- Research article
- Open Access
- Open Peer Review
Regional wall function before and after acute myocardial infarction; an experimental study in pigs
© Pahlm et al.; licensee BioMed Central Ltd. 2014
- Received: 23 March 2014
- Accepted: 9 September 2014
- Published: 13 September 2014
Left ventricular function is altered during and after AMI. Regional function can be determined by cardiac magnetic resonance (CMR) wall thickening, and velocity encoded (VE) strain analysis. The aims of this study were to investigate how regional myocardial wall function, assessed by CMR VE-strain and regional wall thickening, changes after acute myocardial infarction, and to determine if we could differentiate between ischemic, adjacent and remote segments of the left ventricle.
Ten pigs underwent baseline CMR study for assessment of wall thickening and VE-strain. Ischemia was then induced for 40-minutes by intracoronary balloon inflation in the left anterior descending coronary artery. During occlusion, 99mTc tetrofosmin was administered intravenously and myocardial perfusion SPECT (MPS) was performed for determination of the ischemic area, followed by a second CMR study. Based on ischemia seen on MPS, the 17 AHA segments of the left ventricle was divided into 3 different categories (ischemic, adjacent and remote). Regional wall function measured by wall thickening and VE-strain analysis was determined before and after ischemia.
Mean wall thickening decreased significantly in the ischemic (from 2.7 mm to 0.65 mm, p < 0.001) and adjacent segments (from 2.4 to 1.5 mm p < 0.001). In remote segments, wall thickening increased significantly (from 2.4 mm to 2.8 mm, p < 0.01). In ischemic and adjacent segments, both radial and longitudinal strain was significantly decreased after ischemia (p < 0.001). In remote segments there was a significant increase in radial strain (p = 0.002) while there was no difference in longitudinal strain (p = 0.69). ROC analysis was performed to determine thresholds distinguishing between the different regions. Sensitivity for determining ischemic segments ranged from 70-80%, and specificity from 72%-77%. There was a 9% increase in left ventricular mass after ischemia.
Differentiation thresholds for wall thickening and VE-strain could be established to distinguish between ischemic, adjacent and remote segments but will, have limited applicability due to low sensitivity and specificity. There is a slight increase in radial strain in remote segments after ischemia. Edema was present mainly in the ischemic region but also in the combined adjacent and remote segments.
- Cardiac Magnetic Resonance
- Acute Myocardial Infarction
- Late Gadolinium Enhancement
- Longitudinal Strain
- Radial Strain
Acute myocardial infarction (AMI) is a major cause of death worldwide despite diagnostic and therapeutic improvements . Mortality is especially high in patients with AMI and out of hospital cardiac arrest.
Regional left ventricular function is altered during and after AMI. This includes changes in the infarcted and ischemic regions as well as stunning in adjacent and remote areas of the myocardium [2–6]. Most studies describe changes in the infarcted myocardium while there is less information about changes in remote myocardium. It is still somewhat controversial whether remote myocardium after AMI is hypo-functioning  or hyper-functioning . This has not been well studied in the hyper acute setting.
Cardiac magnetic resonance (CMR) is a comprehensive diagnostic tool that can provide accurate and reproducible measurements of cardiac volumes , dimensions , regional cardiac function [9, 10] and infarct size [11, 12]. It has emerged as the gold standard for assessing systolic wall thickening . Studies have shown that regional wall function can be assessed using CMR strain analysis [13, 14]. Strain is a measure of the change in size and shape of an object and can be derived from CMR by using grid-tagging , displacement encoding with stimulated echoes (DENSE)  or velocity-encoded (VE) imaging [14, 17].
Myocardial function in patients with AMI reaching the hospital has been well studied [5, 6, 18]. Without knowledge of the pre-AMI function it precludes a detailed quantitative analysis of absolute and relative changes in function. The function in the superacute stage (hours) of infarction and in those suffering out of hospital cardiac death is also unknown.
