Improving risk stratification after acute myocardial infarction : focus on emerging applications of echocardiography
Antoni, M.L.
Citation
Antoni, M. L. (2012, January 19). Improving risk stratification after acute myocardial infarction : focus on emerging applications of echocardiography. Retrieved from https://hdl.handle.net/1887/18376
Version: Corrected Publisher’s Version
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Part III
Diastolic Function after Acute Myocardial Infarction
.
Chapter 11
Comprehensive Assessment of Changes in Left Atrial Volumes and Function after ST-segment Elevation Acute Myocardial Infarction: Role of 2-
Dimensional Speckle Tracking Strain Imaging
M. Louisa Antoni, Ellen A. ten Brinke, Nina Ajmone Marsan, Jael Z. Atary, Eduard R. Holman, Ernst E. van der Wall, Martin J. Schalij, Jeroen J. Bax, Victoria Delgado
J Am Soc Echocardiogr 2011; 24: 1126-1133
Abstract
Objectives
Left atrial (LA) size has been associated with adverse outcome in patients after acute myocardial infarction (AMI). However, data about the occurrence of late LA enlargement and changes in LA function during follow-up are scarce. The purpose of the current study was to evaluate changes in LA size and function during 1-year follow-up.
Methods and results
The study population comprised 407 patients with AMI who were treated with primary percutaneous coronary intervention. At baseline and 12 months, 2-dimensional echocardiography was performed to assess LA volumes and function using speckle- tracking strain and strain rate.
Mean age was 60 ± 11 years and most patients were men (78%). LA maximal volume increased from 25 ± 8ml/m2 to 28 ± 8ml/m2 (p <0.001) from baseline to 1-year.
Echocardiographic assessment at 1-year follow-up defined that 92 patients (25%) developed LA remodeling (defined as an increase of 8 ml/m2 in LA maximal volume).
At multivariate analysis, only LA maximal volume at baseline (odds ratio (OR) 0.95, 95%confidence interval (CI) 0.91–0.98, p = 0.003) and LA strain at baseline (OR 0.94, 95%CI 0.92–0.97, p <0.001) were independent predictors of LA remodeling during follow-up. Interestingly in patients without LA remodeling, no changes were observed in LA function during follow-up. However, in patients with LA remodeling, LA function significantly worsened during follow-up. In line, LA strain and strain rate were
significantly lower at 12 months compared to baseline (24 ± 7% vs. 27 ± 6%, p <0.001 and 1.8 ± 0.5s-1 vs. 2.4 ± 0.7s-1, p <0.001, respectively).
Conclusions
In patients after AMI, LA remodeling occurs in 22% of the patients. In patients without LA remodeling, no changes in LA function were observed, however in patients with LA remodeling, LA function deteriorated significantly.
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IntroductionLeft atrial (LA) dilatation after acute myocardial infarction (AMI) has been associated with an adverse outcome in several studies.1-3 Most studies have evaluated the presence of LA enlargement immediately after AMI.1 2 However, complex alterations in ventricular architecture and function after AMI can result in diastolic dysfunction and therefore dilatation of the LA during follow-up after AMI.4 Data about the occurrence of LA remodeling during the follow-up of patients after AMI are scarce. Some evidence is available that LA remodeling occurs during follow-up in patients after high-risk AMI.3 However, in the current population of AMI patients treated with primary percutaneous coronary intervention, the prevalence of LA remodeling and the effects on LA function during follow-up are unknown. Accordingly, the purpose of the current study was to evaluate the changes in LA dimensions and function during 1 year follow-up in patients after AMI. LA function was assessed extensively using mechanical function derived from LA volumes and myocardial deformation using novel speckle-tracking imaging.
Furthermore, clinical and echocardiographic predictors of LA remodeling were established and the effect of LA remodeling on changes in LA function was assessed.
