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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Chapter 15
Prevalence of Dyssynchrony and Relation with Long-Term Outcome in Patients after Acute Myocardial Infarction
M. Louisa Antoni, Helèn Boden, Georgette E. Hoogslag, See Hooi Ewe, Dominique Auger, Eduard R. Holman, Ernst E. van der Wall, Martin J. Schalij,
Jeroen J. Bax, Victoria Delgado
Am J Cardiol 2011; in press
Abstract
Objectives
The impact of left ventricular (LV) dyssynchrony on long-term outcome of patients with acute myocardial infarction (AMI) remains unknown. The purpose of the current study was to evaluate the prevalence of LV dyssynchrony after AMI and the potential relation with adverse events.
Methods and results
A total of 976 consecutive patients admitted with AMI treated with primary percutaneous coronary intervention were evaluated. Two-dimensional echocardiography was performed within 48 hours of admission. LV dyssynchrony was assessed with speckle-tracking imaging and calculated as the time difference between the earliest and latest activated segments. Patients were followed-up for the occurrence of all-cause mortality (primary endpoint) or the composite secondary endpoint (heart failure hospitalization and all-cause mortality). Within 48 hours of admission for the index infarction, mean LV dyssynchrony was 61 ± 79 ms and 14% of the patients demonstrated 130 ms time difference defined as significant LV dyssynchrony. During a mean follow-up of 40 ± 17 months, 82 patients (8%) reached the primary endpoint. In addition, 36 patients (4%) were hospitalized for heart failure. The presence of LV dyssynchrony was associated with an increased risk of all-cause mortality and hospitalization for heart failure during long-term follow-up (adjusted HR 1.06, 95%CI 1.05–1.08, p <0.001, per 10 ms increase). Moreover, LV dyssynchrony provided incremental value over known clinical and echocardiographic risk factors for the prediction of adverse outcome.
Conclusions
LV dyssynchrony is a strong predictor of long-term mortality and hospitalization for heart failure in a population of patients admitted with ST-segment elevation AMI treated with primary percutaneous coronary intervention.
Introduction
Left ventricular (LV) dyssynchrony has been extensively evaluated in patients with heart failure undergoing cardiac resynchronization therapy. The presence of LV dyssynchrony is significantly associated with increased morbidity and mortality of patients with heart failure.1 2 In contrast, reduction of LV dyssynchrony by cardiac resynchronization therapy has shown to improve the quality of life, LV function and survival of patients with heart failure.3 4 In the past few years, the prevalence and clinical implications of LV
dyssynchrony in other subgroups of patients have been evaluated. Several studies have investigated the predictive value of LV dyssynchrony for the development of LV remodeling after acute myocardial infarction (AMI).5-7 More recently, LV dyssynchrony was related to adverse events, including all-cause mortality and heart failure, in high-risk AMI patients with LV dysfunction.8 Currently, most patients admitted with AMI are treated with primary percutaneous coronary intervention (PCI) and therefore, LV function is relatively preserved. A few studies have reported the prevalence of LV dyssynchrony in patients with AMI treated with primary PCI.5 9 However, the clinical relevance of LV dyssynchrony in AMI patients treated with primary PCI remains unclear. Accordingly, the purpose of the present study was to assess the prevalence of LV dyssynchrony in a large population of AMI patients treated with primary PCI and to assess the potential relation between LV dyssynchrony and long-term outcome.
Methods
A total of 976 consecutive patients admitted with ST-segment elevation AMI treated with primary PCI were evaluated.10 Patients were selected from an ongoing registry which evaluates the effects of an all-phase integrated AMI care program (MISSION!) on short- and long-term outcomes.10 Diagnosis of ST-segment elevation AMI was made on the basis of typical electrocardiographic changes with clinical symptoms associated with elevation of cardiac biomarkers.11 All patients were treated according to the institutional AMI protocol (MISSION!), which includes 2-dimensional (2D) echocardiography performed within 48 hours of admission.10 Clinical data were prospectively entered in the departmental Cardiology Information System (EPD-Vision®, Leiden University Medical Center) and retrospectively analyzed.10 12 In addition, echocardiographic data were retrospectively
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analyzed including the assessment of LV dyssynchrony with 2-dimensional speckle tracking imaging. Patients were followed prospectively for the occurrence of all-cause mortality and hospitalizations for heart failure. Among the various clinical and echocardiographic variables, the independent determinants of these endpoints were assessed. Particularly, the prognostic value of LV dyssynchrony was evaluated.
