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Ann Thorac Surg 2005;80:2250-2255
© 2005 The Society of Thoracic Surgeons

Original article: Cardiovascular

Borderzone Geometry After Acute Myocardial Infarction: A Three-Dimensional Contrast Enhanced Echocardiographic Study

Benjamin M. Jackson, MD a , Landi M. Parish, SB a , Joseph H. Gorman, III, MD, Yoshiharu Enomoto, MD a , Hiroaki Sakamoto, MD a , Theodore Plappert, CVT b , Martin G. St. John Sutton, MSSB b , Ivan Salgo, MD c , Robert C. Gorman, MD a , *

a Harrison Department of Surgical Research, Division of Cardiology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania
b Department of Medicine, Division of Cardiology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania
c Philips Medical Systems, Andover, Massachussetts

Accepted for publication May 12, 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, PA 19104-4283 (Email: gormanr{at}uphs.upenn.edu).


Dr Salgo discloses a financial relationship with Philips Medical Systems.

 

   Abstract
Top
 Abstract
Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
BACKGROUND: Regional myocardial geometry, function, and perfusion status are critical variables for understanding infarction-induced left ventricle (LV) remodeling. Three-dimensional contrast echocardiography (3DCE) is uniquely suited to measure these parameters. We evaluate the ability of 3DCE to assess geometric changes in the normally perfused but hypocontractile borderzone myocardium (BZM) immediately after a myocardial infarction (MI) in an ovine model, and we compare 3DCE with two-dimensional contrast echocardiography (2DCE) in the long and short axis.

METHODS: Four sheep were studied with 3DCE and 4 were studied using 2DCE, before and 30 minutes after an anteroapical MI. Each 3DCE data set was acquired over 18 consecutive cardiac cycles. The LV geometry was reconstructed and perfusion data spatially correlated, thereby constituting a 3D model of ventricular geometry and perfusion. The borderzone was defined as the contrast-perfused myocardium adjacent to the infarct.

RESULTS: The 2DCE short-axis analysis demonstrated decreased curvature and decreased wall thickness in the borderzone after MI. These findings are consistent with increased BZM wall stress. However, the long-axis 2DCE analysis demonstrated increased BZM wall thickness and a surprising change in BZM concavity acutely after infarction. The 3DCE analysis confirmed these findings and added additional information regarding regional variability in BZM geometry that was not evident in the two orthogonal 2D views.

CONCLUSIONS: This study provides evidence that regional changes in BZM geometry are more complex than previously believed and are not necessarily indicative of increased regional stress. The superiority of 3DCE over 2DCE for assessing these changes is strongly supported.

Myocardial infarction (MI) is the most common cause of congestive heart failure [1]. The left ventricular (LV) response to MI is dependent on a complex interaction between infarction size, location, transmurality, and perfusion status [2–5]. When conditions favor infarct expansion, LV remodeling leading to ventricular dilatation and congestive heart failure is induced [6]. Ventricular dilatation—once established—is difficult to treat and portends a poor long term outcome [7]; however, the time course and extent of ventricular remodeling after MI is highly variable and difficult to predict in the early postinfarction period [8, 9]. This heterogeneity impedes the ability to identify patients at risk for MI-induced remodeling and subsequent congestive heart failure.

Recent laboratory studies have emphasized the importance of the normally perfused but hypocontractile borderzone myocardium (BZM) to the remodeling process and the development of congestive heart failure [10–12]. The BZM initially involves a narrow perimeter around the infarct, but as remodeling occurs the BZM extends to involve more normally perfused myocardium, until congestive heart failure develops [12, 13].

Because of the proposed importance of BZM stress to the initiation of the remodeling process [12, 14], a correlation between BZM geometric changes early after MI (as a measurable surrogate for stress) and the outcome of remodeling would allow for the identification of patients at risk for adverse remodeling and congestive heart failure.

Contrast-enhanced echocardiography has the ability to precisely register myocardial perfusion status, function, and geometry, making it a technique with potential for describing the borderzone myocardium during the remodeling process.

Technologic advancements in three-dimensional echocardiography have improved image quality, allowed real-time imaging, and increased the availability of this cardiac imaging modality. Its use in combination with improved echocardiographic contrast agents and delivery techniques may result in an ideal tool for studying the remodeling phenomenon.

In this study we evaluated the ability of two-dimensional contrast echocardiography (2DCE) and three-dimensional contrast echocardiography (3DCE) to assess BZM geometry early after MI in a standardized ovine model of adverse postinfarction remodeling.


