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Ann Thorac Surg 2005;80:2257-2262
© 2005 The Society of Thoracic Surgeons

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Original article: Cardiovascular

Early Postinfarction Ventricular Restraint Improves Borderzone Wall Thickening Dynamics During Remodeling

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

Accepted for publication May 11, 2005.

^_* Address correspondence to Dr Robert C. Gorman, Harrison Department of Surgical Research, University of Pennsylvania School of Medicine, 313 Stemmler Hall, 36th and Hamilton Walk, Philadelphia, PA19104-4283 (Email: gormanr{at}uphs.upenn.edu).

Presented at the Poster Session of the Forty-first Annual Meeting of The Society of Thoracic Surgeons, Tampa, FL, Jan 24–26, 2005.

	Abstract

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BACKGROUND: Early infarct expansion impairs function of normally perfused borderzone myocardium (BZM), initiates adverse remodeling, and portends a poor long-term outcome. Early ventricular restraint has been demonstrated to improve global remodeling but its effect on BZM function has not been assessed. Using an ovine model of infarct induced remodeling and MRI, we tested the hypothesis that ventricular restraint early after MI preserves BZM function and reduces remodeling.

METHODS: Six sheep had a large anterior infarction after ligation of all diagonal branches. One week after infarction 3 sheep had placement of a cardiac support device (CSD) to restrain infarct expansion. Global remodeling and borderzone wall thickening strain were assessed using tagged MRI before and 8 weeks after infarction.

RESULTS: Global remodeling was greatly reduced in the CSD group compared with control. The BZM systolic wall thickening was similar in both groups at baseline (13.5% ± 2.0%, control; 12.8% ± 2.0%, CSD, p = 0.8). After 8 weeks of infarction-induced remodeling, systolic wall thickening strain decreased significantly to 4.9% ± 0.7% in the control group (p = 0.03). In contrast, systolic wall thickening was preserved in the CSD group at 8 weeks (11.0% ± 1.6%, p = 0.3). In the control group all thickening occurred during isovolemic contraction, plateauing during ejection. The CSD improved late systolic borderzone wall thickening, although dynamics remained perturbed.

CONCLUSIONS: Ventricular restraint early after MI improves both contractile function of the BZM and global ventricular remodeling. The dynamics of BZM wall thickening are impaired during remodeling. The CSD significantly improves but does not completely maintain baseline BZM wall thickening dynamics.

	Introduction

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Left ventricular (LV) remodeling caused by a myocardial infarction (MI) is now responsible for almost 70% of 4.9 million cases of heart failure in the United States [1]. Early infarct expansion (namely, stretching) has been identified as the inciting event that initiates adverse remodeling and leads to LV dilatation [2–4]. Once established, ventricular dilatation is difficult to reverse and portends a poor long-term outcome [5]. Recent laboratory studies have suggested that mechanical infarct restraint initiated soon after infarction can influence outcome of remodeling [6–11]. These data, in conjunction with the development of innovative devices suitable for providing LV restraint in patients [12, 13], have increased interest in this surgical strategy as a potential means of preventing rather reversing or palliating congestive heart failure (CHF) due to infarct-induced remodeling. In previous studies using sonomicrometry array localization we have demonstrated that infarct expansion causes increased strain and decreased contractility in the normally perfused borderzone myocardium (BZM) adjacent to the infarct [3]. To date the effect of early postinfarction ventricular restraint on BZM function has not been assessed. Using an ovine model of infarct induced remodeling and tagged magnetic resonance imaging (MRI), we tested the hypothesis that ventricular restraint early after MI preserves BZM function and reduces remodeling.

	Material and Methods

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Animal Model and Surgical Protocol
Six male sheep weighing 35 to 45 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 National Institutes of Health's "Guide for the Care and Use of Laboratory Animals" (NIH publication 85-23, revised 1985). For all the procedures described, animals were induced with thiopental sodium (10 to 15 mg/kg intravenously) and intubated. Anesthesia was maintained with isofluorane (1.5% to 2.0%) and oxygen.