All patients were imaged in the left lateral decubitus position using a commercially available system (Vivid 7 and e9, General Electric-Medical Systems, Horton, Norway).
Images were obtained, with a simultaneous ECG signal, using a 3.5-MHz transducer in the parasternal and apical views. Standard M-mode and 2D-images were acquired during breath hold and saved in cine-loop format from 3 consecutive beats. Analysis of echocardiographic images was performed offline by 2 independent observers using dedicated software (EchoPac version 108.1.5, General Electric-Vingmed).
The LV end-systolic and end-diastolic volumes were assessed, and LV ejection fraction was calculated using the biplane Simpson’s method.13 Thereafter, the LV was divided into 16 segments and each segment was analyzed individually and scored based on its motion and systolic thickening (1=normokinesis, 2=hypokinesis, 3=akinesis, 4=dyskinesis). Wall motion score index was calculated as the sum of the segment scores divided by the number of segments scored.13 Severity of mitral regurgitation was graded semi-quantitatively from the jet area of color-flow Doppler data and by measuring the width of the vena contracta.
Mitral regurgitation was characterized as: mild = jet area/left atrial area <20% and vena contracta width <0.30 cm, moderate = jet area/left atrial area 20% – 40% and vena contracta width 0.30 – 0.69 cm, and severe = jet area/left atrial area >40% and vena contracta width 0.70 cm.14 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.15 LV dyssynchrony was evaluated using speckle- tracking analysis (Figure 1). This software analyses motion by tracking frame-to-frame movement of natural acoustic markers on standard ultrasonic images in two dimensions.16 17 All images were recorded with a frame rate of 40 fps for reliable analysis. To obtain LV dyssynchrony, peak radial strain was assessed on the LV short-axis images at the level of the papillary muscles. The LV endocardial border was manually traced and the
automatically created region of interest was adjusted to the thickness of the myocardium.
Thereafter, the traced endocardium was automatically divided into 6 standard segments (septal, anteroseptal, anterior, lateral, posterior, and inferior). Segments were discarded if tracking was of poor quality. Finally, the software automatically provides the time to peak systolic strain for all 6 segments and LV dyssynchrony was calculated as the time
difference between the earliest and latest activated segments.6 Inter- and intra-observer agreement for LV dyssynchrony assessment was 87%, as previously published.6
Figure 1.
Examples of LV dyssynchrony measurements usual speckle-tracking radial strain analyses. Panel A demonstrates a patient without LV dyssynchrony. Panel B depicts a patient with LV dyssynchrony and a time delay of 200 ms, where the anterior (yellow) segment was the latest activated segments.
The arrows depict the timings of the earliest and latest activated segments.
All patients were followed prospectively and the occurrence of adverse events was noted.
Patients, of whom more than 1 year follow-up data were lacking, were considered as lost to follow-up. Data of these patients were included until the last date of follow-up. All-cause mortality was defined as the primary endpoint. The secondary endpoint was defined as a composite of all-cause mortality and hospitalization for heart failure. Hospitalization for heart failure was defined as hospitalization for new-onset or worsening of heart failure.
Continuous data are presented as mean ± standard deviation and categorical data are presented as frequencies and percentages. Differences in characteristics between patient
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groups were evaluated using the unpaired Student’s t-test and chi-square test. Differences in dyssynchrony between the different groups of LV ejection fraction were compared using the one-way analysis of variance (ANOVA). Post hoc comparisons were performed using the Bonferroni adjustments for multiple comparisons. Event rates were plotted in Kaplan- Meier curves for primary and secondary endpoints, and the study population was divided into patients with and without LV dyssynchrony. Patients with LV dyssynchrony were defined as patients with a time difference of 130 ms between the earliest and latest activated segments. The cut-off value of 130 ms was derived from previous studies, which have demonstrated that a time difference of 130 ms is the optimal cut-off value for the prediction of LV remodeling in patients after AMI, but also for the prediction of response after cardiac resynchronization therapy.6 18 The event rates between patients with and without LV dyssynchrony were compared using the log-rank test. To assess the relationship between LV dyssynchrony and the primary and secondary endpoints, multivariable Cox proportional hazards analysis was performed. Selection of parameters for consideration for entry in the multivariable models was based both on clinical judgment and univariable statistical significance. Based on these considerations, the multivariable models were corrected for age, Killip class 2, diabetes, QRS duration, the left anterior descending coronary artery as culprit vessel, multivessel coronary disease, peak cardiac troponin T level, LV ejection fraction, wall motion score index and E/E’-ratio.
