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

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DOI: 10.1016/j.athoracsur.2005.05.103 2005;80:2250-2255 Ann Thorac Surg C. Gorman Robert Hiroaki Sakamoto, Theodore Plappert, Martin G. St. John Sutton, Ivan Salgo and Benjamin M. Jackson, Landi M. Parish, Joseph H. Gorman, III, Yoshiharu Enomoto, Contrast Enhanced Echocardiographic Study Borderzone Geometry After Acute Myocardial Infarction: A Three-Dimensional http://ats.ctsnetjournals.org/cgi/content/full/80/6/2250 located on the World Wide Web at: The online version of this article, along with updated information and services, is Print ISSN: 0003-4975; eISSN: 1552-6259. Southern Thoracic Surgical Association. Copyright © 2005 by The Society of Thoracic Surgeons. is the official journal of The Society of Thoracic Surgeons and the The Annals of Thoracic Surgery by on June 1, 2013 ats.ctsnetjournals.org Downloaded from

Transcript of Borderzone Geometry After Acute Myocardial Infarction: A Three-Dimensional Contrast Enhanced...

DOI: 10.1016/j.athoracsur.2005.05.103 2005;80:2250-2255 Ann Thorac Surg

C. Gorman RobertHiroaki Sakamoto, Theodore Plappert, Martin G. St. John Sutton, Ivan Salgo and

Benjamin M. Jackson, Landi M. Parish, Joseph H. Gorman, III, Yoshiharu Enomoto, Contrast Enhanced Echocardiographic Study

Borderzone Geometry After Acute Myocardial Infarction: A Three-Dimensional

http://ats.ctsnetjournals.org/cgi/content/full/80/6/2250located on the World Wide Web at:

The online version of this article, along with updated information and services, is

Print ISSN: 0003-4975; eISSN: 1552-6259. Southern Thoracic Surgical Association. Copyright © 2005 by The Society of Thoracic Surgeons.

is the official journal of The Society of Thoracic Surgeons and theThe Annals of Thoracic Surgery

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orderzone Geometry After Acute Myocardialnfarction: A Three-Dimensional Contrast Enhancedchocardiographic Study

enjamin M. Jackson, MD, Landi M. Parish, SB, Joseph H. Gorman III, MD,oshiharu Enomoto, MD, Hiroaki Sakamoto, MD, Theodore Plappert, CVT,artin G. St. John Sutton, MSSB, Ivan Salgo, MD, and Robert C. Gorman, MD

arrison Department of Surgical Research and Department of Medicine, Division of Cardiology, University of Pennsylvania

chool of Medicine, Philadelphia, Pennsylvania, and Philips Medical Systems, Andover, Massachussetts

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Background. Regional myocardial geometry, function,nd perfusion status are critical variables for understand-ng infarction-induced left ventricle (LV) remodeling.hree-dimensional contrast echocardiography (3DCE) isniquely suited to measure these parameters. We evalu-te the ability of 3DCE to assess geometric changes in theormally perfused but hypocontractile borderzone myo-ardium (BZM) immediately after a myocardial infarc-ion (MI) in an ovine model, and we compare 3DCE withwo-dimensional contrast echocardiography (2DCE) inhe long and short axis.

Methods. Four sheep were studied with 3DCE and 4ere studied using 2DCE, before and 30 minutes after an

nteroapical MI. Each 3DCE data set was acquired over8 consecutive cardiac cycles. The LV geometry waseconstructed and perfusion data spatially correlated,hereby constituting a 3D model of ventricular geometrynd perfusion. The borderzone was defined as the con-

rast-perfused myocardium adjacent to the infarct.

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2005 by The Society of Thoracic Surgeonsublished by Elsevier Inc

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Results. The 2DCE short-axis analysis demonstratedecreased curvature and decreased wall thickness in theorderzone after MI. These findings are consistent with

ncreased BZM wall stress. However, the long-axis 2DCEnalysis demonstrated increased BZM wall thicknessnd a surprising change in BZM concavity acutely afternfarction. The 3DCE analysis confirmed these findingsnd added additional information regarding regionalariability in BZM geometry that was not evident in thewo orthogonal 2D views.

Conclusions. This study provides evidence that re-ional changes in BZM geometry are more complex thanreviously believed and are not necessarily indicative of

ncreased regional stress. The superiority of 3DCE overDCE for assessing these changes is strongly supported.

