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Ann Thorac Surg 2007;84:2004-2010. doi:10.1016/j.athoracsur.2007.06.062
© 2007 The Society of Thoracic Surgeons
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Original Articles: Cardiovascular

Ventricular Restraint Prevents Infarct Expansion and Improves Borderzone Function After Myocardial Infarction: A Study Using Magnetic Resonance Imaging, Three-Dimensional Surface Modeling, and Myocardial Tagging

Aaron S. Blom, DOa, James J. Pilla, PhDa,b, Jeffrey Arkles, MSa, Larry Dougherty, PhDb, Liam P. Ryan, MDa, Joseph H. Gorman, III, MDa, Michael A. Acker, MDa, Robert C. Gorman, MDa,*

a Harrison Department of Surgical Research, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania
b Department of Radiology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania

Accepted for publication June 21, 2007.

* Address correspondence to Dr Robert C. Gorman, University of Pennsylvania School of Medicine, 313 Stemmler Hall, 36th and Hamilton Walk, Philadelphia, PA 19104-4283 (Email: gormanr{at}uphs.upenn.edu).


   Abstract
Top
 Abstract
Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
Background: Infarct expansion is associated with impaired borderzone function, adverse remodeling, and poor long-term prognosis. We hypothesized that left ventricular restraint early after myocardial infarction limits infarct expansion, preserves borderzone function, and reduces remodeling.

Methods: We used an ovine model as well as high spatial and temporal resolution cardiac magnetic resonance imaging to quantify total and infarcted left ventricular epicardial surface area at baseline and 1 week and 12 weeks after anterior wall infarction in 10 animals. Five animals were randomly assigned to treatment with left ventricular restraint (Acorn cardiac support device) 1 week after infarction. Five animals were untreated controls. Total left ventricular surface area was measured by importing the end-diastolic magnetic resonance imaging–derived epicardial contours into custom software, which creates a three-dimensional surface from the two-dimensional magnetic resonance imaging contours. Infarct area was calculated from magnetic resonance imaging–detectable titanium markers placed at the infarct border. Borderzone radial and circumferential strains during systole were also assessed using myocardial tagging techniques as a measure of contractile function.

Results: The infarct area 1 week after infarction was 1,177 ± 386 mm2 in the control group and 1,124 ± 427 mm2 in the cardiac support device group. After 12 weeks, infarct area was 3,666 ± 1,013 mm2 in the control group and 1,227 ± 301 mm2 in the cardiac support device group. Borderzone systolic radial strain decreased from 12.6% ± 0.77% to 3.6% ± 0.3% after infarction in the control group and 13.7% ± 0.87% to 4.7% ± 0.3% in the cardiac support device group. At 12 weeks after infarction, radial strain was 3.4% ± 0.5% in the control group and 6.7% ± 0.4% in the cardiac support device group.

Conclusions: Early postinfarction left ventricular restraint limits infarct expansion and improves borderzone contractile function.


   Introduction
Top
 Abstract
 Introduction
Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
Left ventricular (LV) remodeling caused by a myocardial infarction (MI) is now responsible for almost 70% of 5 million cases of heart failure in the United States [1]. Early infarct expansion, or stretching, has been correlated with adverse remodeling and a poor long-term prognosis [2–4]. In previous experimental studies using sonomicrometry [5], echocardiography [6, 7], and magnetic resonance imaging (MRI) [8–10], it has been demonstrated that infarct expansion is associated with stretching and decreased contractile function in the neighboring normally perfused borderzone (BZ) myocardium. Additionally, although the perfused but hypocontractile myocardium is initially isolated to the region immediately adjacent to the infarct, the process extends with time to involve progressively more myocardium remote from the infarcted region [5, 11].

Early ventricular restraint or infarct stiffening has been demonstrated to have a salutary effect on global ventricular remodeling in animal infarction models [10, 12–17]. However, a quantitative assessment of the extent to which these restraint strategies prevent infarct expansion has not been previously performed. In this study, we used cardiac MRI and a novel technique for three-dimensional surface modeling to measure the degree of infarct expansion and global LV remodeling in an ovine infarction model with and without ventricular restraint with the CorCap cardiac support device (CSD; Acorn Cardiovascular, St. Paul, MN). Borderzone radial strain during systole was also assessed with MRI using myocardial tagging techniques as a measure of contractile function [10].


