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. Author manuscript; available in PMC: 2022 Dec 2.
Published in final edited form as: J Biomech. 2021 Oct 5;129:110794. doi: 10.1016/j.jbiomech.2021.110794

Regional End-Systolic Circumferential Strain Demonstrates Compensatory Segmental Contractile Function in Patients with ST-segment Elevation Myocardial Infarction

Steve W Leung 1, Theresa M Ratajczak 1, Mohamed Abo-Aly 1,2, Elica Shokri 1, Ahmed Abdel-Latif 1, Jonathan F Wenk 3,4,*
PMCID: PMC8671364  NIHMSID: NIHMS1747198  PMID: 34634593

Abstract

Myocardial strain has shown tremendous promise as a potential diagnostic tool for characterizing ventricular function. With regards to myocardial infarction, global circumferential strain (CS) can be used to assess overall function, while regional CS can identify local alterations in contractility. Currently, there is a lack of data related to regional strain in patients with ST-segment elevation myocardial infarction (STEMI). Thus, the goal of this study was to quantify regional strain patterns in STEMI and normal control patients, measuring both peak CS and end-systolic (ES) CS in the mid-ventricular region. This was done by conducting cardiac magnetic resonance (CMR) imaging acutely after STEMI patients underwent primary percutaneous coronary intervention. The CMR datasets were then analyzed using feature-tracking of the cine images. The patients were broken into three groups: (1) control patients (N=18), (2) STEMI patients with ejection fraction (EF) ≥ 50% (N=20), and (3) STEMI patients with EF < 50% (N=20). The key result of the analysis was that ES CS detected a significant increase in the magnitude of strain in the non-infarcted tissue of STEMI patients with EF ≥ 50% when compared to STEMI patients with EF < 50%, whereas peak CS did not detect any differences. This implies that the tissue in this region is contracting more strongly compared to non-infarcted tissue in STEMI patients with EF < 50%. Thus, regional ES CS could potentially be utilized as a diagnostic tool for assessing STEMI patients, by detecting regional changes in contractility after PCI, which could assist in treatment planning.

Keywords: Cardiac Magnetic Resonance, Feature Tracking, Left Ventricle

Introduction

Studies have demonstrated that myocardial strain patterns in the left ventricle (LV), measured using echocardiography or cardiac magnetic resonance (CMR) imaging, are strongly linked to contractile function (Abraham and Nishimura, 2001; Chitiboi and Axel, 2017; Mamidi et al., 2019; Pedrizzetti et al., 2016; Wenk et al., 2011). Using the American Heart Association (AHA) guidelines, the LV can be broken down into 16 segments, which are associated with different branches of the coronary anatomy (Cerqueira et al., 2002). In the case of myocardial infarction (MI), where coronary vessels are blocked, strain can be used to assess reduced contractility in damaged regions of tissue.

The majority of previous studies have focused on the use of global peak strain (i.e., the average of peak strain values from all 16 AHA segments) (Buss et al., 2015; Cha et al., 2019; Nucifora et al., 2018; Wong et al., 2014). Due to the influence of the dysfunctional MI region, the peak value of strain in each myocardial segment may occur at different time points during the cardiac cycle. Thus, global averages of peak strain are based on inconsistent time points. Of the studies that do present regional (also referred to as segmental) strain distributions, most have centered around the regional values in healthy volunteers (Mangion et al., 2019; Mangion et al., 2016; Marcus et al., 1997; Suever et al., 2017; Wu et al., 2014). Thus, there is a lack of data in the literature related to regional end-systolic strain distributions in patients with MI. In addition, prior studies have shown that the regional strain patterns in the mid-ventricle of the LV are the most reproducible, with regards to intra- and interobserver variability (Mangion et al., 2016; Wehner et al., 2018).

Therefore, the goal of the current study was to quantify regional strain patterns in patients with MI, measuring both the peak circumferential strain and end-systolic circumferential strain in the 6 AHA segments of the mid-ventricular region. More specifically, a cohort of patients with a ST-segment elevation myocardial infarction (STEMI) in the inferior region of the LV underwent CMR, as well as a cohort of normal control patients. The STEMI patients were broken into two groups, one with an ejection fraction (EF) ≥ 50% and the other with an EF < 50% (since this typically represents a state of depressed function). The control and STEMI patient CMR datasets were analyzed using feature-tracking, and regional circumferential strain was compared between the three groups. The main hypothesis is that regional end-systolic circumferential strain will be able to detect compensatory segmental contractile function in STEMI patients with an EF ≥ 50%, as compared to patients with an EF < 50%.