Methods
Patient population and protocol
The study population comprised 407 patients from the ongoing clinical registry (MISSION!) with a ST-segment elevation AMI, who were treated with primary percutaneous coronary intervention.5 Clinical and echocardiographic data were
prospectively entered into the departmental Cardiology Information System (EPD-Vision®, Leiden University Medical Center) and the echocardiography database, respectively, and retrospectively analyzed.5 6 All patients were treated according to the institutional protocol (MISSION!), which includes standardized medical care according to the most recent guidelines.5 7 8 Within 24 hours of admission, medication is initiated and within 24-48 hours of admission an echocardiogram is performed. Thereafter, patients are scheduled for visits at the outpatient clinic and echocardiography is repeated at 12 months follow-up. LA dimensions and function using conventional and speckle-tracking echocardiography were evaluated at baseline and at 12 months follow-up. The purpose of the current study was to
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investigate the changes in LA dimensions and function during 1 year follow-up in patients after AMI. Furthermore, the patient population was divided according to the presence of LA remodeling during follow-up and clinical and echocardiographic predictors of LA remodeling were established. Finally, the effect of LA remodeling on changes in LA function was assessed and the occurrence of new-onset fibrillation during 1 year follow-up was noted. Atrial fibrillation was determined on the basis of electrocardiographic findings consistent with the diagnosis of atrial fibrillation on 12-lead electrocardiograms and Holter recordings during hospitalization and follow-up at the outpatient clinic.
Echocardiography
According to the protocol (MISSION!), within 24-48 hours of admission for the index infarction and after 12 months follow-up, extensive 2-dimensional (2D) echocardiographic evaluation was performed.5 Patients were imaged using a commercially available system (Vivid 7, General Electric-Vingmed, Horton, Norway). Analysis of echocardiographic images was performed randomly offline by experienced observers (EchoPac version 108.1.5, General Electric-Vingmed). Left ventricular (LV) end-systolic volume, LV end- diastolic volume and LV ejection fraction were calculated with the biplane Simpson’s technique from the apical 4- and 2-chamber views.9 Thereafter, the LV was divided into 16 segments to calculate wall motion score index.9 Mitral regurgitation was characterized as:
mild = jet area/LA area <20% and vena contracta width <0.30 cm, moderate = jet area/LA area 20% – 40% and vena contracta width 0.30 – 0.69 cm, and severe = jet area/LA area
>40% and vena contracta width 0.70 cm.10 The early (E) and late (A) peak diastolic velocities and E-wave deceleration time were measured. The E/E’-ratio was obtained by dividing E by E’, which was measured using color-coded tissue Doppler imaging at the septal side of the mitral annulus in the apical 4-chamber view.11 Diastolic function was graded according to the most recent recommendations of the American Society of
Echocardiography.12 Diastolic function was graded as normal, when septal E’ was 8, E/A ratio was 1 and <2 and deceleration time of E-wave was between 160-200 ms. Diastolic dysfunction was graded as grade I (mild), when septal E’ was <8, E/A ratio <0.8 and deceleration time >200 ms; grade II (moderate), when septal E’ was <8, E/A ratio 0.8 – 1.5 and deceleration time 160 – 200 ms; grade III (severe), when septal E’ was <8, E/A ratio 2
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and deceleration time <160 ms. All measurements were performed by two experienced observers and any discordances were discussed in order to obtain accurate measurements.
Analysis of left atrial dimensions and function
The apical 2- and 4-chamber views were used to measure LA volumes with the biplane Simpson’s method. LA volumes were measured at 3 time points during the cardiac cycle:
(1) maximal volume (LA max) at end-systole, just before mitral valve opening;
(2) minimal volume (LA min) at end-diastole, just before mitral valve closure;
(3) volume before atrial active contraction (LA preA) obtained from the last frame before mitral valve reopening or at time of the P wave on the surface electrocardiogram.
All LA volumes were indexed to the body surface area, as recommended.9 LA mechanical function was derived from the LA volumes and expressed with the following formulas: (1) total atrial emptying fraction: LA total ejection fraction = [(LA max – LA min)/LA max] *100; (2) active atrial emptying fraction: LA active ejection fraction = [(LA preA – LA min)/LA preA] *100, which is considered an index of LA active contraction; (3) passive atrial emptying fraction: LA passive ejection fraction = [(LA max – LA preA)/LA max] *100, which is considered an index of LA conduit function; (4) atrial expansion index: LA expansion index = [(LA max – LA min)/LA min] *100, which is considered an index of LA reservoir function.13 In addition, longitudinal LA wall deformation was assessed in the apical views using speckle-tracking analysis (Figure 1).14 This novel software analyzes motion by tracking frame-to-frame movement of natural acoustic markers in 2 dimensions. All images were recorded with a frame rate of > 40fps for reliable analysis. The LA endocardial border was manually traced and the automatically created region of interest was adjusted to the thickness of the myocardium. The extent of LA wall stretching during the reservoir period may be important for maintaining adequate LV filling.15 Therefore, LA peak systolic longitudinal strain and strain rate were assessed as a measure of LA compliance.16 Strain and strain rate analysis of the LA was feasible in 89% of segments. All LA volume, function and strain measurements were performed with EchoPac version 108.1.5, General Electric-Vingmed.