   Material and Methods
Top
 Abstract
 Introduction
 Material and Methods
Results
 Comment
 Acknowledgments
 References
 
Surgical Protocol
Eight sheep were induced with thiopental sodium (10 to 15 mg/kg), intubated, anesthetized with isoflurane (1.5% to 2.0%), and ventilated with oxygen (Drager anesthesia monitor; North American Drager, Telford, Pennsylvania). All animals received glycopyrrolate (0.4 mg, intravenously) and cefazolin (1 g, intravenously, both before and after operation). Animals were treated in compliance with "Guide for the Care and Use of Laboratory Animals," published by the National Institutes of Health (NIH publication 85-23, revised 1985). The surface electrocardiogram (ECG) and arterial blood pressure were continuously monitored.

Using sterile surgical technique, a left anterolateral thoracotomy was performed in the fifth interspace. Polypropylene snares were placed around the left anterior descending artery (LAD) and second diagonal (D2) coronary arteries (approximately 40% from the apex). The animal was allowed to recover. Ligation of these arteries leads to a transmural apical infarction involving 22% ± 3% of the LV mass. Infarct expansion (stretching) occurs immediately [12] but heart failure does not occur acutely. Congestive heart failure and left ventricular aneurysm formation ensue over 8 weeks as infarction-induced remodeling ensues [15].

Infarction
After 10 to 14 days, sheep were again anesthetized and placed supine. Four animals underwent 2DCE; subsequently, another group of 4 animals was studied using 3DCE. Baseline echocardiographic images were recorded as described below, without injection of contrast. The exteriorized subcutaneous snares were tightened. Once the animal stabilized (approximately 1 hour), postinfarction contrast-enhanced echocardiographic measurements were made.

Echocardiographic Data Collection
Subdiaphragmatic echocardiographic images were obtained through a sterile, midline laparotomy as previously described [16]. In the first group of 4 animals, 2DCE was performed using a second harmonic technique (SONOS 5500; Philips, Andover, Massachusetts). For each recording of perfusion and wall motion, 0.5 mL Optison (albumen with octafluoropropane gas) echocardiographic contrast agent (GE Healthcare, London, United Kingdom) was injected directly into the left coronary ostium through a percutaneously inserted coronary angiographic catheter. Short-axis cross-sectional images at the level of the midpapillary muscles and long-axis images (four-chamber) were recorded continuously during the injection of contrast. Subsequently, in the second group of 4 sheep, 3DCE was performed using the Philips SONOS 5500 module with a R50-12 rotational ultrasound probe. At the initiation of each 3D data set acquisition, 0.5 mL Optison contrast agent was injected directly into the left coronary ostium. Using electrocardiographic gating, images were acquired over 18 consecutive heartbeats at angular increments of 10 degrees.

Data Analysis
All images were analyzed off-line. All measurements were made at end systole, identified as the frame at which LV cavity area was smallest. All plots representing three-dimensional renderings were created using Tecplot (Version 10; Amtec Engineering, Bellevue, Washington). Spline surface fits and Gaussian curvatures were calculated in Matlab. All measurements are presented as means ± SD. Comparisons are made between baseline and postinfarction using paired t tests.

The image processing and data analysis performed for the 2DCE data in both long and short axis has been described previously, and the techniques are illustrated in Figures 1 and 2 Go (unpublished data: Jackson BM, Gorman JH III, Parish LB, et al. Early changes in borderzone geometry after myocardial infarction: a contrast echocardiographic study, 2005) [17]. Briefly, the endocardial curvature (K) and the ventricular wall thickness (h) were measured in the borderzone before and 1 hour after infarction.



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  		Fig 1. Method of measuring endocardial radius of curvature (R) demonstrated for a single postinfarction short-axis contrast echocardiogram. In all sheep, there was a sharp demarcation of the infarct at its septal border. The line of demarcation was decidedly distinct on cine echocardiogram; reference to the video allowed precise location of the infarct line in the still images. (APM = anterior papillary muscle; PPM = posterior papillary muscle; point 1 = septal border of the infarct; point 2 = posterior border or observed flattening; point 3 = midpoints of points 1 and 2.)

 


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  		Fig 2. A two-dimensional contrast echocardiographic image showing borderzone (BZ) endocardial curvature in a long-axis plane; the endocardium is convex toward the left ventricle (LV) cavity after myocardial infarction. Arrow on drawing indicates infarct line. (RV = right ventricle.)