Therefore, the aim of this study was to investigate how regional myocardial wall function, assessed by CMR velocity encoded strain and regional wall thickening, changes after acute myocardial infarction. In order to quantify absolute and relative regional changes we used an experimental pig model with induced ischemia and reperfusion using each animal as its own control. We also aimed to find out if we could differentiate between ischemic, adjacent and remote myocardium as determined by myocardial perfusion MPS by looking at regional myocardial function.
The study conforms to the Guide for the Care and Use of Laboratory Animals, US National Institute of Health (NIH Publication No. 85–23, revised 1996) and was approved by the Ethics Committee of Lund University, Sweden.
Ten domestic pigs weighing 40–50 kg were fasted overnight with free access to water and all were premedicated with 2 mg/kg azaperone (Stresnil; Leo, Helsingborg, Sweden) administered intramuscularly 30 minutes before the procedure. Induction of anesthesia was performed with 5–25 mg/kg of thiopental (Pentothal; Abbott, Stockholm, Sweden). Administration of the anaesthetic was complemented with intermittent doses of meprobamat (Mebumal; DAK, Copenhagen, Denmark) and thiopental, if needed. Prior to inducing ischemia all pigs underwent a baseline CMR for assessment of wall thickening and velocity encoded strain. Ischemia was induced with inflation of an angioplasty balloon in the left anterior descending coronary artery distal to the first diagonal branch for 40 minutes. An angiogram was performed after inflation of the balloon and before deflation of the balloon in order to verify total occlusion of the coronary vessel and correct balloon positioning. After deflation of the balloon, a second angiogram was performed to verify restoration of blood flow in the previously occluded artery. During occlusion of the artery, 99mTc tetrofosmin was administered intravenously prior to reperfusion and MPS was performed 2–3 hours after occlusion for determination of the area subjected to ischemia. A second CMR examination was performed approximately 3–4 hours after reperfusion. After the second CMR examination the animals were euthanized.
CMR imaging and analysis
Magnetic resonance imaging was performed on a Philips Intera CV 1.5 T (Philips, Best, the Netherlands) with a five element cardiac synergy coil before and after ischemia. All pigs were placed in supine position and scout images in the three orthogonal planes were acquired as guidance for determination of the standard imaging planes.
For assessment of regional wall thickening steady state free precession (SSFP) cine images were acquired in the short-axis plane covering the entire left ventricle from base to apex. Images were also acquired in the 2, 3 and 4 chamber imaging planes. Image parameters were: repetition time 3.2 ms, echo time 1.6 ms, flip angle 60°, image resolution 1.36 × 1.36, slice thickness 8 mm, retrospective ECG gated reconstruction.
From the short-axis cine images systolic wall thickness, wall thickening, and fractional wall thickening (defined as wall thickening divided by end diastolic wall thickness) were assessed before and after ischemia by manual tracing of the endocardial and epicardial borders. The left ventricle was divided in the American Heart Association 17 segment model. Papillary muscles were excluded from the myocardium. The most basal slice included in the analysis was the most basal short-axis slice containing myocardium in 360° of the left ventricular myocardial circumference in end-systole.
All 2D in-plane velocity encoded data was acquired in the 2, 3 and 4 chamber imaging planes. Imaging parameters were: repetition time 23.4 ms echo time 4.6 ms, velocity encoding gradient 20 cm/s, flip angle 15°. Image resolution was typically 1.6 × 1.6 mm, and slice thickness 7 mm with 18–22 time frames per cardiac cycle, retrospective ECG gating.
Late gadolinium enhancement (LGE)
An extracellular contrast agent (gadopentetate dimeglumine, Bayer Pharma, Berlin, Germany) was administered intravenously at 0.2 mmol/kg 15 minutes before late gadolinium enhancement (LGE) images were acquired. Standard clinical imaging parameters were used for LGE imaging covering the left ventricle from base to apex by using an inversion-recovery gradient-echo sequence (slice thickness, 8 mm; field of view, 340 mm; repetition time, 3.14 ms; echo time, 1.58 ms), with manually adjustment of the inversion time to null the signal from viable myocardium.