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Definition of left atrial remodelingChanges in LA volumes and function were assessed between baseline and 12 months follow-up. To study the determinants of LA remodeling, patients were divided in 2 groups based on the change in LA maximal volume. LA remodeling was defined as an increase of
8 ml/m2 of the LA maximal volume between baseline and 12 months follow-up. The cut- off value of an increase of 8 ml/m2 in LA maximal volume was derived from the patient population as the highest quartile of change in LA maximal volume between baseline and 12 months follow-up and is in line with previous studies assessing the extent of LA remodeling.3 Finally, changes in LV volumes, LV ejection fraction and E/E’-ratio between baseline and 12 months follow-up were compared between patients with and without LA remodeling.
Statistical analysis
Continuous data are presented as mean ± standard deviation and were compared between patients with and without LA remodeling with unpaired Student t- test. Categorical data are presented as frequencies and percentages and were compared using chi-square test.
Differences in continuous variables between baseline and follow-up were evaluated using paired Student t-test. In addition, univariate and multivariate logistic regression analyses were performed to identify baseline clinical and echocardiographic parameters that predict remodeling of the LA during follow-up. Clinical and echocardiographic characteristics with
Figure 1.
Representative examples of patients with normal (A, C) and impaired (B, D) longitudinal strain and strain rate of the LA from the apical 4-chamber view.
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a p-value <0.15 at univariate analysis were introduced in the multivariate regression analyses. Finally, 15 patients were selected to test the intra- and interobserver
reproducibility of LA measurements. Bland–Altman analyses were performed and the intraclass correlation coefficient and coefficient of variation were calculated. All statistical analyses were performed with SPSS software (version 16.0, SPSS Inc., Chicago, Illinois).
All statistical tests were two-sided and a p value <0.05 was considered to be statistically significant.
Results
Baseline characteristics of the patient population
A total of 407 consecutive patients were evaluated. Baseline clinical characteristics of the patients are summarized in Table 1. Mean age was 60 ± 11 years and most patients were men (317 patients, 78%). Twenty-five patients (6%) had a prior myocardial infarction and in more than half of the patients (184 patients, 45%) the left anterior descending coronary artery was the culprit vessel. Baseline echocardiographic characteristics are summarized in Table 2. All patients were treated with primary percutaneous coronary intervention and therefore mean LV ejection fraction was relatively preserved (46 ± 9%). In 40 patients echocardiographic assessment was not available at 12 months (including 19 patients who died during the first year) and were therefore excluded from the analysis. Patients who were excluded from the analysis more often presented with a Killip class 2, had higher peak cardiac enzymes and lower LV ejection fraction (41± 9 vs. 46 ± 8%, p <0.001) and higher wall motion score index (1.6 ± 0.3 vs. 1.5 ± 0.3, p = 0.001), indicating a larger myocardial infarction when compared to the remaining 367 patients. Although LA max was
comparable between the excluded and included patients (24 ± 11 vs. 24 ± 8 ml/m2, p = 0.67), LA function was worse in the excluded patients. LA total ejection fraction (43 ± 9 vs.
54 ± 11%, p = 0.03), LA active ejection fraction (19 ± 11 vs. 36 ± 13%, p = 0.01), LA reservoir function (80 ± 32 vs. 132 ± 62%, p = 0.09) and LA strain (18 ± 8 vs. 33 ± 11%, p
= 0.007) and strain rate (1.3 ± 0.2 vs. 2.3 ± 0.7 s-1, p <0.001) were worse in the excluded patients.