The incremental value of LV dyssynchrony for the prediction of the primary and secondary endpoints was evaluated by comparing the area under the curve (AUC) of receiver-
operating characteristic (ROC) curves. For this purpose 2 models were constructed: model 1 consisted of traditional clinical and echocardiographic risk factors including age, Killip class 2, diabetes, QRS duration, the left anterior descending coronary artery as culprit vessel, peak cardiac troponin T level, LV ejection fraction, and E/E’-ratio; and model 2 consisted of model 1 including LV dyssynchrony. All statistical tests were two-sided, and a P value <0.05 was considered statistically significant.
Results
The baseline clinical and echocardiography characteristics of the patients are summarized in Tables 1 and 2. Mean age of the population was 61 ± 12 years and most patients were
men (747 patients, 77%). The left anterior descending coronary artery was the culprit vessel in 446 patients (46%) and mean peak cardiac enzymes were 2374 ± 3143 U/l and 6.4 ± 6.7 ȝg/l for peak creatine phosphokinase level and peak cardiac troponin T level, respectively.
Baseline echocardiography performed within 48 hours of admission revealed a relatively preserved LV ejection fraction (47 ± 9%) and moderate or severe mitral regurgitation in 65 patients (7%). Strain analysis was feasible in 98% of the segments. Interestingly, mean LV dyssynchrony, as assessed with speckle-tracking analysis, was 61 ± 79 ms. As much as 14% of the patient population (129 patients) demonstrated 130 ms time difference between the earliest and latest activated segments and where defined as patients with significant LV dyssynchrony. Patients with LV dyssynchrony were significantly older (63 ± 12 vs. 60 ± 12 years, p = 0.01) and more likely to present with Killip class 2 (14% vs. 5%, p <0.001) and diabetes (18% vs. 9%, p = 0.002), when compared to patients without LV dyssynchrony. In addition, patients with LV dyssynchrony were more likely to have the left anterior descending coronary artery as culprit vessel (56% vs. 44%, p = 0.01), multivessel coronary disease (64% vs. 46%, p = 0.002), higher peak cardiac troponin T level (9.0 ± 10.1 vs. 5.9 ± 5.5 ȝg/l, p <0.001) and longer QRS duration (99 ± 19 vs. 94 ± 15 ms, p = 0.005). When comparing echocardiographic characteristics between patients with and without dyssynchrony, patients with LV dyssynchrony had lower LV ejection fraction (43 ± 11 vs. 47 ± 9%, p <0.001) and higher wall motion score index (1.6 ± 0.4 vs. 1.5 ± 0.3, p = 0.02). In addition, LV filling pressures estimated with E/E’-ratio were higher (16 ± 11 vs.
13 ± 6, p = 0.02). When dividing the population according to LV ejection fraction (<40%, 40 – 50% and 50%), there were significant differences in the amount of LV dyssynchrony (ANOVA, p <0.001). These differences were more pronounced within the group of patients with an LV ejection fraction <40% (86 ± 90 ms; post-hoc Bonferroni test p <0.001) whereas no differences were observed between patients with a LV ejection fraction of 40 – 50% and 50% (52 ± 76 vs. 54 ± 72 ms).
During a mean follow-up of 40 ± 17 months, 82 patients (8%) reached the primary endpoint defined as all-cause mortality. In addition, 36 patients (4%) were hospitalized for heart failure. The Kaplan-Meier curves for patients with and without LV dyssynchrony who reached the primary and secondary endpoints are shown in Figure 2.