   Material and Methods
Top
 Abstract
 Introduction
 Material and Methods
Results
 Comment
 Acknowledgments
 References
 
Animal Model and Surgical Protocol
Ten male sheep weighing between 35 and 40 kg were used for this study. Animals were treated under an experimental protocol approved by the University of Pennsylvania’s Institutional Animal Care and Use Committee and in compliance with the National Institutes of Health’s "Guide for the Care and Use of Laboratory Animals" (NIH publication 85-23, revised 1996). For all of the procedures described, anesthesia was induced with thiopental sodium (10 to 15 mg/kg intravenously) before intubation. Anesthesia was maintained with isoflurane (1.5% to 2.0%) and oxygen. All animals had a baseline MRI after which they were allowed to recover and were returned to the animal colony. After 1 week, the animals were returned to the operating room. Under general anesthesia and aseptic conditions, animals underwent left thoracotomy and pericardiotomy. The surface electrocardiogram and arterial blood pressure were continuously monitored throughout the procedure. All animals received magnesium sulfate (1 g intravenous bolus), amiodarone (150 mg intravenously), and lidocaine (3 mg/kg intravenous bolus, then 2 mg/min infusion) before infarction to prevent or treat arrhythmias. After premedication, all diagonal branches of the left anterior descending coronary artery were ligated. This infarction typically involves 25% of the LV mass and, because sheep lack preformed collaterals, always results in a transmural infarction [10, 18, 19]. Additionally, 3-mm by 1-mm titanium disks were placed along the left anterior descending coronary artery to mark the lateral extent of the infarct to delineate and follow the infarct area with MRI (Fig 1). The ischemic region was easily discerned by the blue-purple discoloration in the normally brick-red myocardium that occurred after coronary ligation.


Figure 1
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  		Fig 1. The ovine heart as viewed through a left thoracotomy. Infarctions were created by ligating all diagonal branches of the left anterior descending coronary artery (in this case four vessels, denoted as D1–D4) and can be differentiated by the discoloration of the myocardium. Titanium markers (denoted by white circles) were placed at the interface of the infarcted and perfused regions to delineate the infarct on magnetic resonance imaging.

 
When hemodynamic and rhythm stability were assured, the thoracotomy was closed in layers using standard techniques. The pericardium was not closed. The animals were allowed to recover and were returned to the animal colony when able to ambulate.

One week after infarction, the 10 animals were randomly assigned to receive either no treatment (control group, n = 5) or ventricular restraint with the CorCap CSD (CSD group, n = 5). The CSD animals were returned to the operating room, and the thoracotomy incision was reopened. The CSD was placed by sliding the device over the epicardium, up to the level of the atrioventricular junction. Polypropylene sutures (4-0) were placed along the base of the heart, starting on the posterior surface and working anteriorly, with a total of between 8 and 10 sutures, depending on the size of the heart. The excess device material was gathered up along a line parallel to the long axis of the heart and excised. The free edges of the CSD were sewn to allow for the device to be in loose contact with the epicardium. The CSD was placed in a manner that would allow the restraining material to be "tented" off the anterior wall by less than 10 mm. This is the same technique we have used in our extensive clinical experience with the CSD. The thoracotomy was again closed, and the animal was allowed to recover. A second thoracotomy was not performed in the control group. After 12 weeks, all animals underwent a final MRI, after which they were euthanized under general anesthesia with a potassium overdose.