All animals had a baseline MRI after which they were recovered and 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 all diagonal branches of the left anterior descending artery were ligated. The surface electrocardiogram and arterial blood pressure were continuously monitored. All animals received magnesium sulfate (1 g intravenously), amiodarone (150 mg intravenously), and lidocaine (3 mg/kg intravenous bolus, then 2 mg/min infusion) before infarction to prevent arrhythmias. The thoracotomy was closed using standard techniques. Animals were recovered and returned the animal colony when able to ambulate.

One week after infarction, the 6 animals were randomized to receive either no treatment (control group, n = 3) or ventricular restraint with the CorCap (Acorn Cardiovascular, St. Paul, Minnesota) cardiac support device (CSD group, n = 3). 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 heart starting on the posterior surface and working around anteriorly, with total of between 8 and 10 sutures, depending on the size of the heart. The excess material was gathered up along a line parallel with the long axis of the heart and excised. The ends where resewn such that the CSD was in contact with the epicardium but exerted little or no tension. The thoracotomy was again closed, and the animal recovered. The control group did not have a second thoracotomy.

After 8 weeks, the animals were again anesthetized and underwent a final MRI after which they were euthanized.

The infarction model used in this experiment is similar but not identical to the one previously described by our group [14]. We have previously reported ligation of the first and second diagonal branches of the left anterior descending artery, which infarcts 23.9% ± 2.2% of the LV mass and results in a twofold increase in left ventricular end systolic volume (LVESV) after 8 weeks of remodeling as assessed by echocardiography. In this experiment we ligated all identifiable diagonals, with an estimated infarct size of 30% of the left ventricle. These infarcts are, therefore, a slightly stronger stimulus for remodeling than our previously reported model (Fig 1).

View larger version (122K): [in this window] [in a new window]   Fig 1. An intraoperative photograph of the ovine heart after the infarct was created by ligating all diagonal vessels (in this case four vessels: D 1 , D 2 , D 3 , and D 4 ). The heart is viewed through a left thoracotomy. The base of the heart is at the top of the photograph.

The MR imaging was performed using a fast gradient echo pulse sequence with a SPAMM preparatory pulse and the following parameters: field of view = 22 cm, acquisition matrix = 256 x 128, flip angle 15 degrees, 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.

Data Analysis
An experienced observer performed all MRI image analysis in a masked fashion. The short-axis tagged images were analyzed using a custom cardiac MRI analysis program, SPAMMVU [15]. Left ventricular endocardial and epicardial contours were automatically delineated and tag tracking was performed using an automated algorithm based on recently declassified military software adapted for cardiac MR image analysis [15, 16]. This algorithm determines myocardial displacement by means of optical flow, which uses intensity to track the individual pixels throughout the cardiac cycle. From the displacement field radial and circumferential strains are calculated.

Left ventricular end diastolic volume (LVEDV) and LVESV at baseline and 8 weeks were determined as a global assessment of remodeling.

The borderzone was determined to be the area bounded by a 20-degree arc toward the septum in the noninfarcted region (Fig 2). 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 cm to 1.5 cm portion of normally perfused septum immediately adjacent to the infarcted anterior wall. This is the approximate size of the acute borderzone that we have previously measured using sonomicrometry array localization [3]. The same region was also analyzed for the baseline studies. Strain was calculated over this region by averaging the radial and circumferential strain magnitudes from three adjacent tag intersection points. Borderzone radial and circumferential strain was 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 parameter settings resulted in a phase temporal resolution of approximately 18 ms, which covered the systole in 13 acquisitions phases. End diastole and end systole were assigned to image acquisitions with the largest and smallest LV volumes, respectively. The end of isovolemic contraction was defined as the acquisition phase just before LV volume began to decline. This was fifth acquisition phase in most studies. The BZM strain was assessed for each period (and normalized to end diastole) in control animals and in CSD treated animals.

View larger version (177K): [in this window] [in a new window]   Fig 2. Localization of borderzone myocardium. The borderzone was determined to be the area bounded by a 20-degree arc on the septal side of the infarct. The arc was generated from the centroid of the left ventricle by projecting two lines separated by 20 degrees to the epicardial surface. The same region was also analyzed for the baseline studies.

