The aim of this study was to investigate the changes and time course of recovery of regional myocardial function within the first week following successful primary coronary intervention in patients with first-time ST-segment elevation myocardial infarctions using myocardial deformation analysis, which is more quantitative and thus more objective than the wall motion score.
Thirty-one consecutive patients admitted with ST-segment elevation myocardial infarctions were studied on days 1, 2, 3, and 7 using strain and strain rate tissue Doppler echocardiography.
The mean peak troponin T level was 7.0 μg/L, and 15 patients had anterior and 16 had inferior infarct localization. Peak systolic strain rate and end-systolic strain increased significantly on day 2, both in segments with moderately reduced function (−0.6 to −1.0 s −1 vs −8% to −15%, P < .001) and in severely reduced function (−0.2 to −1.0 s −1 vs 1% to −12%, P < .001), but there were no further changes. Mean wall motion score in infarct related segments decreased significantly from day 1 to day 2 (2.7 to 2.4, P = .001) and from day 3 to day 7 (2.3 to 2.2, P = .001).
Recovery of regional function after ST-segment elevation myocardial infarction occurred within 2 days and could be detected by wall motion score, strain rate, and strain. However, strain and strain rate were better discriminative parameters for the changes in function as well as being better to assess near normalization on day 2. This could have a clinical impact on early management in patients who undergo percutaneous coronary intervention.
Primary angioplasty for ST-segment elevation myocardial infarction (STEMI) is recommended if symptom duration is <12 hours. However, substantial myocardial salvage can be obtained beyond the 12-hour limit even when the infarct-related artery (IRA) is totally occluded, but with a larger final infarct size. Spontaneous reperfusion before treatment occurs in 7% to 27% of the patients with STEMIs and is associated with a decreased infarct size and an improved prognosis. Percutaneous coronary intervention (PCI) ensures better long-term outcomes than thrombolysis, with reduced mortality. Regional myocardial deformation can be quantified by strain and strain rate (SR) using B-mode or tissue Doppler imaging and can assess regional myocardial dysfunction due to ischemia. In the acute setting, the assessment of global and regional left ventricular function is complicated by myocardial stunning, and as a consequence, final infarct size is hard to predict at this stage. However, recent studies have found global strain to correlate well with myocardial infarct mass quantified by contrast-enhanced magnetic resonance imaging in the early and late stages. Strain has also been shown to be a good predictor of left ventricular remodeling in infarcted patients who undergo primary PCI. Time series of the recovery of regional function after acute myocardial infarction (AMI) can be achieved using magnetic resonance imaging, single photon-emission computed tomography, and echocardiography (wall motion score [WMS] index [WMSI]). We have earlier shown the improvement of strain and SR to occur during the first week after AMI, indicating recovery of stunned myocardium. The patients were examined at 1 and 7 days and at 3 months. In patients with STEMIs examined 3 days after PCI, Weidemann et al found that peak systolic SR (SR s ) increased significantly only in the regions that were not transmurally infarcted. On the basis of these findings, we investigated the change in deformation on a segmental basis during the first 3 days after AMI compared to after 1 week.
Thirty-one consecutive patients with first-time AMIs admitted to the coronary care department at St Olav’s Hospital were asked to participate. The inclusion criteria were first-time STEMI regardless of initial treatment (on the basis of electrocardiographic findings or the biochemical markers troponin T and creatine kinase-MB), visually recognized regional dyssynergy on echocardiography, clinical and hemodynamic stability, and age > 18 years. Exclusion criteria were previous AMI, atrial flutter, atrioventricular block, left bundle branch block, and known cardiomyopathy. No patients were excluded because of poor image quality. The study was approved by the regional ethics committee, and all patients gave written consent.
Echocardiographic Data Acquisition
Complete echocardiographic examinations, including B-mode parasternal long-axis and short-axis views and apical views for Doppler studies, were performed using a Vivid 7 scanner (GE Vingmed Ultrasound AS, Horten, Norway) with a phased-array transducer. Three cine loops from the 3 standard apical planes (4-chamber, 2-chamber, and long-axis) were recorded in harmonic B-mode and color tissue Doppler mode simultaneously and separately. The loop with the best quality was chosen for analysis. The mean frame rates were 157 frames/s (range, 114-183 frames/s) for tissue Doppler imaging and 93 frames/s (range, 44-119 frames/s) for B-mode imaging. The pulse repetition frequency was 1000 Hz.