Magnetic Resonance Imaging Protocol
Before imaging, the animals were placed under general anesthesia (as described above) and a high-fidelity LV pressure transducer catheter (Spc-350; Millar Instruments, Houston, TX) was inserted through a 7F introducer sheath placed in the femoral artery to allow for LV pressure cardiac gating. All images were cardiac and respiratory gated to ensure consistent spatial positioning of the heart during each acquisition. A complete set of high temporal resolution tissue-tagged T1-weighted images was acquired in the short-axis plane using a 1.5-T whole-body high-speed imaging system (General Electric, Milwaukee, WI). Noninvasive tagging of cardiac tissue in magnetic resonance images was achieved by perturbing the local magnetization using spatial modulation of magnetization (SPAMM) to create MRI-visible tags within the myocardial wall. As these tags move with the underlying myocardial wall, the motion of the tags during the cardiac cycle reveals the internal motion of the otherwise featureless myocardial wall allowing for the measurement of regional strain. The MRI was performed using a fast-gradient echo pulse sequence with a SPAMM preparatory pulse and the following variables: field of view, = 22 cm; acquisition matrix, = 256 x 128; flip angle, = 15 degrees; repetition time to echo time (TR/TE), = 8.8/2.2 ms; slice thickness, = 6 mm; interslice gap, = 0; tag spacing, = 5 mm; two signal averages; and 2 k-space lines acquired per cardiac frame. Images were acquired in the short-axis plane using two 12.7-cm surface coils placed on the left and right chest. The images were archived and stored for off-line analysis.

Determination of Infarct Area
After the images were acquired, they were imported into our custom cardiac MRI analysis software. Endocardial and epicardial LV contours were drawn in a single phase for each slice in the short-axis stack. The contours for the remaining phases were automatically determined using an optical flow method [20], which tracked each point on the contour during the entire cardiac cycle, resulting in a complete set of contours being generated from a single initial contour. The position of the titanium markers, which appear as circular signal voids on the gradient recalled echo MRI images, were determined as the coordinates with minimum signal intensity (Fig 2).


Figure 2
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  		Fig 2. (A) Tissue tagged short-axis magnetic resonance image of a sheep 1 week after infarction. The titanium markers placed at the infarct border can be seen as signal voids in the image—the anterior wall, the posterior wall, and the right ventricle (RV) have been labeled. (B) Epicardial contours derived from the short-axis magnetic resonance images. Positions of the markers on the epicardial surface are depicted by asterisks placed on the contours.

 
The set of epicardial contours at end-diastole formed the basis for the three-dimensional model of the LV. All data analysis was performed using custom Matlab (The Mathworks, Natick, MA) algorithms. The vertices from all the two-dimensional contours were fed into a Delaunay tessellation algorithm to generate a three-dimensional surface model of the LV that was a mesh of interlocking triangles. A spline function fit was used to improve the overall smoothness of the model. Left ventricular volumes at end-systole and end-diastole were calculated from the endocardial contours.

The marker coordinates were then translated into spherical coordinates, and a polygon was created that, when applied to surface of the model, delineated the borders of the infarct. The region bounded by the intersection between the marker polygon and the model represented the area of the MI.

Determination of Borderzone Contractile Function
The BZ was defined as the area bounded by a 20-degree arc toward the septum in the noninfarcted region (Fig 3). The arc was generated from the centroid of the LV by projecting two lines separated by 20 degrees to the epicardial surface. This 20-degree arc in all cases represented a 1- to 1.5-cm portion of normally perfused septum immediately adjacent to the infarcted anterior wall [10]. This is the approximate size of the acute BZ that we have previously measured using sonomicrometry array localization [5]. The same approximate region was also analyzed for the baseline studies.


Figure 3
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  		Fig 3. Short-axis tagged images of control (A) and cardiac support device–treated (B) animals 12 weeks after infarction. Titanium markers, which create voids in the images, are used to delineate the edge of the infarct. The borderzone was defined as the region within a 20-degree arc on the noninfarcted septal side of the marker.

 
Borderzone radial strain (or wall thickening) and circumferential strain (circumferential shortening) were calculated from displacement flow fields generated using the optical flow method, which tracks each pixel in the myocardium throughout the cardiac cycle using intensity [20]. This method of automatic tracking is based on declassified military software that has been adapted for cardiac MRI analysis.

Borderzone radial and circumferential strains were determined through the cardiac cycle by calculating the percentage change in strain at each image acquisition phase during systole relative to end-diastole. The image variable settings resulted in a temporal resolution of approximately 18 ms, which covered systole in an average of 13 phases. End-diastole was the initial phase, and end-systole was assigned to the imaging phase with the smallest LV volume. Borderzone radial and circumferential strains were assessed for each phase (and normalized to end-diastole) in control animals and in CSD-treated animals.