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Table 1. Baseline clinical characteristics
Dyssynchrony (ms) All Patients
(N = 976)
130 (N = 129)
<130
(N = 829) P
Age (years) 61 ± 12 63 ± 12 60 ± 12 0.01
Men 747 (77%) 103 (80%) 631 (76%) 0.35
Killip class 2 63 (7%) 17 (14%) 42 (5%) <0.001
Current smoking 477 (49%) 61 (48%) 412 (50%) 0.66
Diabetes emllitus 102 (11%) 23 (18%) 75 (9%) 0.002
Hypercholesterolemia* 192 (20%) 30 (23%) 161 (19%) 0.29
Hypertension† 310 (32%) 46 (36%) 254 (31%) 0.23
Prior myocardial infarction 76 (8%) 12 (9%) 61 (7%) 0.42
QRS duration (ms) 95 ± 16 99 ± 19 94 ± 15 0.005
LAD culprit artery 446 (46%) 72 (56%) 364 (44%) 0.01 Multivessel disease 477 (49%) 79 (64%) 385 (46%) 0.002
TIMI 2-3flow 954 (98%) 124 (97%) 814 (98%) 0.22
Peak CPK level (U/l) 2374 ± 3143 2985 ± 2773 2255 ± 3153 0.007 Peak cTnT level (ȝg/l) 6.4 ± 6.7 9.0 ± 10.1 5.9 ± 5.5 <0.001 Medication at discharge
ACE inhibitor/ARB 925 (97%) 114 (97%) 798 (97%) 0.83 Antiplatelets 952 (100%) 117 (100%) 822 (100%) 0.69
Beta-blocker 891 (94%) 108 (92%) 771 (94%) 0.54
Statins 942 (99%) 113 (97%) 816 (99%) 0.008
* Total cholesterol 190 mg/dl or previous pharmacological treatment. † Blood pressure 140/90 mmHg or previous pharmacological treatment. 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; TIMI: thrombolysis in myocardial infarction.
Table 2. Baseline echocardiographic characteristics
Dyssynchrony (ms) All Patients
(N = 976)
130 (N = 129)
<130
(N = 829) P LV end-systolic volume (ml) 57 ± 23 64 ± 28 56 ± 21 0.002 LV end-diastolic volume (ml) 106 ± 35 111 ± 39 105 ± 34 0.09 LV ejection fraction (%) 47 ± 9 43 ± 11 47 ± 9 <0.001 Wall motion score index 1.5 ± 0.3 1.6 ± 0.4 1.5 ± 0.3 0.02
E/A-ratio 1.0 ± 0.4 1.0 ± 0.4 1.0 ± 0.4 0.79
Deceleration time (ms) 212 ± 73 206 ± 83 213 ± 72 0.30
E/E’-ratio 14 ± 7 16 ± 11 13 ± 6 0.02
Moderate or severe MR 65 (7%) 12 (9%) 51 (6%) 0.17
LV dyssynchrony (ms) 61 ± 79 224 ± 92 35 ± 33 *
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 atrium; LV: left ventricular;
MR: mitral regurgitation; *: by definition.
At 3 years follow-up, the cumulative survival was significantly lower in patients with LV dyssynchrony as compared to patients without (73% vs. 96%, p <0.001). In addition, during 3 years of follow-up, the frequency of heart failure hospitalizations in the group of patients with LV dyssynchrony was significantly higher as compared to patients without LV dyssynchrony (17% vs. 2%, p <0.001). Finally, the event-free survival for the secondary endpoint at 3 years follow-up was significantly lower in patients with LV dyssynchrony (64% vs. 95%, p <0.001). Univariate Cox regression analysis demonstrated that in addition to known predictors of clinical outcome (LV ejection fraction and E/E’ ratio), LV
dyssynchrony (HR 1.08, 95%CI 1.06 – 1.09, p <0.001 per 10 ms increase) was significantly associated with all-cause mortality after AMI. Of note, patients with LV dyssynchrony demonstrated increased risk of all-cause mortality (HR 7.13, 95%CI 4.53 – 11.23, p
<0.001) compared to patients without significant LV dyssynchrony. In addition, the presence of significant LV dyssynchrony was associated with increased risk of all-cause mortality and hospitalization for heart failure (HR 7.93, 95% CI 5.38 – 11.69, p <0.001).