Methods

Patient Population

This retrospective study was conducted at a single center. The study consisted of 40 patients with inferior STEMI (N=20 with EF ≥ 50% and N=20 with EF < 50%) enrolled at the University of Kentucky hospital between January 2014 and September 2019. Patients who were hemodynamically unstable with evidence of cardiogenic shock, mechanically intubated, on dual antiplatelet therapy, or received thrombolytics were excluded. CMR was performed within 1–2 days after primary percutaneous coronary intervention (PCI). The control patients (N=18), without history of coronary artery disease, were age and sex matched to the STEMI cohorts. These patients underwent CMR but had normal function, no more than mild valvular disease, and no late gadolinium enhancement. The study protocol complies with the Declaration of Helsinki and was approved by the University of Kentucky Institutional Review Board and Ethics Committees.

CMR Imaging

CMR was performed on a 1.5T MR scanner (Magnetom Aera, Siemens Medical, Erlangen, Germany) with 18-channel body coil and 12-channel spine coil. Patients underwent breath-held steady-state free precession cine imaging in the 2-, 3-, 4-chamber long axis view, and full LV coverage with short axis stack from base to apex (typical parameters: field of view: 380mm × 380mm, matrix: 256 × 256, slice thickness 8mm, interslice gap 2mm, echo time (TE): 1.2ms, repetition time (TR): 3.2ms, flip angle 50°, temporal resolution 50ms, reconstructed into 25 phases).

CMR Image Processing

All CMR analyses were performed by a level-3 trained CMR reader (S.L. and T.R.) on CMR42 v5.6.2 (Circle Cardiovascular Imaging, Inc., Calgary, Canada). The readers were blinded to the clinical data.

Left Ventricular Quantification

Using the CMR42 Short 3D module, LV endocardial borders were drawn on short axis cines in the end-diastolic phase and end-systolic phase. Ejection fraction was calculated based on the end-diastolic volume and end-systolic volume.

CMR Image Feature-Tracking

Feature-tracking was performed on the CMR42 Tissue Tracking module. Endocardial and epicardial borders were manually drawn on all short axis and long axis cines at end-diastole. The mitral valve plane and apex were determined on long axis cines. Anterior and inferior right ventricular insertion points were drawn to determine the AHA segments (Cerqueira et al., 2002). Circumferential strain was calculated at 25 phases during the cardiac cycle. The end-systolic time point was determined during the EF calculation and was used to identify the end-systolic circumferential strain values in each of the 6 AHA segments in the mid-ventricular region (segments 7–12). The peak circumferential strain in each segment was taken to be the largest magnitude of strain (i.e., the absolute value) regardless of time point. A representative example of the circumferential strain vs. time curves are shown for a control patient and a STEMI patient in Figure 1.

Figure 1:

Figure 1:

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Example of circumferential strain vs. time curves measured in (A) control patient and (B) STEMI patient. Each curve represents the strain in AHA segments 7 through 12 of the left ventricle. The solid black dot indicates the peak value of strain in that segment. The vertical lines at ~400ms and ~300ms, respectively, indicate the end-systolic time point where the end-systolic value of strain was measured. The maximum time-to-peak strain delay is shown as a time difference (arrow) between the earliest and the latest segment.

Statistical Analysis

All data are presented as mean ± standard error (SE) or median [Q1, Q3], depending on distribution. Multiple comparisons between the 3 groups (i.e., controls, STEMI patients with EF ≥ 50%, and STEMI patients with EF < 50%) were performed using one-way ANOVA with post-hoc Tukey-Kramer tests. Comparisons of strain were conducted within each of the 6 AHA segments at mid-ventricle. Comparisons of categorical variables were performed with Fischer’s exact test. A value of P < 0.05 was considered significant.

Datasets from ten randomly identified STEMI patients were selected for intraobserver and interobserver variability studies, in which the intraclass correlation coefficient (ICC) was computed with the regional strain, as well as 95% confidence intervals (CI). Bland-Altman analysis was also conducted to assess intraobserver and interobserver variability. The datasets were analyzed by S.L. for intraobserver reproducibility, and by S.L. and T.R. for interobserver reproducibility. Control datasets were not assessed since mid-ventricular strain, computed via feature-tracking, has been shown in previous studies to be reproducible in normal functioning hearts (Mangion et al., 2016; Wehner et al., 2018).

Results

Clinical Characteristics

The patient characteristics of the included patients are shown in Table 1. The groups are similar in age, body mass index, and risk factors for coronary artery disease. Control group has lower percentage of patients who smoked compared to the STEMI patients. The group of STEMI patients with EF < 50% has higher percentage of male patients compared to the group of STEMI patients with EF ≥ 50%. Both STEMI patient groups had similar pain to balloon time, and median days from STEMI to CMR. Ejection fraction was significantly different between the three groups of patients.

