Background
The aim of this study was to examine whether left atrial (LA) strain and synchrony can be assessed using three-dimensional (3D) speckle-tracking echocardiography (STE) and how 3D STE parameters are modified by atrial fibrillation (AF).
Methods
LA peak ventricular systolic longitudinal strain (LSs), circumferential strain (CSs), and area strain (ASs) and LA peak pre–atrial contraction longitudinal strain, circumferential strain (CSa), and area strain were determined using 3D STE, and SDs of times to peaks of regional LA strain were calculated as indices of LA dyssynchrony. Three-dimensional speckle-tracking was able to measure LA strain in 75 of the 77 healthy subjects and in all 47 patients with AF (31 with paroxysmal AF [PAF] and 16 with permanent AF).
Results
The mean time for analysis with 3D STE was 18% shorter than with two-dimensional (2D) STE ( P < .05). On 3D STE, values of interobserver and intraobserver variability of LA strain were <10% and <12%, respectively. LSs, CSs, ASs, and 2D STE LSs were reduced in patients with PAF compared with controls, and further reductions of these parameters were observed in patients with permanent AF. SDs of LSs, CSs, and ASs were similarly larger in patients with PAF and in those with permanent AF compared with controls. Patients with PAF showed smaller LA peak pre–atrial contraction longitudinal strain, CSa, and LA peak pre–atrial contraction area strain and larger SDs of CSa and LA peak pre–atrial contraction area strain compared with controls. In multivariate analysis, 2D STE LSs ( P = .044), LSs ( P = .040), ASs ( P = .007), and CSa ( P = .020) were independent predictors of PAF.
Conclusions
Three-dimensional speckle-tracking enables the measurement of both LA strain and synchrony with excellent reproducibility. Three-dimensional LA strain appears to be beneficial compared with 2D LA strain for identifying patients with PAF.
Left atrial (LA) size and function assessed using volumetric methods and Doppler echocardiography have been shown to predict adverse cardiovascular outcomes. However, such indices of LA function depend on hemodynamic loading conditions and on geometric assumptions. These problems have been overcome by strain rate imaging and two-dimensional (2D) speckle-tracking echocardiography (STE). These imaging techniques enable the assessment of LA myocardial function with better reproducibility and less load dependence than with conventional methods. Two-dimensional STE is a basically angle independent technique, and the analysis of longitudinal LA function by 2D STE has been increasingly used for various purposes, including the assessment of effects of paroxysmal atrial fibrillation (PAF), the prediction of atrial fibrillation (AF) recurrence after pulmonary venous isolation, the estimation of left ventricular (LV) filling pressure, the assessment of LA dyssynchrony, and the prediction of adverse cardiac events in patients after acute myocardial infarction. However, there are several limitations to 2D STE for the assessment of LA function. The measurement of LA strain by 2D STE is dependent on image quality and suffers from errors due to the loss of some speckles that move out of the image plane (i.e., through-plane motion). LA myocardial fibers are arranged in both longitudinal and circumferential directions, and cardiac magnetic resonance imaging has demonstrated that LA fibrosis occurred heterogeneously in patients with AF. Thus, it is likely that the assessment of longitudinal LA function by 2D STE overlooks some LA dysfunction.
Three-dimensional (3D) STE has recently been developed, and its advantages for the determination of LV strain and LV synchrony have been shown. However, whether 3D STE is applicable for the evaluation of LA function remains unclear. To address this issue, we first examined the feasibility and reproducibility of 3D STE for the determination of LA strain and synchrony in healthy subjects. In the second part of the study, we investigated the effects of AF on LA parameters by 3D STE. Finally, we examined whether LA strain determined by 3D STE is more efficient than strain determined by 2D STE for identifying patients with PAF.
Methods
Study Population
This was a single-center, cross-sectional study conducted at Sapporo Medical University Hospital, and informed consent was obtained from all study subjects. From October 2010 to November 2010, 77 healthy subjects without cardiovascular disease, hypertension (HT) or diabetes mellitus were enrolled as controls to assess the feasibility and reproducibility of 3D STE for the determination of LA deformation and synchrony ( Table 1 ). In this group of subjects, physical findings, electrocardiographic findings, and the results of conventional echocardiography were all normal. As shown in previous studies, age is an important determinant of LA strain. To compare patients with AF with controls of comparable age, 15 healthy subjects aged > 50 years were selected as control group ( Table 2 ). Eighty-five patients with AF were consecutively recruited in November 2010, March 2011, November 2011, and July 2012, when the Artida system (Toshiba Medical Systems, Tokyo, Japan) was available for us to conduct the present study. Thirty-eight patients with AF were excluded on the basis of the exclusion criteria, which were poor image quality, the presence of regional or global LV systolic dysfunction (ejection fraction < 55%), LV dilatation (end-diastolic diameter > 55 mm), significant valvular diseases, and/or a history of cardiac surgery. Thus, 47 patients with nonvalvular AF (31 with PAF and 16 with permanent AF) were selected to assess the effects of AF on LA function ( Table 2 ). Fourteen of the patients with PAF had organic heart disease and/or underlying systemic disease (six with HT, three with diabetes mellitus, three with aortitis, and two with hypothyroidism), and six of the patients with permanent AF had HT. PAF was diagnosed when both AF and sinus rhythm had been documented on electrocardiographic or Holter monitoring. All study subjects, except for the patients with permanent AF, were in sinus rhythm at the time of echocardiographic examination.