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Table 1. Baseline clinical characteristics All patients (N = 407)
LA remodeling
(N = 92)
No LA remodeling
(N = 275)
P
Age(years) 60 ± 11 61 ± 11 59 ± 11 0.10
Male gender 317 (78%) 64 (70%) 224 (82%) 0.02
Current smoking 206 (51%) 40 (44%) 141 (51%) 0.20
Diabetes 30 (7%) 6 (7%) 18 (7%) 0.99
Family history of CAD 170 (42%) 38 (42%) 118 (43%) 0.85
Hyperlipidemia 78 (19%) 20 (22%) 51 (19%) 0.52
Hypertension 134 (33%) 37 (40%) 80 (29%) 0.05
Prior myocardial infarction 25 (6%) 5 (5%) 16 (6%) 0.89
Prior revascularization 18 (4%) 5 (5%) 11 (4%) 0.56
Killip class 2 29 (7%) 4 (5%) 15 (6%) 0.70
Culprit vessel LAD RCA LCX
184 (45%) 152 (37%) 71 (17%)
50 (54%) 31 (34%) 11 (12%)
114 (42%) 109 (40%) 52 (14%)
0.08
Multivessel disease 196 (48%) 44 (48%) 130 (48%) 0.97
TIMI flow 2.9 ± 0.3 3.0 ± 0.2 2.9 ± 0.4 0.59
Peak CPK level(U/l) 2377 ± 1953 2429 ± 2072 2243 ± 1795 0.41 Peak cTnT level(ȝg/l) 6.6 ± 6.2 6.7 ± 6.3 6.1 ± 5.2 0.40 ACE inhibitor/ARB at
discharge
390 (99%) 91 (99%) 272 (99%) 0.99
Antiplatelets at discharge 395 (100%) 92 (100%) 275 (100%) 1.00 Beta-blocker at discharge 363 (92%) 85 (94%) 251 (91%) 0.50
Statin at discharge 386 (98%) 89 (97%) 270 (98%) 0.41
ACE: angiotensin-converting enzyme; ARB: angiotensin receptor blocker; CAD: coronary artery disease; CPK: creatine phosphokinase; cTnT: cardiac troponin T; LAD: left anterior descending coronary artery; LCX: left circumflex coronary artery; RCA: right coronary artery; TIMI:
thrombolysis in myocardial infarction.
Intraobserver reproducibility was good with mean differences, an intraclass correlation coefficient and coefficient of variation of 1.6 ± 2.4 ml/m2, 0.97 and 6 ± 11% for LA maximal volume, 0.5 ± 3.0%, 0.95 and 2 ± 16% for LA strain and 0.06 ± 0.22 s-1, 0.89 and 3 ± 13% for LA strain rate, respectively. Interobserver reproducibility was also good with
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mean differences, intraclass correlation coefficient and coefficient of variation for LA maximal volume, LA strain and LA strain rate of 2.1 ± 4.2 ml/m2, 0.92 and 5 ± 19%, 1.0 ± 4.4%, 0.91and 2 ± 23%and -0.12 ± 0.24s-1, 0.88 and 10 ± 13%.
Table 2. Baseline echocardiographic characteristics All
patients (N = 407)
LA remodeling
(N = 92)
No LA remodeling
(N = 275)
P
LV end-systolic volume (ml) 59 ± 22 61 ± 26 58 ± 20 0.20
LV end-diastolic volume (ml) 108 ± 34 112 ± 37 108 ± 32 0.31
LV ejection fraction (%) 46 ± 9 46 ± 8 46 ± 9 0.57
Wall motion score index 1.5 ± 0.3 1.5 ± 0.3 1.5 ± 0.2 0.19
LV mass index (g/m2) 104 ± 31 103 ± 29 104 ± 30 0.90
E/A ratio 0.9 ± 0.3 0.9 ± 0.3 0.9 ± 0.3 0.22
Deceleration time (ms) 210 ± 77 219 ± 89 209 ± 70 0.535
E/E’ ratio 13 ± 5 13 ± 6 12 ± 5 0.11
Moderate or severe MR 31 (8%) 4 (4%) 19 (7%) 0.38
Diastolic function Grade 0 Grade I Grade II Grade III
24 (6%) 198 (49%)
84 (21%) 101 (25%)
4 (4%) 47 (51%) 12 (13%) 29 (32%)
18 (7%) 131 (48%)
66 (24%) 60 (22%)
0.06
LA max (ml/m2) 25 ± 8 22 ± 8 25 ± 7 <0.001
LA total ejection fraction (%) 54 ± 12 54 ± 11 54 ± 11 0.94 LA passive ejection fraction (%) 28 ± 9 28 ± 9 29 ± 10 0.57 LA active ejection fraction (%) 34 ± 13 36 ± 13 36 ± 13 0.71
LA expansion index (%) 131 ± 62 131 ± 58 132 ± 63 0.86
LA strain (%) 31 ± 11 27 ± 6 33 ± 11 <0.001
LA strain rate (s-1) 2.3 ± 0.7 2.3 ± 0.7 2.3 ± 0.7 0.45
E/A: mitral inflow peak early velocity (E)/mitral inflow peak late velocity (A); E/E’: mitral inflow peak early velocity (E)/mitral annular peak early velocity (E’); LA: left atrial; LV: left ventricular;
MR: mitral regurgitation.