	Results

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Ventricular Volumes
The LVESV and LVEDV for all animals at baseline were 36.4 ± 4.4 mL and 56.3 ± 7.8 mL, respectively. In the control group, at 8 weeks LVESV and LVEDV were 91.4 ± 5.8 mL and 110 ± 9.8 mL, respectively (p < 0.05 for both compared with baseline). In the CSD group, at 8 weeks LVESV and LVEDV were 47.8 ± 2.8 mL and 67.6 ± 4.6 mL, respectively (p < 0.05 for both compared with baseline and control).

Borderzone Myocardium Systolic Circumferential and Radial Thickening Strain
The BZM systolic wall thickening strain was similar in both groups at baseline (13.5% ± 2.0%, control; 12.8% ± 2.0%, CSD). After 8 weeks of infarction-induced remodeling, systolic wall thickening strain in the control group decreased significantly to 4.9% ± 0.7% (p = 0.03). Systolic wall thickening was, however, preserved in the CSD group at 8 weeks (11.0% ± 1.6%, p = 0.3; Fig 3). There was no significant change in circumferential strain during remodeling in either control or CSD group.

View larger version (23K): [in this window] [in a new window]   Fig 3. Total systolic borderzone (BZ) wall thickening. The BZ myocardium in the control group (left) and the cardiac support device (CSD) group (right) had similar systolic thickening at baseline. After 8 weeks of remodeling, BZ myocardium wall thickening was greatly reduced in the control group. The BZ myocardium wall thickening was preserved in the CSD group. *p = 0.03 control at 8 weeks versus control at baseline. p = 0.04 control at 8 weeks versus CSD at 8 weeks.

View larger version (27K): [in this window] [in a new window]   Fig 4. Dynamic borderzone (BZ) wall thickening during systole as a percentage increase relative to end diastole. In both the control group (left) and in the cardiac support device group (right) there is constant wall thickening throughout systole before infarction. Eight weeks after infarction in the control group wall thickening only occurs during isovolemic contraction with no further thickening during the ejection phase of systole. In the cardiac support device treated group there is improvement in BZ thickening in the late ejection phase compared to the control group. Numbers on the left = fractional thickening (eg, 2 = 0.02, 4 = 0.04, etc). (ED = end diastole; EIVC = end isovolemic contraction; ES = end systole.)

	Comment

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The etiologic importance of infarct expansion in the initiation and progression of infarct-induced LV remodeling is confirmed by the results of this study. Laboratory and clinical data have shown that expansion (stretching) of a transmural myocardial infarction initiates a progressive myopathic process in normally perfused myocardium [2–4]. 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 [3, 17]. The stretch-induced myopathic process has been associated with myocyte apoptosis [18] and disruption of the extracellular matrix secondary to activation of matrix metalloproteinases [19]. The failure of surgical reshaping operations and interventions for ischemic mitral regurgitation to improve survival in ischemic cardiomyopathy patients strongly suggests that infarct-induced myopathy is very difficult to reverse once established [20–23]. A recent study using a finite element analysis by Guccione and associates [24] has demonstrated that the decreased function in the chronically remodeled BZM cannot be attributed solely to a mechanical disadvantage due to increased regional stress [24]. This is further evidence to suggest 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.

Although experimental results have demonstrated the potential of early ventricular restraint to influence global remodeling after MI, little work has been performed to directly support the hypothesis that prevention of infarct expansion has salutary effects on BZM function. This study represents a first attempt to confirm that hypothesis. Experiments such as these are important because of the mechanistic and therapeutic insights that they can provide.

We found that total systolic BZM thickening was profoundly reduced in control animals and preserved in the CSD group (Fig 3). However, the time course of systolic thickening was abnormal in both groups (Fig 4).

Before infarction, systolic wall thickening occurred in a nearly linear fashion from end diastole to end systole. No distinction was evident between the thickening rate during isovolemic contraction and the ejection phase of systole.

In control animals, total BZM systolic wall thickening was decreased by more than 50%, with essentially all of it occurring during the isovolemic contraction phase of systole. This finding adds further and unique evidence to support the impact of infarct expansion on BZM function. These results suggest that BZM contractility is not only reduced as a result of remodeling but occurs only against low ventricular pressure and does not effectively contribute to the ejection.