The digitally stored recordings were analyzed offline using EchoPAC software (GE Vingmed Ultrasound AS). Wall motion was visually assessed by an experienced observer according to the American Society of Echocardiography’s 16-segment model and rated 1 to 4 (1 = normal, 2 = hypokinesia, 3 = akinesia, 4 = dyskinesia). Normal segments and segments with reduced function identified by WMS were analyzed on days 1, 2, 3, and ≥7. The WMSI was calculated in each patient as the average WMS of segments studied in that patient.
For automated analysis of myocardial deformation, a customized postprocessing system was used (GcMat; GE Vingmed Ultrasound AS) that runs under MATLAB (The MathWorks Inc, Natick, MA). Three segments in each wall were delineated automatically. Tracking of segment borders was done axially (along the ultrasound beam) by tissue Doppler data and laterally by speckle tracking. Speckle tracking was used only for tracking, not in the analysis of strain and SR. A region of interest for measuring SR was placed in the middle of the segment, and the region of interest followed the segment tracking automatically (dynamic velocity gradient method ). Eulerian SR was calculated from the velocity gradient along the ultrasound beam, and strain was calculated as the temporal integral of SR, with correction to Lagrangian strain. The strain length was 10 to 15 mm, and temporal averaging was 25 ms. The timing of aortic valve opening and closure was automatically defined by an algorithm using tissue Doppler imaging of the mitral annulus.
Tissue Doppler imaging measurements included SR s , determined as the maximal negative SR value during ejection time, and end-systolic strain (S es ), determined as the magnitude of strain at aortic valve closure. Postsystolic strain and SR were defined as the peak negative values after aortic valve closure. Measurements were made in 18 segments from 3 apical views automatically, but only 16 were used for both SR index and WMS by deleting the apical segments of the apical long-axis view. Global SR and strain were calculated as the mean values of all 16 segments.
Tissue Doppler velocities were based on color Doppler images and were measured at the 4 mitral annular sites in the 4-chamber and 2-chamber views, and the mean of these points was used for peak systolic (S′), and peak early diastolic (E′) velocities. Mitral annular excursion (MAE) was measured as displacement from the same sites as tissue Doppler velocities. The ratio of mitral inflow E velocity to tissue Doppler e′ (E/e′), plays an important role in estimating filling pressure, and a value > 15 is a criterion for elevated left atrial pressure. However, E/e′ has limitations, being dependent on age, and recent studies have shown a poor correlation between filling pressure and E/e′ in patients with critical illnesses and noncardiac illnesses. Ejection fraction (EF) was calculated from the 4-chamber and 2-chamber views using the modified Simpson’s method.
The reproducibility of the customized echocardiographic software was investigated in an earlier study of 30 patients with myocardial infarctions and 30 normal subjects, showing a coefficient of variability for intraobserver variability of 16% and for interobserver variability of 17% as well as in a study including 10 healthy subjects.
Definition of Reduced Function
A WMS value > 1 was defined as indicating a dysfunctional segment. For tissue Doppler, a segment with severely reduced function was defined as SR ≥ −0.5 s −1 and S es ≥ −5%, and a segment with moderately reduced function was defined as an SR of −0.5 to −0.75 s −1 and an S es between −5% and −10%. In addition, the segments were defined according to the IRA, per the recommendations of the American Heart Association. If the IRA defined on coronary angiography was the left anterior descending coronary artery, the following segments were defined as infarct-related segments; apical and mid septal; apical, mid, and basal anterior; apical inferior; and mid and basal anterior segments. For the right coronary artery the basal and mid inferior and basal septal segments were defined as infarct related, and for the circumflex coronary artery, the basal and mid lateral and basal and mid inferolateral segments were defined as infarct related. The non-infarct-related segments were defined as normal.
Coronary angiography was performed using standard techniques, and all patients underwent coronary angiography and PCI. The angiograms were evaluated by experienced observers. Stenosis severity was measured by either eyeballing or quantitative coronary angiography, using an automated edge detection system (Philips Medical Systems, Eindhoven, the Netherlands). A maximal luminal diameter stenosis of >50% in any plane was classified as significant. Segmental disease was evaluated using the previously described 15-segment American Heart Association model of the coronary tree to ensure that only stenoses in major epicardial vessels were assessed. A culprit lesion was defined for each patient. Spontaneous reperfusion was defined as coronary angiography showing Thrombolysis In Myocardial Infarction (TIMI) flow grade ≥ 2 before PCI, in a combination with decrease in pain and a decrease of ST-segment elevation on electrocardiography.