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Changes in left atrial dimensions and functionDuring 1 year follow-up, 19 patients (5%) developed new-onset atrial fibrillation.
Interestingly, patients with atrial fibrillation had larger LA volumes at baseline compared to patients without atrial fibrillation, although not statistically significant (28 ± 10 vs. 24 ± 8 ml/m2, p = 0.07). However, no other differences were observed in LA function between the two groups except in LA strain, which was significantly lower at baseline in patients with new-onset atrial fibrillation (25 ± 11 vs. 33 ± 11%, p = 0.007). In the remaining population of 367 patients with a follow-up echocardiogram, LA max increased from 25 ± 8 ml/m2 to 28 ± 8 ml/m2 (p <0.001) and LA reservoir function decreased from 131 ± 62% to 121 ± 44% (p = 0.002) from baseline to 12 months. In addition, mean LA strain and strain rate which reflect the compliance of the LA decreased significantly from 31 ± 11% to 30 ± 12%
(p = 0.03) and 2.3 ± 0.7 s-1 to 2.1 ± 0.7 s-1 (p <0.001), respectively. Of note, no significant changes were observed in LA total ejection fraction, LA passive ejection fraction or LA active ejection fraction between baseline and follow-up in the total population. Overall, LV function improved during 1 year follow-up. LV end-systolic and end-diastolic volumes decreased (from 61 ± 22 to 50 ± 20ml, p <0.001 and 114 ± 33 to 98 ± 28ml, p <0.001, respectively), resulting in an increase in LV ejection fraction (from 46 ± 9 to 50 ± 8%, p
<0.001). In line, wall motion score index decreased from 1.5 ± 0.2 to 1.3 ± 0.3 (p <0.001).
Finally, LV filling pressures as reflected by E/E’-ratio decreased during 1 year follow-up (from 12 ± 4 to 11 ± 5, p=0.003).
Left atrial remodeling
Echocardiographic assessment at 1 year after the index infarction identified 92 patients (25%) developed LA remodeling (defined as an increase of 8 ml/m2 in LA maximal volume, corresponding with the highest quartile of the population).3 No significant differences in clinical characteristics were observed between patients with and without LA remodeling except for male gender (70% vs. 82%, p = 0.02). Interestingly, patients with and without LA remodeling demonstrated no differences in baseline LV systolic and diastolic function. However, when the baseline LA parameters are assessed, LA max was significantly smaller (22 ± 8 ml/m2 vs. 25 ± 7 ml/m2, p <0.001) and LA strain was significantly lower (27 ± 6% vs. 33 ± 11%, p <0.001) in patients with LA remodeling
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compared to patients without LA remodeling after 1 year. When comparing the changes in LV function during 1 year follow-up between patients with and without LA remodeling, no differences were observed in LV volumes or LV ejection fraction between the 2 groups.
Both groups demonstrated a decrease in LV volumes resulting in an improvement in LV ejection fraction (from 46 ± 8 to 50 ± 8%, p <0.001 and from 46 ± 9 to 50 ± 7%, p <0.001 for patients with and without LA remodeling, respectively). However, patients with LA remodeling showed an increase in LV filling pressures during follow-up whereas patients without LA remodeling showed a decrease in E/E’-ratio (from 13 ± 5 to 15 ± 5, p=0.001 and from 12 ± 4 to 11 ± 6, p = 0.02, respectively).
Prediction of left atrial remodeling
To investigate predictors of LA remodeling, univariate and multivariate regression analyses were performed (Table 3). Predictors for LA remodeling at univariate analyses were male gender, LA max and LA strain. At multivariate analysis, only LA max (odds ratio(OR) 0.94, 95%confidence interval(CI) 0.91 – 0.98, p = 0.001) and LA strain (OR 0.94, 95%CI 0.92 – 0.97, p <0.001) remained independent predictors of LA remodeling.