| Variable | Value |
|---|---|
| Age (y) | 32.3 ± 14.2 |
| Men | 48 (62%) |
| Body mass index (kg/m 2 ) | 21.9 ± 2.7 |
| Heart rate (beats/min) | 67.6 ± 12.3 |
| Systolic blood pressure (mm Hg) | 112.7 ± 10.2 |
| Diastolic blood pressure (mm Hg) | 72.5 ± 9.5 |
| 2D LA volume (mL/m 2 ) | 22.7 ± 7.3 |
| 3D LA volume (mL/m 2 ) | 21.7 ± 6.3 |
| LV mass index (g/m 2 ) | 68.5 ± 18.4 |
| LV ejection fraction (%) | 68.6 ± 4.6 |
| E/A ratio | 1.7 ± 0.6 |
| Deceleration time of E (msec) | 171 ± 24 |
| Medial e′ (cm/sec) | 13.8 ± 3.2 |
| Lateral e′ (cm/sec) | 15.8 ± 5.2 |
| Medial a′ (cm/sec) | 9.6 ± 2.1 |
| Lateral a′ (cm/sec) | 9.5 ± 2.7 |
| E/medial e′ | 5.4 ± 1.3 |
| E/lateral e′ | 4.6 ± 1.1 |
| LSs by 2D STE (%) | 35.8 ± 7.7 |
| LSs (%) | 28.1 ± 7.4 |
| CSs (%) | 32.6 ± 11.6 |
| ASs (%) | 71.0 ± 22.9 |
| LSa (%) | 7.7 ± 5.2 |
| CSa (%) | 13.9 ± 8.7 |
| ASa (%) | 23.8 ± 15.4 |
| SD of LSs (%) | 9.0 ± 4.5 |
| SD of CSs (%) | 14.4 ± 5.9 |
| SD of ASs (%) | 9.7 ± 5.5 |
| SD of LSa (%) | 22.9 ± 9.6 |
| SD of CSa (%) | 19.1 ± 9.9 |
| SD of ASa (%) | 19.6 ± 10.2 |
| Variable | Controls ( n = 15) | Patients with PAF ( n = 31) | Patients with permanent AF ( n = 16) |
|---|---|---|---|
| Age (y) | 57.9 ± 5.4 | 62.5 ± 8.2 | 62.4 ± 10.4 |
| Men | 12 (80%) | 19 (71%) | 14 (88%) |
| Body mass index (kg/m 2 ) | 23.9 ± 2.4 | 24.2 ± 2.8 | 24.3 ± 3.3 |
| Heart rate (beats/min) | 64.5 ± 10.0 | 60.0 ± 9.8 | 64.9 ± 14.0 |
| Systolic blood pressure (mm Hg) | 117.6 ± 13.0 | 113.3 ± 15.0 | 121.4 ± 14.7 |
| Diastolic blood pressure (mm Hg) | 79.3 ± 9.4 | 71.6 ± 9.1 | 77.9 ± 13.4 |
| Duration of AF (y) | 7.5 ± 7.1 | 9.7 ± 7.3 | |
| CHADS 2 score | 0.8 ± 1.2 | 1.8 ± 1.3 † | |
| Hypertension | 7 (23%) | 6 (38%) | |
| Diabetes mellitus | 3 (10%) | 6 (38%) | |
| Calcium antagonists | 11 (35%) | 7 (44%) | |
| ACE inhibitors or ARBs | 4 (13%) | 5 (31%) | |
| β-blockers | 16 (52%) | 3 (19%) | |
| Antiarrhythmic drugs | 23 (74%) | 6 (38%) † | |
| 2D LA volume (mL/m 2 ) | 27.1 ± 7.5 | 35.8 ± 13.3 ∗ | 48.6 ± 17.3 ∗,† |
| 3D LA volume (mL/m 2 ) | 25.6 ± 6.8 | 35.4 ± 15.3 ∗ | 48.0 ± 18.3 ∗,† |
| LV mass index (g/m 2 ) | 78.9 ± 17.3 | 98.3 ± 25.2 ∗ | 94.1 ± 19.9 |
| LV ejection fraction (%) | 68.6 ± 4.6 | 68.5 ± 4.6 | 67.2 ± 4.2 |
| E (cm/sec) | 60 ± 12 | 67 ± 17 | 85 ± 17 ∗,† |
| A (cm/sec) | 62 ± 11 | 61 ± 22 | |
| Deceleration time of E (msec) | 189 ± 34 | 196 ± 54 | 165 ± 31 † |
| Medial e′ (cm/sec) | 10.1 ± 1.9 | 9.0 ± 2.7 | 10.1 ± 2.6 |
| Lateral e′ (cm/sec) | 11.4 ± 2.1 | 10.7 ± 3.1 | 13.5 ± 2.5 † |
| Medial a′ (cm/sec) | 11.5 ± 1.8 | 8.8 ± 2.6 ∗ | |
| Lateral a′ (cm/sec) | 12.1 ± 1.9 | 8.5 ± 3.0 ∗ | |
| E/medial e′ | 6.1 ± 1.4 | 8.0 ± 2.6 ∗ | 8.9 ± 2.8 ∗ |
| E/lateral e′ | 5.4 ± 1.3 | 6.8 ± 2.8 | 6.5 ± 1.6 |
| LSs by 2D STE (%) | 32.6 ± 6.5 | 23.8 ± 8.6 ∗ | 11.1 ± 3.5 ∗,† |