Continuous variables are presented as mean ± SD. Ranges are used instead of standard deviations for frame rates. To compare two samples, either paired-samples t tests or independent-samples t tests were used. Time series were analyzed by repeated measurements of analysis of variance, with post hoc analysis by Bonferroni’s correction for multiple pairwise corrections. A P value < .05 was considered statistically significant. Spearman’s rank correlation was used for regression coefficients. SPSS version 15 (SPSS, Inc, Chicago, IL) was used for analyis.
All patients were treated using PCI. Patient characteristics are listed in Table 1 . Anterior STEMIs were found in 15 patients and inferior STEMIs in 16. The culprit lesion was located in the left anterior descending coronary artery in 15 patients, in the right coronary artery in 9 patients, and in the circumflex coronary artery in 7 patients. Single-vessel disease was found in 19 patients and multivessel disease in 12 patients. Wall motion on day 1 was scored as 1 in 320 segments (57.5%), 2 in 78 segments (14%), 3 in 155 segments (28%), and 4 in 3 segments (0.5%). In total, 209 segments were defined as infarct-related segments.
|Age (y)||56 ± 13|
|Systolic blood pressure (mm Hg)||134 ± 29|
|Diastolic blood pressure (mm Hg)||81 ± 18|
|Heart rate (beats/min)||74 ± 11|
|Peak troponin T (μg/L)||7 ± 5|
|Thrombolytic therapy and primary angioplasty||18|
|IRA patent after treatment||30|
|IRA patent before treatment||9|
|Time to primary angioplasty (h)||15.9 (5-24)|
|Angiotensin II receptor antagonists||4|
|Angiotensin-converting enzyme inhibitors||1|
In total, 2232 segments were analyzed. Feasibility was 85 % for SR s , 83% for S es , and 98% for WMS. Segments were excluded because of angle deviation > 25°, reverberations, poor tracking, and poor image quality with dropouts.
The global indices of MAE, S′, strain, and SR improved significantly from day 1 to 2 but not from day 2 to 7 ( Table 2 ). EF increased significantly from day 1 to 3 ( P = .039). Regional function by strain and SR improved significantly from day 1 to 2 in the segments with severely reduced function as well as in the segments with moderately reduced function, whereas no significant improvement was seen after day 2 ( Table 3 ). WMSI decreased from day 3 to 7, and mean WMS in infarct-related segments decreased from day 1 to 2 and from day 3 to 7 ( Table 3 ).
|Global value||Day 1||Day 2||Day 3||Day 7||Day 1-2||Day 2-3||Day 3-7||Day 1-7||Day 2-7|
|WMSI||1.65 ± 0.22||1.56 ± 0.26||1.54 ± 0.26||1.48 ± 0.25||.25||1||.01||.007||.006|
|EF (%)||51.9 ± 7.3||53.3 ± 7.8||55.5 ± 8.9||56.5 ± 8.8||.84||.34||1||.007||.03|
|MAE (mm)||9.6 ± 2.1||10.7 ± 1.9||10.7 ± 2.3||11.9 ± 2.3||.004||1||.11||<.001||.14|
|Global SR (s −1 )||−1.03 ± 0.22||−1.14 ± 0.19||−1.19 ± 0.16||−1.19 ± 0.14||.03||.88||1||.009||1|