The area of hyperenhancement was defined on the LGE short-axis images and was quantified using a previously described and validated semi-automatic algorithm  incorporating manual adjustments. Finally, all LGE data was transformed into polar plots according to a 17 segment model .
MPS imaging and analysis
Five hundred MBq of 99mTc tetrofosmin (Amersham Health, Buckinghamshire, UK) was administered intravenously ten minutes before deflation of the angioplasty balloon. The pigs were then imaged in a supine position using a dual head camera (ADAC Vertex, Milpitas, CA, USA) at 32 projections (40s per projection) with a 64 x 64 matrix yielding a digital resolution of 5 x 5 x 5 mm. Short- and long-axis images, covering the left ventricle, gated to ECG, were then reconstructed.
For MPS analysis, automatic segmentation of the LV was performed . In short, the automatic segmentation finds the centerline through the LV wall and identifies the endocardium and epicardium based on an individually estimated wall thickness and signal intensity values within the image. Following delineation, the ischemic area was assessed in contiguous short-axis slices from base to apex using a method for semi-automatic quantification . All myocardium below a threshold of 50 percent of the maximum counts was considered ischemic and expressed as a percentage of the LV volume. Manual adjustment of the automatic delineation was sometimes required in the LV outflow region. Finally, the MPS delineations with ischemia were transformed into colour coded blacked-out polar plots.
Definition of left ventricular areas: ischemic, adjacent and remote myocardium
Wilcoxon Sign Rank test was used to assess changes in volumes, ejection fraction, cardiac output and heart rate. For changes in regional CMR wall thickening and VE strain we used a paired t-test. For all analysis, a p-value below 0.05 was considered significant. Values are expressed as mean ± SEM. To find thresholds to be able to discriminate between ischemic, adjacent and remote areas ROC analysis was performed. The ROC analysis was performed by evaluating sensitivity and specificity for different thresholds of wall thickening, radial strain, and longitudinal strain, respectively. The thresholds was tested in 1000 steps from minimum value to maximum value for each parameter.
Heart rate, cardiac volumes, ejection fraction (EF) and cardiac output (CO) before and after ischemia
Heart rate [bpm]
81 ± 21
113 ± 30
Left ventricular mass [ml]
86 ± 7
94 ± 15
End diastolic volume [ml]
82 ± 11
71 ± 10
End systolic volume [ml]
47 ± 7
48 ± 9
Stroke volume [ml]
36 ± 8
23 ± 5
Ejection fraction [%]
44 ± 7
32 ± 6
Cardiac output [l/min]
2.8 ± 0.7
2.6 ± 0.8
There was a significant increase in left ventricular mass from 86 ± 7 ml to 94 ± 15, an increase in 9% (p = 0.01) after ischemia. The increase in mass was not homogenous, and the increase in ischemic areas was 38% ± 3% (mean ± SEM) (p < 0.01), adjacent was 4% ± 2% (mean ± SEM) (p = ns), and in remote areas the increase was 7% ± 3% (mean ± SEM) (p = ns). When combining the results from remote and adjacent areas there was an increase in mass of 6% ±2% (p = ns).
Thresholds for wall thickening, radial strain and longitudinal strain determined by ROC analysis for differentiations between ischemic, adjacent and remote areas
Wall thickening ischemic
< 1.4 mm
Wall thickening adjacent
1.4 - 2.1 mm
Wall thickening remote
Radial strain ischemic
Radial strain adjacent
Radial strain remote
Long. strain ischemic
Long. strain adjacent
−0.04 - -0.07
Long. strain remote
In this study we found that there is a significant decrease in regional wall function in the ischemic and adjacent segments of the left ventricle measured by CMR wall thickening and VE-strain after induced myocardial infarction. There is a slight increase in regional wall function seen by wall thickening and VE radial strain in remote myocardium. The non-significant increase in longitudinal strain seen in the remote myocardium was likely attributed to the limited number of subjects.