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Multivariable analysis was performed to evaluate the independent effect of LV dyssynchrony on the primary and secondary endpoint after correcting for known risk factors that predict adverse outcome after AMI. Table 3 shows that LV dyssynchrony remained an independent predictor of the primary endpoint (HR 1.06, 95%CI 1.04 – 1.08, p
<0.001, per 10 ms increase) and secondary endpoint (HR 1.06, 95%CI 1.05 – 1.08, p
<0.001, per 10 ms increase) after correcting for age, Killip class2, diabetes, QRS duration, the left anterior descending coronary artery as culprit vessel, multivessel coronary disease, peak cardiac troponin T level, LV ejection fraction, wall motion score index and E/E’-ratio.
ROC curves were used to assess the incremental predictive value of LV dyssynchrony over traditional clinical and echocardiographic risk factors of adverse outcome. For the primary endpoint, the model with traditional risk factors (age, Killip class 2, diabetes, QRS duration, the left anterior descending coronary artery as culprit vessel, peak cardiac troponin T level, LV ejection fraction and E/E’-ratio) provided a good discrimination of survival with an AUC of 0.80 (95%CI 0.77 – 0.83). The addition of LV dyssynchrony increased the AUC to 0.85 (95%CI 0.82 – 0.87) providing a significantly improved discrimination of the primary endpoint (Figure 3A, p = 0.009 for the comparison of the added value of LV dyssynchrony over traditional clinical and echocardiographic risk factors). For the secondary endpoint, similar results were observed. The addition of LV dyssynchrony to the model with traditional clinical and echocardiographic risk factors significantly increased the area under the curve from 0.78 (95%CI 0.75 – 0.81) to 0.85
Figure 2.
Kaplan Meier curves of time to the primary endpoint (all-cause mortality, panel A) and the secondary endpoint (composite of all-cause mortality and hospitalization for heart failure, panel B) by LV dyssynchrony <130 ms and
130 ms.
(95%CI 0.82 – 0.87), p = 0.001 for the prediction of the composite endpoint of all-cause mortality and hospitalization for heart failure (Figure 3B).
Table 3. Cox multivariable analysis for adverse outcome
Discussion
The main findings of the current study can be summarized as follows: 1) in patients admitted with ST-segment elevation AMI treated with primary PCI, 14% show significant LV dyssynchrony (130 ms) as assessed with speckle-tracking imaging early after the index admission. 2) The presence of LV dyssynchrony was associated with an increased risk of all-cause mortality and hospitalization for heart failure at long-term follow-up. 3)
Primary endpoint Hazard Ratio 95%CI P
Age (per year) 1.05 1.02 – 1.07 0.001
Killip class 2 2.34 1.21 – 4.55 0.01
Peak cardiac troponin T level (ȝg/l) 1.06 1.03 – 1.10 0.001 Left ventricular dyssynchrony (per 10 ms) 1.06 1.04 – 1.08 <0.001 Secondary endpoint
Killip class 2 2.31 1.24 – 4.30 0.008
Peak cardiac troponin T level (ȝg/l) 1.06 1.03 – 1.09 <0.001 Left ventricular ejection fraction (%) 0.97 0.94 – 0.99 0.01 Left ventricular dyssynchrony (per 10 ms) 1.06 1.04 – 1.08 <0.001
Figure 3.
Receiver-operating characteristic curves for the primary endpoint (all-cause mortality, panel A) and secondary endpoint (composite of all-cause mortality and
hospitalization for heart failure, panel B).
* P value comparing the added value of LV dyssynchrony beyond the traditional clinical and echocardiographic risk factors.