Statistical Analysis
Repeated measures analysis of variance (Statistical Package for the Social Sciences, SPSS Inc, Chicago, IL) was used to evaluate changes in LV areas and BZ strain. Data are presented as mean ± standard deviation. Significance was defined as a probability value less than 0.05. The funding sources had no role in interpreting the data.


   Results
Top
 Abstract
 Introduction
 Material and Methods
 Results
Comment
 Acknowledgments
 References
 
Representative 3-month postinfarction control and CSD-treated MI surface models generated from the MRI contours and marker positions are shown in Figure 4. Red triangles depict the surface area of normal myocardium whereas the blue triangles are the area bounded by the markers and represent the infarcted myocardium. Total LV surface was 7,660 ± 1,464 mm2 and 7,870 ± 1,271 mm2 at baseline in the control and CSD groups, respectively, and increased to 9,779 ± 1,450 mm2 and 9,892 ± 1,200 mm2 at 1 week after infarction. In the CSD group, LV total surface area was stabilized at 12 weeks after infarction but increased to 14,088 ± 1,487 mm2 in the control group (Fig 5A). Infarct area 1 week after infarction was 1,177 ± 387 mm2 and 1,124 ± 427 mm2 in the control and CSD groups, respectively. In the control group the infarct area more than tripled to 3,666 ± 1,014 mm2 12 weeks after infarction. The CSD application essentially stabilized infarct size (1,228 ± 302 mm2) from 1 to 12 weeks after infarction (Fig 5B).


Figure 4
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  		Fig 4. Three-dimensional epicardial surface model for representative control (A) and cardiac support device–treated (B) animals 12 weeks after infarction. Models were generated from magnetic resonance images in which detectable markers were used to delineate the infarct from perfused myocardium. Red triangles indicate the area of perfused myocardium, and the blue triangles are the area bounded by the markers and represent infarcted myocardium. Note the difference in overall left ventricular size and infarct area between the control animal and the cardiac support device–treated animal.

 

Figure 5
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  		Fig 5. (A) Total left ventricular (LV) epicardial surface area calculated from the three-dimensional surface model. Total area increased from baseline to 1 week after infarction in all animals and continued to increase in the control group during the 12-week follow-up interval. Cardiac support device (CSD) placement stabilized total left ventricular area from 1 to 12 weeks after infarction. (B) Infarct area calculated from three-dimensional epicardial surface model using points generated from magnetic resonance imaging visible markers. Twelve weeks after infarction, the infarct area in the control animals increased significantly compared with 1-week values, whereas cardiac support device placement prevented further infarct expansion during the 12-week follow-up interval. *p < 0.05 versus baseline; #p < 0.05 versus 1 week after infarction; {ddagger}p < 0.05 versus control.

 
Borderzone systolic radial strain was 12.6% ± 0.77% and 13.7% ± 0.87% at baseline and decreased markedly to 3.6% ± 0.3% and 4.7% ± 0.3% in the control and CSD groups, respectively, at 1 week after infarction. Twelve weeks after infarction radial strain in the BZ was unchanged in the control group (3.4% ± 0.5%) but improved significantly to 6.7% ± 0.4% in the CSD-treated group (Fig 6). Left ventricular volume and hemodynamic data are presented in Table 1. Circumferential BZ strain was not significantly improved in the CSD-treated group compared with the control group.


Figure 6
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  		Fig 6. Borderzone radial strain decreased dramatically in both groups 1 week after infarction. Although radial strain improved after cardiac support device (CSD) placement, there was no change in the control group. *p < 0.05 versus baseline; #p < 0.05 versus 1 week after infarction; {ddagger}p < 0.05 versus control.

 

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  		Table 1 Left Ventricular Volumes and Hemodynamics a
 

   Comment
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
Acknowledgments
 References
 
All animals in this study sustained a large transmural anterior MI—a strong remodeling stimulus. During the first week after infarction both infarcted and perfused regions of the heart expanded. In control animals the surface area of the infarct region expanded more than 300% between postinfarction weeks 1 and 12, whereas the total LV surface area increased by nearly 200%. This was associated with a significant and sustained reduction in BZ contractile function as assessed by radial wall thickening. In the CSD treatment group, neither the infarcted nor perfused regions experienced further expansion after the CSD was placed. Borderzone radial strain (wall thickening) also improved after device placement and was significantly better than the control group 12 weeks after infarction.