Table 1:

Patient Characteristics

Control (N=18) EF ≥ 50% (N=20) EF < 50% (N=20) 1 vs. 2 1 vs. 3 2 vs. 3
Age (years, ± SE) 54.3 ± 2.8 58.5 ± 2.0 55.8 ± 2.0 0.22 0.65 0.35
Male (N, %) 11 (61%) 11 (55%) 18 (90%) 0.75 0.06 0.03*
Body Mass Index (kg/m2, ± SE) 28.1 ± 1.5 29.2 ± 1.4 26.7 ± 1.1 0.60 0.47 0.17
Past Medical History
 Hypertension (N, %) 7 (39%) 8 (40%) 11 (55%) 1.00 0.35 0.53
 Diabetes (N, %) 0 (0%) 4 (20%) 4 (20%) 0.11 0.11 1.00
 Dyslipidemia (N, %) 2 (11%) 6 (30%) 7 (35%) 0.24 0.13 1.00
 Coronary Artery Disease (N, %) 0 (0%) 1 (5%) 3 (15%) 1.00 0.23 0.61
 Myocardial Infarction (N, %) 0 (0%) 1 (5%) 1 (5%) 1.00 1.00 1.00
Tobacco Use
 Never Smoker (N, %) 15 (72%) 5 (25%) 8 (40%) <0.01* 0.06 0.50
 Former Smoker (N, %) 2 (11%) 5 (25%) 3 (15%) 0.41 1.00 0.69
 Current Smoker (N, %) 1 (6%) 10 (50%) 9 (45%) <0.01* <0.01* 1.00
Pain to Balloon (minutes, IQR [1,3]) - 205 [177, 294] 231 [157.5, 367.5] - - 0.14
Days to CMR (days, IQR [1,3]) - 1 [1, 2] 1 [1, 2] - - 0.50
Left Ventricular Ejection Fraction (%, ± SE) 64 ± 0.8 55.2 ± 1.0 42.7 ± 1.3 <0.01* <0.01* <0.01*
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Note: (1) Control patients, (2) STEMI patients with EF ≥ 50%, and (3) STEMI patients with EF < 50%. Values of *P<0.05 were significant.

Regional Strain Distributions

It can be seen in Figure 1A that for the control case, the peak and end-systolic circumferential strain values within a given segment are similar in magnitude and occur in a narrow time range, which is close to end-systole. However, Figure 1B shows that in the case of STEMI, the peak and end-systolic circumferential strain values can be more disparate and occur over a larger range of time. For example, the end-systolic circumferential strain value in segment 9 (inferoseptal tissue) is 4.1%, while the peak circumferential strain value is −9.4% and occurs 140 ms after end-systole. This disparity between peak and end-systolic circumferential strain values and times occurred frequently in the inferior region of the STEMI patient datasets.

To further investigate these timing differences--most likely driven by the damaged myocardium in the MI region (causing akinetic or dyskinetic segments) and the remote tissue that moves inward during systole--the maximum time-to-peak strain delay between the earliest and the latest segment (Figure 1) was calculated for each patient involved in the study (Bauer et al., 2013). There was a significant difference between the delay time for the control patients and the two groups of STEMI patients (control vs. EF ≥ 50; 109.3 ± 7.4 vs. 218.1 ± 15.5 ms; P < 0.001) and (control vs. EF < 50; 109.3 ± 7.4 vs. 225.2 ± 25.3 ms; P < 0.001), respectively. However, there was no statistical difference between the delay times for the STEMI patients with an EF ≥ 50 and those with EF < 50.

Figure 2 shows the peak and end-systolic circumferential strain values for the control patients, STEMI patients with EF ≥ 50%, and STEMI patients with EF < 50%. In segments 9, 10, and 11 (representing the inferoseptal, inferior, and inferolateral tissue, respectively), both the peak and end-systolic circumferential strain were significantly lower in magnitude for all STEMI patients when compared to the control patients. In segment 12 (anterolateral tissue), both the peak and end-systolic circumferential strain were significantly lower in magnitude for the STEMI patients with EF < 50% when compared to the control patients. Most notably, in segments 7, 8, and 12 (representing the anterior, anteroseptal, and anterolateral tissue, respectively), only the end-systolic circumferential strain was significantly higher in magnitude for the STEMI patients with EF ≥ 50% when compared to the STEMI patients with EF < 50%. All other comparisons between the 3 groups in each segment were not significant.

Figure 2:

Figure 2:

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(A) Peak and (B) end-systolic circumferential strain values in AHA segments 7 through 12 of the left ventricle (located at mid-ventricle). Comparisons were made within each segment between control patients (N=18), STEMI patients with EF ≥ 50% (N=20), and STEMI patients with EF < 50% (N=20); *P<0.05 vs. control; †P<0.05 vs. EF < 50%.