 
All 18 3DCE rotational cross-sectional images were analyzed as follows. Endocardial and epicardial contours were traced (UTHSCSA ImageTool; Department of Dental Diagnostic Science, University of Texas Health Science Center, San Antonio, Texas) by an echocardiography technician unaware of the hypotheses of the study. The endocardium and epicardium were reconstructed at end systole by tracing each in every individual rotational cross-section. At each endocardial and epicardial location, the presence or absence of myocardial perfusion was determined; thereby, perfusion status was registered with LV geometry, allowing precise and unambiguous determination of borderzone myocardium. The cross-sectional data were then combined to recreate a three-dimensional representation of the LV endocardial and epicardial surfaces, indexed by perfusion status. The endocardial and epicardial surfaces were fit using a smoothing thin-plate spline (x), and the characteristics of this surface, including spatially resolved Gaussian curvature, were calculated. Gaussian curvature (K) is defined as:


{2250.05010027.si1}

(1)


   Results
Top
 Abstract
 Introduction
 Material and Methods
 Results
Comment
 Acknowledgments
 References
 
The results of the 2DCE study performed on the first group of 4 animals are summarized in Table 1. In the short-axis cross-sectional direction the endocardial contour became flatter as borderzone K decreased with infarction from 0.86 ± 0.33 cm–2 to 0.35 ± 0.19 cm–2 (p < 0.05). Borderzone wall thickness also decreased from 1.14 ± 0.26 cm to 1.01 ± 0.25 cm (p < 0.05) in the short axis.


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  		Table 1. Two-Dimensional Contrast Echocardiography Results a
 
In contrast, in the long-axis cross-sectional direction, borderzone wall thickness increased (1.06 ± 0.17 cm to 1.27 ± 0.21 cm, p = 0.05) and curvature became negative with infarction indicating that the endocardial contour, concave toward the ventricular cavity before infarction (K = 0.28 ± 0.08 cm–2), became convex toward the ventricular cavity (K = –0.61 ± 0.15 cm–2) in the infarcted LV. These results indicate that the geometric conformation of the LV endocardial surface changes from an elliptic paraboloid before infarction to a hyperbolic paraboloid after infarction.

These complex changes in borderzone geometry as assessed by 2DCE were compared with a group of 4 additional sheep that were studied using 3DCE, as described above. Figure 3 demonstrates a representative rotational cross-sectional image from a postinfarction 3DCE data set. For each sheep, 18 of these cross-sectional images were combined into a postinfarction wire-mesh model of the LV, as illustrated in Figure 4. Surfaces representing the endocardial and epicardial contours were laid over the wire-mesh structure, as in Figure 5.



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  		Fig 3. A representative rotational cross-sectional image from a postinfarction three-dimensional contrast echocardiogram data set. The yellow line represents the endocardial contour. The green line represents the epicardial contour. The red line encloses unperfused myocardium.

 


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  		Fig 4. (Left) A postinfarction wire-mesh model of the left ventricle in one sheep. These models were generated by tracing the endocardial and epicardial contours, as well as the perfusion defect, in the 18 cross-sectional images comprising a complete rotational three-dimensional echo data set. The green lines represent perfused epicardium, yellow lines represent perfused endocardium, and red lines represent the perfusion defect. (Right) The same ventricle viewed from its base, illustrating the rotational nature of the data set.

 


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  		Fig 5. A wire-mesh structure with surfaces representing the endocardial and epicardial contours overlaid. (Green area = perfused endocardium; dark red area = ischemic endocardium; dark purple = ischemic epicardium; LAD = left anterior descending artery.)

 
Finally, the Gaussian curvature over spline surface fits to both the endocardial and epicardial surface models. Representative results of this geometric analysis are presented for a single postinfarction sheep LV in Figure 6. This figure confirms a regional heterogeneity in both endocardial and epicardial surface curvature, in that the borderzone myocardium at the margin of the nonperfused infarct assumes a deformed geometrical conformation. Both endocardial and epicardial curvature was found to be highly dependent on the location within the ventricle. As one would have predicted from the prior 2DCE results, azimuthal (short axis) curvature tended to decrease in the area of the BZM that was closest to the septum and base of the heart, while the paradoxical change in concavity (ie, negative curvature) in the direction of zenith was consistently demonstrated in the lateral and more apical segments of the BZM (Fig 6).



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  		Fig 6. The left ventricle of a single postinfarction sheep. Gaussian curvature, calculated from spline surface fits to the epicardial (left) and endocardial (right) surfaces, is indicated by pseudocolor (medium blue = 1.5 cm-2; blue gray = 0.5 cm-2; olive green = 0.0 cm-2; light olive green = –0.5 cm-2; and yellow = –1.5 cm-2). The borderzone myocardium at the margin of the nonperfused infarct assumes a deformed geometrical conformation, confirming a regional heterogeneity in surface curvature.

 

   Comment
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
Acknowledgments
 References
 
The incidence of heart failure has risen steadily in developed countries during the last 50 years while 5-year survival after diagnosis has remained stubbornly around 50% [18]. Infarction-induced remodeling is now responsible for nearly 70% of all cases of heart failure [1].