These data demonstrate clearly the profound propensity of a large transmural MI to promote progressive expansion and how such expansion results in global remodeling and reduced contractile function in normally perfused myocardium both adjacent to and remote to the infarct. The data further confirm that such expansion can be arrested by mechanical ventricular restraint, which, in turn, results in improved BZ contractile function and reduced global remodeling.

Laboratory and clinical data have shown that expansion (stretching) of a transmural MI initiates a progressive myopathic process in normally perfused myocardium [5, 11, 21]. This phenomenon is initially localized to myocardium immediately adjacent to the infarct but extends during the remodeling process to convert contiguous normally perfused myocardium into hypocontractile, remodeled myocardium [5, 21]. This stretch-induced myopathic process has been associated with myocyte apoptosis [22] and disruption of the extracellular matrix secondary to activation of matrix metalloproteinases [17, 23].

Although surgical reshaping operations such as aneurysm resection, surgical anterior ventricular restoration, and the Dor procedure effectively reduce LV volumes, they have not been definitively demonstrated improve survival in ischemic cardiomyopathy patients [24–26]. No randomized data exist comparing these procedures with medical management or surgical revascularization alone. A recent report of a large cohort of patients who had the surgical anterior ventricular restoration operation demonstrated a significant increase in LV diastolic volumes less than 1 year after the operation, further raising concern about the long-term benefit of reshaping procedures [27]. A recent randomized trial comparing surgical anterior ventricular restoration and coronary revascularization with revascularization alone showed no survival advantage for surgical anterior ventricular restoration at 2 years follow-up but did demonstrate improvement in symptoms [28]. Definitive conclusions regarding the efficacy and durability of the surgical anterior ventricular restoration procedure await the conclusion of large randomized prospective trials with at least a 5-year follow-up.

Clinical experience with the CSD device in a large series of end-stage heart failure patients has recently been presented. This randomized prospective study demonstrated small but significant reductions (approximately 10%) in LV volumes 1 year after device placement and significantly less need for subsequent interventions for heart failure; however, no improvement in 1-year survival occurred in the CSD-treated cohort when compared with control patients [29].

These clinical results indicate that the inherent myopathic process associated with LV remodeling is very difficult to reverse once established. A recent finite element analysis of BZ mechanics by Guccione and colleagues [30] using MRI and a similar ovine infarction model has demonstrated that the decreased contractile function in the chronically remodeled BZ myocardium cannot be attributed solely to a mechanical disadvantage caused by increased regional stress. This analysis provides further evidence that the remodeling process leads to an inherent myopathy of normally perfused myocardium that is unlikely to be reversed by procedures designed to reshape the chronically remodeled heart.

Our results support the conclusion that ventricular restraint is effective when placed early after an MI with the intent of limiting the remodeling stimulus associated with infarct expansion. However, the window of opportunity during which ventricular restraint can be most effectively applied remains to be determined. In this study intervention was delayed until 1 week after infarction. Although definite functional and structural benefits were identified with this approach, BZ contractile function was extensively degraded by 1 week after infarction and did not completely recover after 12 weeks despite CSD placement even though further infarct expansion was prevented. Earlier ventricular restraint may allow for further improvement of long-term BZ contractile function.

The results of this study confirm the importance of infarct expansion as the driving impetus for adverse postinfarction ventricular remodeling. More importantly, this study reports the use of a novel technique for precisely measuring infarct size and expansion as well as BZ function using a clinically relevant imaging modality. Although we used titanium markers to demarcate the infarct from normally perfused myocardium, the use of concomitant first-pass contrast MRI should allow for the delineation of the infarcted from perfused myocardium, obviating the need for markers in future work and permitting clinical application of this technique. As effective and less invasive techniques for preventing infarct expansion are developed, it will be essential to have imaging modalities that precisely quantify infarct expansion so patients most at risk for adverse remodeling can be identified and treated.


   Acknowledgments
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
References
 
This study was funded in part by grants from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD (HL63954 [RCG], HL71137 [RCG], and HL76560 [JHG]), an American Heart Association Post-Doctoral Fellowship (0625455U [LPR]), and a grant from Acorn Cardiovascular, Inc, St. Paul, MN (MAA).


   References
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 

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