(Ann Thorac Surg 2005;80:2250–6)

© 2005 by The Society of Thoracic Surgeons

yocardial infarction (MI) is the most common causeof congestive heart failure [1]. The left ventricular

LV) response to MI is dependent on a complex interac-ion between infarction size, location, transmurality, anderfusion status [2–5]. When conditions favor infarctxpansion, LV remodeling leading to ventricular dilata-ion and congestive heart failure is induced [6]. Ventric-lar dilatation—once established—is difficult to treat andortends a poor long term outcome [7]; however, the timeourse and extent of ventricular remodeling after MI isighly variable and difficult to predict in the early postin-

arction period [8, 9]. This heterogeneity impedes thebility to identify patients at risk for MI-induced remod-ling and subsequent congestive heart failure.Recent laboratory studies have emphasized the impor-

ance of the normally perfused but hypocontractile bor-erzone myocardium (BZM) to the remodeling process

ccepted for publication May 12, 2005.

ddress correspondence to Dr Robert C. Gorman, Harrison Departmentf Surgical Research, University of Pennsylvania School of Medicine, 313

nd the development of congestive heart failure [10–12].he BZM initially involves a narrow perimeter around

he infarct, but as remodeling occurs the BZM extends tonvolve more normally perfused myocardium, until con-estive heart failure develops [12, 13].Because of the proposed importance of BZM stress to

he initiation of the remodeling process [12, 14], a corre-ation between BZM geometric changes early after MI (as

measurable surrogate for stress) and the outcome ofemodeling would allow for the identification of patientst risk for adverse remodeling and congestive heartailure.

Contrast-enhanced echocardiography has the ability torecisely register myocardial perfusion status, function,nd geometry, making it a technique with potential forescribing the borderzone myocardium during the re-odeling process.Technologic advancements in three-dimensional echo-

Dr Salgo discloses a financial relationship with Philips

Medical Systems.

0003-4975/05/$30.00doi:10.1016/j.athoracsur.2005.05.103

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ardiography have improved image quality, allowedeal-time imaging, and increased the availability of thisardiac imaging modality. Its use in combination withmproved echocardiographic contrast agents and deliv-ry techniques may result in an ideal tool for studyinghe remodeling phenomenon.

In this study we evaluated the ability of two-imensional contrast echocardiography (2DCE) and

hree-dimensional contrast echocardiography (3DCE) tossess BZM geometry early after MI in a standardizedvine model of adverse postinfarction remodeling.

aterial and Methods

urgical Protocolight sheep were induced with thiopental sodium (10 to5 mg/kg), intubated, anesthetized with isoflurane (1.5%

ig 1. Method of measuring endocardial radius of curvature (R)emonstrated for a single postinfarction short-axis contrast echocar-iogram. In all sheep, there was a sharp demarcation of the infarctt its septal border. The line of demarcation was decidedly distinctn cine echocardiogram; reference to the video allowed precise loca-ion of the infarct line in the still images. (APM � anterior papil-ary muscle; PPM � posterior papillary muscle; point 1 � septalorder of the infarct; point 2 � posterior border or observed flatten-ng; point 3 � midpoints of points 1 and 2.)

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o 2.0%), and ventilated with oxygen (Drager anesthesiaonitor; North American Drager, Telford, Pennsylvania).ll animals received glycopyrrolate (0.4 mg, intrave-ously) and cefazolin (1 g, intravenously, both before andfter operation). Animals were treated in complianceith “Guide for the Care and Use of Laboratory Ani-als,” published by the National Institutes of Health

NIH publication 85-23, revised 1985). The surface elec-rocardiogram (ECG) and arterial blood pressure wereontinuously monitored.

Using sterile surgical technique, a left anterolateralhoracotomy was performed in the fifth interspace.olypropylene snares were placed around the left ante-ior descending artery (LAD) and second diagonal (D2)oronary arteries (approximately 40% from the apex).he animal was allowed to recover. Ligation of theserteries leads to a transmural apical infarction involving2% � 3% of the LV mass. Infarct expansion (stretching)ccurs immediately [12] but heart failure does not occurcutely. Congestive heart failure and left ventricularneurysm formation ensue over 8 weeks as infarction-nduced remodeling ensues [15].

nfarctionfter 10 to 14 days, sheep were again anesthetized andlaced supine. Four animals underwent 2DCE; subse-uently, another group of 4 animals was studied usingDCE. Baseline echocardiographic images were recordeds described below, without injection of contrast. Thexteriorized subcutaneous snares were tightened. Oncehe animal stabilized (approximately 1 hour), postinfarc-ion contrast-enhanced echocardiographic measure-

ents were made.

chocardiographic Data Collectionubdiaphragmatic echocardiographic images were ob-

ained through a sterile, midline laparotomy as previ-usly described [16]. In the first group of 4 animals, 2DCEas performed using a second harmonic technique

SONOS 5500; Philips, Andover, Massachusetts). Forach recording of perfusion and wall motion, 0.5 mLptison (albumen with octafluoropropane gas) echocar-iographic contrast agent (GE Healthcare, London,nited Kingdom) was injected directly into the left cor-nary ostium through a percutaneously inserted coro-ary angiographic catheter. Short-axis cross-sectional

mages at the level of the midpapillary muscles andong-axis images (four-chamber) were recorded continu-usly during the injection of contrast. Subsequently, in

Fig 2. A two-dimensional contrast echocardio-graphic image showing borderzone (BZ) endo-cardial curvature in a long-axis plane; theendocardium is convex toward the left ventri-cle (LV) cavity after myocardial infarction.Arrow on drawing indicates infarct line. (RV� right ventricle.)