Intra- and Interobserver Variability

The ICCs for interobserver variability were 0.91 (95% CI=0.85–0.94) for peak circumferential strain and 0.94 (95% CI=0.91–0.97) for end-systolic circumferential strain. The ICCs for intraobserver variability were 0.96 (95% CI=0.94–0.98) for peak circumferential strain and 0.97 (95% CI=0.96–0.98) for end-systolic circumferential strain. The results of the Bland-Altman analysis are shown in Table 2 and Figure 3. Overall, the interobserver and intraobserver variabilities were similar between peak and end-systolic circumferential strain.

Table 2:

Bland-Altman results for interobserver and intraobserver reproducibility of regional circumferential strain.

Parameter Mean difference ± SD Limits of agreement
Interobserver Peak circumferential strain −0.70 ± 3.20 −6.97 to 5.57
End-systolic circumferential strain −0.63 ± 3.07 −6.65 to 5.40
Intraobserver Peak circumferential strain 0.32 ± 2.67 −4.92 to 5.55
End-systolic circumferential strain 0.21 ± 2.57 −4.81 to 5.24
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Figure 3:

Figure 3:

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Bland-Altman plots with limits of agreement (1.96 standard deviations) demonstrate the interobserver and intraobserver reproducibility of regional circumferential strain. The middle-dashed line is the mean of the difference between measurements. The upper and lower dotted lines are ±1.96 standard deviation (SD).

Discussion

In the current study, regional circumferential strain was assessed using CMR feature-tracking in control and STEMI patients with an inferior infarct. The key result of the analysis was that end-systolic circumferential strain detected a significant difference between the non-infarcted tissue in STEMI patients with EF ≥ 50% when compared to the STEMI patients with EF < 50%, whereas peak circumferential strain did not detect any differences. More specifically, the magnitude of end-systolic circumferential strain was significantly higher in the STEMI patients with EF ≥ 50%, which implies that the tissue in this region is contracting more strongly compared to the non-infarcted tissue in STEMI patients with EF < 50%. The fact that this compensatory mechanism was only detected when using end-systolic circumferential strain could be related to the fact that the EF and end-systolic circumferential strain use information that is collected at the same time points. Namely, EF measures the ratio of blood ejected between end-diastole and end-systole, and end-systolic circumferential strain measures the amount of wall deformation between end-diastole and end-systole. Since peak circumferential strain occurs at different time points in the presence of MI, it is less representative of systolic function.

As demonstrated in previous studies, the current study showed a significant reduction in contractile function in the inferior infarct region compared to normal controls (Dobrovie et al., 2019; Gavara et al., 2018; Khan et al., 2015; Marcus et al., 1997). Additionally, the STEMI patient datasets were found to be reproducible, which is in agreement with prior studies that focused on mid-ventricular strain in healthy volunteers (Mangion et al., 2016), as well as the few studies that looked at regional strain in diseased and healthy hearts (Wehner et al., 2018). The current study utilized cardiac CMR data that was acquired with cine images as part of standard care and analyzed using feature-tracking to assess regional strain. Other studies have evaluated the efficacy of using tagged CMR and displacement encoding with stimulated echoes (DENSE) CMR to assess strain (Kihlberg et al., 2015; Mangion et al., 2016; Marcus et al., 1997; Suever et al., 2017; Wong et al., 2014). While these studies have yielded good results, one disadvantage of these imaging sequences is that they require the patient to remain in the scanner for additional time. Thus, feature-tracking of cine images collected as part of the standard of care is less burdensome to the patient.

Limitations

Limitations of this study include the retrospective design and sample size. However, the patient cohort was representative of the typical STEMI population in terms of comorbidities. Another limitation is that the study did not have long-term follow-up data to evaluate cardiovascular outcomes. Finally, this study was conducted at a single center and more work is needed to further investigate this approach.

Conclusion

Regional end-systolic circumferential strain could be used as a means of detecting regional changes in contractility after PCI. This could potentially be utilized as a diagnostic tool for assessing STEMI patients and assist in treatment planning by identifying which patients have reduced function in both the infarcted and remote regions of their LV. This could also be helpful in determining which patients are at high risk of persistently low EF and thus higher risk of sudden cardiac death, and provide a means of informing clinicians about which patients may require closer monitoring post-PCI, in terms of pharmaceutical treatment or the need for an implantable or wearable cardioverter defibrillator.

Acknowledgments

This research was supported by National Institutes of Health grants U01 HL133359 (J.W.) and R01 HL124266 (A.A-L.).

Footnotes

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Conflict of Interest Statement

None of the authors have any commercial or other interest that are in conflict with the integrity of this work.

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