The decreased function in the ischemic region is well known and has obvious causes.
The reduced regional function in adjacent areas have been described previously  and represents myocardial stunning as described by Braunwald et al. [3, 4]. This prolonged dysfunction remain present for hours, days or even a few weeks after ischemia and may be explained by the presence of edema . Similar results were demonstrated by Engblom et al. in a human population . The significant decrease in EDV in conjunction with unaffected ESV after ischemia suggests diastolic dysfunction as a result of the ischemia. The decreased regional function in ischemic regions indicates regional systolic dysfunction.
In this study we found that there was a slight, but statistically significant, increase in regional myocardial function in remote areas measured both by wall thickness and radial strain. There was, however, no change in function seen by longitudinal strain. Increased function in remote areas has been described previously [6, 7, 28] but most other studies have found a decreased function in both animals [29, 30] and humans [6, 27, 31, 32]. Reasons for the lack of consensus between studies are unknown but may be related to duration of ischemia, reperfusion and timing of imaging. An advantage of our study is the analysis of strain and wall thickening measurements in the same animal both prior to and after infarction. The presented method for measuring regional left ventricular function in ischemic, adjacent and remote areas may be used in controlled experimental settings to investigate the effect of cardioprotective treatments, such as cooling .
In a direct comparison between strain tagging and wall thickening, a previous study by Götte et al.  using CMR has shown that the former was more accurate in discriminating infarcted from remote myocardium. In our study, however, we found that wall thickening and radial VE strain were similar in discriminating between ischemic and non-ischemic areas. We found that both wall thickening and strain are able to differentiate between ischemic and non-ischemic, remote and non-remote myocardium, respectively. However, the sensitivity to detect adjacent regions was poor, 33% for wall thickening and 15% for strain. The thresholds have limited applicability due to the low sensitivity and specificity. This has implications on trying to differentiate between remote, adjacent and ischemic regions based on regional function regardless of modality. The detection of adjacent sectors alone may be of limited clinical value, however the rational for including adjacent sectors in this study was to differentiate between sectors with high grade ischemia (ischemic sectors) and low grade ischemia (adjacent sectors).
We also found an increase of left ventricular mass of 9% following ischemia that is likely caused by edema. The increase was impressive in the ischemic area, measuring 37% ± 3% (p < 0.01) compared to 6% ± 2 (p = ns) in the combined remote and adjacent areas. This was also supported by end diastolic thickness that was significantly higher in ischemic compared to remote sectors (p < 0.01).
The study was conducted on 10 pigs, all with occlusion of the LAD. How results for CMR wall thickening and VE-strain would be affected by right coronary artery or left circumflex occlusion remains to be studied. In wall thickening, the most basal slices in end-diastole are often excluded since myocardium cannot be found in 360° of the left ventricular myocardial circumference in end-systole due to long-axis AV-plane motion . No standard definition of ischemic, adjacent and remote areas of the ventricle have been established, therefore caution should be taken when comparing results with other studies.
Thresholds for wall thickening and strain could be established for differentiation between ischemic, adjacent and remote areas. These thresholds, however will have limited clinical applicability due to the low sensitivity and specificity. Regional left ventricular function is reduced in the ischemic and areas adjacent to the ischemia after reperfused anterior myocardial infarction, while there is a slight increase in radial function in remote areas of the left ventricle. Edema was present mainly in the ischemic region but also to a slighter degree in the combined adjacent and remote areas.
This study was funded by the Swedish Heart Lung Foundation, the Swedish Research Council (VR-2011-3916,VR- 2012–4944), and Region of Scania, Sweden.
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