Effect of left atrial remodeling on left atrial function
In patients without LA remodeling, no changes were observed in LA mechanical function, strain and strain rate between baseline and follow-up (Figure 2).
Table 3. Prediction of left atrial remodeling
Univariate analysis Multivariate analysis
OR 95%CI P OR 95%CI P
Age (years) 1.02 0.99 – 1.04 0.10 Male gender 0.52 0.30 – 0.89 0.02 Hypertension 1.64 1.00 – 2.68 0.05 Culprit vessel 0.65 0.39 – 1.09 0.10 E/E’ ratio 1.04 0.99 – 1.09 0.12
LA max (ml/m2) 0.93 0.89 – 0.97 <0.001 0.95 0.91 – 0.98 0.003 LA strain (%) 0.94 0.92 – 0.97 <0.001 0.94 0.92 – 0.97 <0.001
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Left atrial remodeling was defined as an increase of 8 ml/m2 in left atrial maximal volume during 1 year follow-up.
E/E’: mitral inflow peak early velocity (E)/mitral annular peak early velocity (E’); LA: left atrial.
However, in patients with LA remodeling, LA mechanical function worsened significantly during follow-up. LA total ejection fraction decreased from 54 ± 11% to 49 ± 10% (p
<0.001), as well as LA active ejection fraction (from 36 ± 13% to 29 ± 16%, p <0.001) and LA expansion index (from 131 ± 58 to 105 ± 41%, p <0.001, Figure 2a). In line, LA strain and strain rate were significantly lower at 12 months compared to baseline (24 ± 7% vs. 27
± 6%, p <0.001 and 1.8 ± 0.5 s-1 vs. 2.4 ± 0.7 s-1, p <0.001, respectively, Figure 2b).
Figure 2a.
Changes in LA mechanical function in patients with and without LA remodeling.
Figure 2b.
Changes in LA strain and strain rate in patients with and without LA remodeling.
Discussion
The main findings of the current study can be summarized as follows. 1) During 1 year follow-up after AMI, 25% of the patients developed LA remodeling (defined as an increase
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of 8 ml/m2 in LA maximal volume, corresponding to the highest quartile of the population). 2) Besides LA max, LA strain assessed early after AMI was an independent predictor of the occurrence of LA remodeling at 1 year follow-up. 3) In patients without LA remodeling, no changes in LA function were observed. However, in patients with LA remodeling, LA mechanical function and LA strain and strain rate deteriorated significantly during follow-up.
Assessment of left atrial function
Current American Society of Echocardiography recommendations include the assessment of LA function by means of LA volume.9 However, assessment of LA mechanical function with phasic changes of the LA volumes provides more information on LA performance.
Abnormal LA reservoir function has been described in several cardiac conditions further impairing LV diastolic filling and reducing LV stroke volume.17 18 In patients with AMI, reservoir function of the LA is important. A preserved LA reservoir function can withstand the impact of the increased LA pressure due to LV dysfunction and maintain an adequate LV filling. However, the assessment of LA reservoir function is derived from LA volume measurements and reflects indirectly the properties of the atrial myocardium. Recently, 2D speckle tracking echocardiography permits direct evaluation of the deformation of the atrial myocardium. Several studies have recently demonstrated that LA peak systolic strain which reflects the passive stretching of the LA during the LV systole, is an accurate measurement of LA reservoir function.15 16 18-20 In addition, LA strain has been related to LA structural remodeling and fibrosis of the atrial wall as assessed with magnetic resonance imaging.21 The present study extends previous results and describes changes in LA function after AMI combining LA volumes, phasic changes of LA volumes and LA strain in patients after AMI. The results show that speckle-tracking derived strain is a promising technique to assess LA function, as baseline LA strain was an independent predictor of the occurrence of LA remodeling and concomitant deterioration of LA function during 1 year follow-up.