In the CSD-treated animals, total BZM systolic wall thickening was nearly normalized; however, the time course of wall thickening was also abnormal, albeit in a manner distinct from that of the control group. Thickening was normal during isovolemic contraction then plateaued during early ejection in a way similar to the control animals. During late ejection in the CSD group, however, wall thickening recommenced and resulted in a total wall thickening not significantly different from baseline. Although the time course of wall thickening in the CSD group seems to represent an improvement, it remains unclear how much this delayed contraction contributes to efficient ejection.

These data emphasize the need to evaluate the time course through systole of BZM geometry and function during the remodeling. The experience with cardiac resynchronization therapy has taught the importance of a coordinated myocardial effort for optimal global systolic function [25]. This may also be the case for BZM.

Study Limitation
We believe this study provides new information regarding the BZM during the remodeling process in a clinically relevant large animal model using a clinically applicable imaging modality.

We employed a large transmural anterior infarction as a remodeling stimulus. These results may, therefore, not be applicable to smaller infarcts, reperfused infarcts or infarcts located in other regions of the ventricle. Recent work has suggested that BZM remodeling is dependent on infarct location [26]. We are currently conducting studies to assess BZM function in ovine infarct models with posterior and apical orientations.

No attempt was made to determine the extent of the abnormal function demonstrated in the 20-degree arc that was selected as borderzone in this study based on our previous experimental work using sonomicrometry [3]. We have previously demonstrated the extension of the borderzone phenomenon as remodeling progresses in the anteroapical ovine infarct model [3]. It may be that application of the CSD reduced the spread of contractile dysfunction that is associated with uncompensated infarction induced remodeling. Confirmation of this possibility awaits further study.

No marker technology was used to definitively identify the BZM. We relied on a visual distinction between the thinned anterior wall and the relatively normal appearing septum (Fig 2). Because of the profound remodeling that can occur in BZM, we have previously reported the potential hazard of such assumptions when studying borderzone mechanics after MI [3]. However, given our results, we feel that this definition of the borderzone, while a distinct limitation, does not invalidate our conclusions.

Three-dimensional strain was not acquired in the BZM. We measured radial and circumferential two-dimensional strain from a two-dimensional tagged data set, which is an accurate depiction of the in-plane deformation. Three-dimensional strain would provide a more complete picture of the deformation in the BZM by supplying longitudinal strain and three-dimensional shear strain measurements, which would furnish more insight into the BZM strain distribution. Our laboratory is currently developing techniques to measure three-dimensional strains.

Finally, the number of animals enrolled in this study is an absolute minimum for studies of infarct-induced remodeling that utilize large animal models. Because of the extreme differences between the control and CSD groups, the highly reproducible nature of sheep coronary anatomy and their lack of collaterals, we are satisfied that phenomenon described are real and represent important new knowledge regarding the importance of BZM in the remodeling process.

	The Society of Thoracic Surgeons: Forty-Second Annual Meeting—New Location

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The city of New Orleans and part of the Gulf region have been devastated by the effects of Hurricane Katrina. Relief efforts have begun, but the clean-up and recovery processes will be slow. For this reason, The Society of Thoracic Surgeons will host its 42nd Annual Meeting in Chicago, Illinois. Please note: the meeting dates have not changed. The Annual Meeting will be held at McCormick Place, January 30–February 1, 2006, and STS/AATS Tech-Con 2006 will be held in the same location, January 28–29.

The Workforce on Annual Meeting's Program Task Force is meeting to discuss program details, and to organize an outstanding educational event. Chicago also offers a wide array of exciting social activities.

Please continue to visit www.sts.org for important program information as it develops!

	Acknowledgments

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Supported by HL63954, HL71137, and HL76560 from the National Heart Lung Blood Institute, National Institutes of Health, Bethesda, Maryland, and by a grant from Acorn Cardiovascular, Inc., St. Paul, Minnesota.

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This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Joseph H. Gorman, III Michael A. Acker Robert C. Gorman Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Pilla, J. J. Articles by Gorman, R. C. Search for Related Content PubMed PubMed Citation Articles by Pilla, J. J. Articles by Gorman, R. C. Related Collections Myocardial infarction