It has been recognized for nearly 3 decades [19] that the myocardium adjacent to an infarction is functionally impaired even though perfusion remains normal. Recent work by our group and others has identified the borderzone as a region of myocardium in which the impetus for remodeling is established and sustained. Studying the perturbation of regional myocardial mechanics and geometry that are initiated by a myocardial infarction has the potential for an improved understanding of this insidious pathologic process as well as the development of better preventative and diagnostic strategies.

A study of regional mechanics after MI is dependent on a tool that allows precise registration of local perfusion status, geometry and function. While a combination of marker imaging technology and microsphere injection has provided valuable data that have helped to elucidate the remodeling phenomenon [12, 20], they cannot be applied clinically and provide, at best, two dimensional strain data that are laborious to analyze. Contrast echocardiography has the potential to overcome these deficiencies with the added benefit of being portable and relatively inexpensive.

Although contrast echocardiography is currently the best clinically relevant imaging modality for identifying and following BZM acutely and chronically, the few existing studies using this technique to assess BZM have been limited to two-dimensional studies and have uniformly focused on assessing contractile function, ignoring the analysis of geometric changes [21, 22].

Using an ovine model of acute anteroapical MI that undergoes early expansion and results in adverse long-term remodeling, we have demonstrated the ability of contrast echocardiography to identify and characterize subtle but consistent changes in BZM geometry that occur immediately after a MI. Early increases in BZM stress resulting from acute changes in the geometry of this region of myocardium have been implicated as an important inciting mechanism for the development of adverse ventricular remodeling and the subsequent development of congestive heart failure [12, 14, 17]. The results of the 2DCE analysis in both long and short axis demonstrated a surprising complexity in borderzone geometry immediately after an acute anteroapical infarction. The short-axis data demonstrated decreased BZM curvature and wall thickness immediately after infarction which is consistent with increased regional stress. However, the analysis in the long-axis direction demonstrated a seemingly paradoxical BZM thickening as well as a change in curvature from concave toward the ventricular cavity before infarction to convex toward the ventricle after infarction. The three-dimensional analysis confirmed these findings, and provided a better and more complete understanding of the regional heterogeneity of BZM geometry.

This study confirms the dynamic nature of BZM geometry early after an acute MI and the probable importance of this region to the phenomenon of infarction-induced remodeling. However, the data suggest that explanations which attribute the initiation and progression of ventricular remodeling to increased regional BZM wall stress may be overly simplistic. For the first time we have demonstrated the ability of 3DCE to assess the complex nature of the geometric changes that affect the BZM after MI. Our data strongly support the use of 3DCE over 2DCE for studies attempting to elucidate the mechanism of infarction-induced LV remodeling.

New pharmacologic, cell-based, and surgical therapies hold promise for improving the outcome of infarction-induced remodeling; however, it is becoming increasingly apparent that results will be optimized when treatment is instituted early after MI with the intent of preventing rather than reversing remodeling.

Determination of efficacy and ultimate clinical acceptance of such innovative therapies will be greatly potentiated by an imaging technique that can reliably assess the long-term risk for adverse remodeling when performed early after MI. Such a tool would also greatly improve the cost effectiveness of such therapy by allowing only those patients at significant risk for adverse remodeling to undergo prophylactic treatment.

Thus, there is a growing need to develop a reliable imaging modality that is capable of identifying patients at high risk for left ventricular dilatation early after MI. We believe that contrast-enhanced three-dimensional echocardiography can be developed to address this critical and expanding, yet unmet clinical need.

Although our results are encouraging, there are, however, important technical issues in this study that limit the immediate application of this modality to patients. All the three-dimensional data were collected with a rotational three-dimensional probe that required long acquisition times and necessitated data acquisition over 18 cardiac cycles. This weakness will be greatly mitigated by the use of the new Phillips iE33 system and xMatrix real-time three-dimensional echocardiographic probe.

The use of contrast in three-dimensional echocardiography is itself a nascent field. In spite of this fact, we were able to achieve excellent delineation between infarcted and perfused myocardium using direct coronary injection of contrast media. Further work will be required to develop a clinically applicable technique for contrast administration (ie, intravenous delivery).

Finally, all the work presented here was obtained in a highly idealized model of a large, transmural, apical infarction that is known to adversely remodel. The effectiveness of 3DCE in assessing BZM geometry will need to be studied in models in which infarct size, location, and reperfusion status are varied to replicate clinically realistic scenarios.


   Acknowledgments
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
References
 
Supported by HL63954, HL71137, HL73021 and HL76560 from the National Heart Lung Blood Institute, National Institutes of Health, Bethesda, Maryland, by a grant from the Mary L. Smith Charitable Trust, Newtown Square, Pennsylvania, and by the W.W. Smith Charitable Trust, Newtown Square, Pennsylvania.


   References
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 

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