Changes in left atrial function after acute myocardial infarction
Preserved reservoir function of the LA is crucial to maintain adequate LV filling despite increased LV filling pressures. However, over time the sustained increase in LA pressure
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overload will lead to LA dilatation and LA dysfunction. This LA remodeling process has been related to worse outcome at long term follow-up.3 Meris et al. described the changes in LA volume in patients after high-risk AMI and found that LA remodeling during follow- up was associated with a worse outcome.3 The authors defined the optimal cut-off value of 9 ml/m2 increase in LA max for the composite endpoint of all-cause mortality or
hospitalization for heart failure. In the current study, the cut-off value of 8 ml/m2 increase in LA max corresponding to the highest quartile, used to divide the population into patients with LA remodeling and without LA remodeling, was in line with the cut-off used in the VALIANT echocardiography study.3 Interestingly, patients with LA remodeling deteriorated significantly in mechanical function reflected by LA total ejection fraction, active ejection fraction and LA expansion index. In a series of 73 patients with an anterior myocardial infarction and repeat echocardiograms performed at time of admission, after 1 week, 1 month and 3 months follow-up, Bozkurt et al. showed that LA active emptying fraction increased whereas LA passive emptying fraction decreased..22 In contrast, in the current study, no changes in active or passive emptying fraction were observed in the overall population. The difference may be explained by the different time points at which LA function was assessed. It may be hypothesized that LA passive emptying fraction deteriorates in the first months after AMI and is compensated by an increase in active emptying fraction as Bozkurt et al describe. During longer follow-up, LA dilatation to some extent may restore LA mechanical function and therefore no changes in active or passive emptying fraction were observed in the current study between baseline and 1 year follow- up. Finally, patients with smaller LA volumes at baseline more often developed remodeling during the follow-up compared to patients with larger LA volumes at baseline. As has been described in previous studies, LA enlargement in the acute phase after myocardial
infarction is a strong predictor of adverse outcome.1-3 This early LA enlargement is probably only partly related to the myocardial infarction, but has been shown to be strongly related to the presence of hypertension and other cardiovascular risk factors and may therefore be already present before the myocardial infarction.3 The development of late LA remodeling is more related to the occurrence of the myocardial infarction and forms a subacute maladaptive response to the acute event. However, the presence of early LA remodeling probably reduces the ability of the LA to develop further remodeling during long-term follow-up and as a result patients with smaller volumes are at higher risk to
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develop LA remodeling. At multivariate analysis, LA strain was also a predictor of LA remodeling and may be a more sensitive parameter of changes in the LA by providing information on mechanical properties and functions of the LA myocardium. Reduced LA strain reflects a reduced compliance of the LA and therefore a LA that is more prone to remodeling. In addition, patients who developed new-onset atrial fibrillation during follow- up already had a reduced LA strain at baseline, whereas LA volumes did not show significant differences yet. This finding supports the hypothesis that LA dysfunction may be detected earlier with LA strain than with volumetric measurements.
Limitations
Baseline echocardiography was performed early after AMI (within 24-48 hours of admission) and therefore may have underestimated LV function due to myocardial stunning. In addition, changes in LV load conditions that may occur at the early phase of AMI may affect the assessment of LV diastolic function. For the current study, the cut-off value for LA remodeling was chosen as the highest quartile from the study population.
However, the cut-off value is in line with the cut-off value defined by Meris et al.3 Although the authors assessed LA remodeling at 1 month follow-up, other cut-off values for LA remodeling, derived from larger populations are currently lacking. Therefore, future research should aim at defining a cut-off value for LA remodeling and validating these cut- offs in relation to clinical endpoints. Finally, patients who were excluded because a follow- up echo was not available at 1 year (due to logistic reasons or because the patient died), had significantly larger myocardial infarctions as reflected by the peak cardiac enzymes and the echocardiographic characteristics. Although, the aim of the study was evaluate the changes between baseline and long-term follow-up, this is a limitation of the study.
Conclusions
In the present study, 25% of the patients demonstrated LA remodeling defined as an increase of 8 ml/m2 in LA maximal volume during 1 year follow-up after AMI. The presence of LA remodeling was associated with deterioration in LA function assessed with phasic changes in LA volumes and novel speckle-tracking LA strain. Baseline LA max and LA strain were identified as independent predictors of LA remodeling at 1 year follow-up.
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References1. Beinart R, Boyko V, Schwammenthal E, et al. Long-term prognostic significance of left atrial volume in acute myocardial infarction. J Am Coll Cardiol 2004;44:327-34.
2. Moller JE, Hillis GS, Oh JK, et al. Left atrial volume: a powerful predictor of survival after acute myocardial infarction. Circulation 2003;107:2207-12.
3. Meris A, Amigoni M, Uno H, et al. Left atrial remodelling in patients with myocardial infarction complicated by heart failure, left ventricular dysfunction, or both: the VALIANT Echo study. Eur Heart J 2009;30:56-65.