|Global strain (%)||−11.8 ± 4.0||−13.7 ± 2.9||−15.2 ± 3.4||−15.7 ± 2.8||.009||.06||1||<.001||.005|
|S′ (cm/s)||5.4 ± 0.2||6.1 ± 0.3||6.3 ± 0.3||6.4 ± 0.2||.046||1||1||.004||1|
|E′ (cm/s)||−5.3 ± 1.7||−6.1 ± 1.7||−6.3 ± 1.5||−6.6 ± 1.7||.001||.38||.81||<.001||1|
|Segmental value||Day 1||Day 2||Day 3||Day 7||Day1-2||Day 2-3||Day 3-7||Day 1-7||Day 2-7|
|WMS in infarct-related segments with WMS > 1||2.71 ± 0.4||2.42 ± 0.7||2.35 ± 0.7||2.16 ± 0.7||<.001||.19||<.001||<.001||<.001|
|Segments with severely reduced function (peak systolic SR > −0.5 s −1 in infarct-related segments)|
|Peak systolic SR (s −1 )||−0.24 ± 0.2||−0.97 ± 0.5||−1.1 ± 0.4||−1.2 ± 0.4||<.001||.76||1.00||<.001||.12|
|SR e (s −1 )||1.16 ± 0.6||1.45 ± 0.6||1.49 ± 0.6||1.84 ± 0.7||.5||1.00||1.00||.039||.89|
|SR a (s −1 )||0.91 ± 0.6||1.0 ± 0.6||1.31 ± 0.6||1.47 ± 0.6||1.00||1.00||1.00||.05||.30|
|Postsystolic SR (s −1 )||−1.05 ± 0.4||−0.63 ± 0.4||−0.50 ± 0.3||−0.20± 0.2||<.001||.10||<.001||<.001||<.001|
|S es (%)||−1.4 ± 1.7||−11.6 ± 5.5||−13.9 ± 5.8||−14.7± 6.5||<.001||.12||1.00||<.001||.81|
|Postsystolic strain (%)||−14.6 ± 8.7||−11.7 ± 5.6||−9.1 ± 4.5||−4.5 ± 4.5||.001||.18||<.001||<.001||<.001|
|PSI||0.85 ± 0.2||0.26 ± 0.2||0.11 ± 0.2||0.09 ± 0.2||<.001||.25||1.00||<.001||1.00|
|Segments with moderately reduced function (peak systolic SR, −0.5 to −0.75 s −1 in infarct-related segments)|
|Peak systolic SR (s −1 )||−0.6 ± 0.06||−1.0 ± 0.3||−1.0 ± 0.4||−1.08± 0.4||.001||1.00||1.00||<.001||1.00|
|SR e (s −1 )||1.41 ± 0.6||1.67 ± 0.6||2.02 ± 0.7||2.20 ± 0.7||1.00||1.00||1.00||.042||1.00|
|SR a (s −1 )||1.04 ± 0.6||1.07 ± 0.6||1.05 ± 0.5||1.06 ± 0.5||1.00||1.00||1.00||1.00||1.00|
|Postsystolic SR (s −1 )||−1.2 ± 0.6||−0.79 ± 0.6||−0.49 ± 0.3||−0.22± 0.2||.004||.28||.045||.001||.10|
|S es (%)||−7.7 ± 1.1||−14.7 ± 4.1||−15.2 ± 4.5||−15.1± 1.1||<.001||.95||1.00||<.001||.38|
|Postsystolic strain (%)||−15.6 ± 7.0||−15.9 ± 5.5||−12.8 ± 5.8||−8.7 ± 5.5||.37||.02||.001||.001||.001|
|PSI||0.51 ± 0.2||0.14 ± 0.1||0.10 ± 0.1||0.02± 0.03||<.001||1.00||.17||<.001||.009|
|Segments with normal function|
|Mean WMS||1.14 ± 0.4||1.15 ± 0.4||1.16 ± 0.4||1.15 ± 0.4||1.00||1.00||1.00||1.00||1.00|
|Peak systolic SR (s −1 )||−1.26 ± 0.3||−1.25 ± 0.3||−1.21 ± 0.3||−1.22± 0.3||1.00||1.00||1.00||1.00||1.00|
|SR e (s −1 )||1.81 ± 0.6||1.83 ± 0.6||1.80 ± 0.5||1.87 ± 0.6||1.00||1.00||1.00||1.00||1.00|
|SR a (s −1 )||1.44 ± 0.6||1.40 ± 0.6||1.39 ± 0.6||1.38 ± 0.5||1.00||1.00||1.00||1.00||1.00|
|Postsystolic SR (s −1 )||−0.28 ± 0.2||−0.24 ± 0.2||−0.23 ± 0.2||−0.20± 0.1||1.00||1.00||1.00||1.00||1.00|
|S es (%)||−16.1 ± 6.7||−15.9 ± 6.5||−15.8 ± 6.5||−16.1± 6.4||1.00||1.00||1.00||1.00||1.00|
|Postsystolic strain (%)||−7.3 ± 5.1||−5.6 ± 4.5||−4.9 ± 5.1||−4.6 ± 2.1||.005||.59||1.00||.001||.65|
|PSI||0.11 ± 0.2||0.06 ± 0.1||0.05 ± 0.1||0.05 ± 0.1||.02||1.00||1.00||1.00||.01|