| LSs (%) | 25.7 ± 7.2 | 16.3 ± 6.8 ∗ | 6.4 ± 2.8 ∗,† |
| CSs (%) | 37.1 ± 10.2 | 20.5 ± 12.2 ∗ | 6.6 ± 3.6 ∗,† |
| ASs (%) | 74.2 ± 20.2 | 41.7 ± 22.3 ∗ | 13.5 ± 6.7 ∗,† |
| LSa (%) | 12.0 ± 4.1 | 7.0 ± 3.9 ∗ | |
| CSa (%) | 22.8 ± 8.1 | 10.7 ± 7.2 ∗ | |
| ASa (%) | 38.2 ± 14.4 | 20.6 ± 12.5 ∗ | |
| SD of LSs (%) | 9.9 ± 5.8 | 16.1 ± 6.8 ∗ | 20.9 ± 4.5 ∗,† |
| SD of CSs (%) | 15.1 ± 5.8 | 20.6 ± 8.3 ∗ | 23.2 ± 6.6 ∗ |
| SD of ASs (%) | 10.0 ± 5.7 | 15.5 ± 8.2 ∗ | 18.2 ± 6.6 ∗ |
| SD of LSa (%) | 20.9 ± 10.9 | 26.4 ± 8.8 | |
| SD of CSa (%) | 16.7 ± 9.0 | 25.8 ± 10.6 ∗ | |
| SD of ASa (%) | 16.5 ± 8.2 | 24.9 ± 9.6 ∗ |
∗ P after Bonferroni’s correction < .05 versus controls.
† P after Bonferroni’s correction < .05 versus patients with PAF.
Transthoracic Echocardiography and Doppler Tissue Imaging (DTI)
Conventional echocardiographic examination and 2D STE were performed using an Artida system equipped with a PST-25SBT transducer. Two-dimensional and spectral DTI modes were used in standard echocardiographic views. Ejection fraction was calculated using the biplane modified Simpson’s method, and LV mass was normalized to body surface area. LA volume was measured using the biplane Simpson’s method and normalized for body surface area (2D LA volume), and LA dilation was defined as 2D LA volume > 29 mL/m 2 . Transmitral flow velocities were determined using pulsed-wave Doppler echocardiography, and mitral flow parameters, including peak velocities during early (E) and late (A) diastole and the deceleration time of E, were measured. Each parameter was evaluated by averaging three to five measurements.
DTI from the apical four-chamber view was performed with a frame rate of 80 to 120 frames/sec. A sample volume was placed at the medial and lateral annulus in the apical four-chamber view, peak myocardial velocities during early (e′) and late (a′) diastole were measured, and the E/e′ ratio was calculated.
Assessment of LA Strain by 2D STE
For 2D STE, apical four-chamber and two-chamber images were obtained using 2D echocardiography. All images were recorded with a frame rate of >40 frames/sec. The LA endocardial border was manually traced in both apical four-chamber and two-chamber views, and the software automatically tracked the contours on the subsequent frames. Adequate tracking can be verified and corrected by adjusting the region of interest or manually correcting the contour to ensure optimal tracking. A single observer blinded to data of the study population performed all analyses offline. As shown in Figure 1 , LA peak ventricular systolic longitudinal strain (LSs), which was calculated by averaging the values of the six LA segments, was measured from apical four-chamber and two-chamber views, and the values were averaged.