4. Thune JJ, Solomon SD. Left ventricular diastolic function following myocardial infarction.
Curr Heart Fail Rep 2006;3:170-4.
5. Liem SS, van der Hoeven BL, Oemrawsingh PV, et al. MISSION!: optimization of acute and chronic care for patients with acute myocardial infarction. Am Heart J 2007;153:14.e1- 11.
6. Borleffs CJ, van Rees JB, van Welsenes GH, et al. Prognostic importance of atrial fibrillation in implantable cardioverter-defibrillator patients. J Am Coll Cardiol 2010;55:879-85.
7. Antman EM, Anbe DT, Armstrong PW, et al. ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction; A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Revise the 1999 Guidelines for the Management of patients with acute myocardial infarction). J Am Coll Cardiol 2004;44:E1-E211.
8. Kushner FG, Hand M, Smith SC, Jr., et al. 2009 focused updates: ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction (updating the 2004 guideline and 2007 focused update) and ACC/AHA/SCAI guidelines on percutaneous coronary intervention (updating the 2005 guideline and 2007 focused update) a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 2009;54:2205-41.
9. Lang RM, Bierig M, Devereux RB, et al. Recommendations for chamber quantification: a report from the American Society of Echocardiography's Guidelines and Standards Committee and the Chamber Quantification Writing Group, developed in conjunction with the European Association of Echocardiography, a branch of the European Society of Cardiology. J Am Soc Echocardiogr 2005;18:1440-63.
10. Zoghbi WA, Enriquez-Sarano M, Foster E, et al. Recommendations for evaluation of the severity of native valvular regurgitation with two-dimensional and Doppler
echocardiography. J Am Soc Echocardiogr 2003;16:777-802.
11. Naqvi TZ, Padmanabhan S, Rafii F, et al. Comparison of usefulness of left ventricular diastolic versus systolic function as a predictor of outcome following primary percutaneous coronary angioplasty for acute myocardial infarction. Am J Cardiol 2006;97:160-6.
12. Nagueh SF, Appleton CP, Gillebert TC, et al. Recommendations for the evaluation of left ventricular diastolic function by echocardiography. J Am Soc Echocardiogr 2009;22:107- 33.
13. Leung DY, Boyd A, Ng AA, et al. Echocardiographic evaluation of left atrial size and function: current understanding, pathophysiologic correlates, and prognostic implications.
Am Heart J 2008;156:1056-64.
Changes in Left Atrial Function
195
14. Sutherland GR, Di SG, Claus P, et al. Strain and strain rate imaging: a new clinical approach to quantifying regional myocardial function. J Am Soc Echocardiogr 2004;17:788-802.
15. Sirbu C, Herbots L, D'hooge J, et al. Feasibility of strain and strain rate imaging for the assessment of regional left atrial deformation: a study in normal subjects. Eur J Echocardiogr 2006;7:199-208.
16. Cameli M, Caputo M, Mondillo S, et al. Feasibility and reference values of left atrial longitudinal strain imaging by two-dimensional speckle tracking. Cardiovasc Ultrasound 2009;7:6.
17. Boyd AC, Ng AC, Tran DT, et al. Left Atrial Enlargement and Phasic Function in Patients Following Non-ST Elevation Myocardial Infarction. J Am Soc Echocardiogr 2010.
18. Eshoo S, Boyd AC, Ross DL, et al. Strain rate evaluation of phasic atrial function in hypertension. Heart 2009;95:1184-91.
19. Di Salvo G, Russo MG, Paladini D, et al. Two-dimensional strain to assess regional left and right ventricular longitudinal function in 100 normal foetuses. Eur J Echocardiogr
2008;9:754-6.
20. Saraiva RM, Demirkol S, Buakhamsri A, et al. Left atrial strain measured by two-
dimensional speckle tracking represents a new tool to evaluate left atrial function. J Am Soc Echocardiogr 2010;23:172-80.
21. Kuppahally SS, Akoum N, Burgon NS, et al. Left Atrial Strain and Strain Rate in Patients with Paroxysmal and Persistent Atrial Fibrillation: Relationship to Left Atrial Structural Remodeling Detected by Delayed Enhancement-MRI. Circ Cardiovasc Imaging 2010.
22. Bozkurt E, Arslan S, Acikel M, et al. Left atrial remodeling in acute anterior myocardial infarction. Echocardiography 2007;24:243-51.
.