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LV dyssynchrony provided incremental value over known clinical and echocardiographic risk factors for the prediction of adverse outcome. Patients with AMI may show significant LV dyssynchrony in an early phase after the index infarction, even in the absence of prolonged ventricular conduction.19 Although dyssynchrony may be present in radial, longitudinal and circumferentional direction, previous studes evaluating the clinical value of speckle-tracking derived dyssynchrony have mostly focused on radial strain. In addition, a recent study showed that only radial strain was able to identify potential responders to cardiac resynchronization therapy.18 The prevalence of LV dyssynchrony after AMI varies in the different published series.5 8 20 For example, Mollema and coworkers demonstrated significant LV dyssynchrony in 18% of patients with AMI treated with PCI.20 LV dyssynchrony was assessed with tissue Doppler imaging and defined as a maximum delay of 65 ms among 4 opposing walls. However, the assessment of LV dyssynchrony with this imaging technique in the setting of AMI may be hampered by the tethering effect of the viable myocardial segments over the scarred segments.21 In contrast, speckle-tracking imaging which evaluates myocardial deformation permits differentiation between segments with active contraction and segments passively tethered.22 Recently, Shin et al. evaluated the prevalence of LV dyssynchrony using speckle-tracking velocity vector imaging in patients after high-risk AMI with LV dysfunction, heart failure, or both.8 The authors used the standard deviation of time to peak velocity as a measure of dyssynchrony and observed that 30% of the population had 65 ms of LV dyssynchrony. In the current study, involving a contemporary population of AMI patients treated with primary PCI, the prevalence of LV dyssynchrony was 14%. LV dyssynchrony was defined as the time difference between the earliest and latest activated LV segments using speckle-tracking radial strain, where the previously defined cut-off value of 130 ms was used.6 18 The clinical importance of LV dyssynchrony after AMI has been mainly investigated in relation to LV remodeling which is a well known surrogate marker of adverse outcome.6 23 Zhang et al. performed sequential echocardiography and contrast-enhanced cardiac magnetic resonance imaging at 2 to 6 days, 3 months and 1 year after AMI.7 The authors confirmed the relation between LV dyssynchrony and LV remodeling. In addition, in patients without LV remodeling a reduction of both infarct size and LV dyssynchrony was observed during follow-up. On the other hand, the study revealed that in patients with LV remodeling, dyssynchrony increased during follow-up, whereas no expansion in infarct size was observed.7 In agreement with
previous findings, the present evaluation also shows that patients with significant LV dyssynchrony had higher peak cardiac troponin T levels and lower LV ejection fraction compared to patients without LV dyssynchrony. More important, patients with LV
dyssynchrony had significantly worse long-term outcome. Survival was significantly lower at 3-years follow-up in patients with LV dyssynchrony (73% vs. 96%, p <0.001) and patients with LV dyssynchrony were more often hospitalized for heart failure (17% vs. 2%
p <0.001). These findings are in agreement with the results of a recent study that investigated the relationship between LV dyssynchrony and adverse outcome in AMI patients.8 Shin and coworkers evaluated high-risk AMI patients with LV dysfunction, heart failure, or both and reported similar results, confirming that LV contraction pattern is strongly related to adverse outcome. In the current evaluation, the relation between LV dyssynchrony and adverse outcome was extended to the contemporary population of patients admitted with an AMI and treated with primary PCI. Echocardiography is a widely available technique and is commonly performed in patients after AMI to assess LV
function. In the current study, novel speckle-tracking echocardiography demonstrated that a significant proportion of patients (14%) admitted with ST-segment elevation AMI treated with primary PCI have significant LV dyssynchrony at the baseline echocardiogram.
Importantly, patients with significant LV dyssynchrony had worse long-term outcome (all- cause mortality and hospitalization for heart failure) as compared to patients without LV dyssynchrony. Moreover, in this growing population of patients, LV dyssynchrony was an independent predictor of adverse outcome and provided incremental prognostic value over known risk factors for the prediction of long-term outcome. Therefore, LV dyssynchrony may be useful in daily clinical practice to improve risk stratification and therapeutic management of post-AMI patients. The indication of device-based therapies, such as cardiac resynchronization therapy for example, in patients with LV dyssynchrony early after AMI needs to be investigated in clinical trials.
Conclusions
LV dyssynchrony is a strong predictor of long-term mortality and hospitalization for heart failure in a population of patients admitted with ST-segment elevation AMI treated with primary percutaneous coronary intervention.
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