine whether LA strain can play the role of an indicator of treatment response.

Finally, we would suggest incorporating the use of LA strain for improved clinical practice. “How about using LA strain in your clinical practice?”

Disclosures

None.

References
 
© 2021, THE JAPANESE CIRCULATION SOCIETY

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