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2252 JACKSON ET AL Ann Thorac SurgBORDERZONE GEOMETRY AFTER ACUTE MI 2005;80:2250–6

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he second group of 4 sheep, 3DCE was performed usinghe Philips SONOS 5500 module with a R50-12 rotationalltrasound probe. At the initiation of each 3D data setcquisition, 0.5 mL Optison contrast agent was injectedirectly into the left coronary ostium. Using electrocar-iographic gating, images were acquired over 18 consec-tive heartbeats at angular increments of 10 degrees.

ata Analysisll images were analyzed off-line. All measurementsere made at end systole, identified as the frame athich LV cavity area was smallest. All plots representing

hree-dimensional renderings were created using Tec-lot (Version 10; Amtec Engineering, Bellevue, Washing-

on). Spline surface fits and Gaussian curvatures werealculated in Matlab. All measurements are presented aseans � SD. Comparisons are made between baseline

nd postinfarction using paired t tests.The image processing and data analysis performed for

he 2DCE data in both long and short axis has beenescribed previously, and the techniques are illustrated

n Figures 1 and 2 (unpublished data: Jackson BM,orman JH III, Parish LB, et al. Early changes in border-

one geometry after myocardial infarction: a contrastchocardiographic study, 2005) [17]. Briefly, the endocar-ial curvature (K) and the ventricular wall thickness (h)ere measured in the borderzone before and 1 hour after

nfarction.All 18 3DCE rotational cross-sectional images were

nalyzed as follows. Endocardial and epicardial contoursere traced (UTHSCSA ImageTool; Department of Den-

al Diagnostic Science, University of Texas Health Sci-nce Center, San Antonio, Texas) by an echocardiogra-hy technician unaware of the hypotheses of the study.he endocardium and epicardium were reconstructed atnd systole by tracing each in every individual rotationalross-section. At each endocardial and epicardial loca-ion, the presence or absence of myocardial perfusionas determined; thereby, perfusion status was registered

able 1. Two-Dimensional Contrast Echocardiographyesultsa

Baseline1 HourPost-MI Significance

ong-axis cross-sectionalechocardiography

K (cm�2) 0.28 � 0.08 �0.61 � 0.15 p � 0.01h (cm) 1.06 � 0.17 1.27 � 0.21 p � 0.05

hort-axis cross-sectionalechocardiography

K (cm�2) 0.86 � 0.33 0.35 � 0.19 p � 0.05h (cm) 1.14 � 0.26 1.01 � 0.25 p � 0.05

Borderzone wall thickness (h) and Gaussian curvature (K) calculatedrom long-axis and short-axis cross-sectional echocardiogram in 4 sheepefore and 1 hour after myocardial infarction. Negative curvature isonvex toward the ventricular cavity.

ith LV geometry, allowing precise and unambiguous m

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etermination of borderzone myocardium. The cross-ectional data were then combined to recreate a three-imensional representation of the LV endocardial andpicardial surfaces, indexed by perfusion status. Thendocardial and epicardial surfaces were fit using amoothing thin-plate spline (x), and the characteristics ofhis surface, including spatially resolved Gaussian curva-ure, were calculated. Gaussian curvature (K) is defineds:

K �det �XuuXuXv� det �XvvXuXv� � �det �XuvXuXv��2

��Xu�2�Xv�2 � �Xu · Xv�2�2

(1)

esults

he results of the 2DCE study performed on the firstroup of 4 animals are summarized in Table 1. In thehort-axis cross-sectional direction the endocardial con-our became flatter as borderzone K decreased withnfarction from 0.86 � 0.33 cm�2 to 0.35 � 0.19 cm�2 (p �.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.In contrast, in the long-axis cross-sectional direction,

orderzone wall thickness increased (1.06 � 0.17 cm to.27 � 0.21 cm, p � 0.05) and curvature became negativeith infarction indicating that the endocardial contour,

oncave toward the ventricular cavity before infarction (K0.28 � 0.08 cm�2), became convex toward the ventric-

lar cavity (K � �0.61 � 0.15 cm�2) in the infarcted LV.hese results indicate that the geometric conformation of

he LV endocardial surface changes from an ellipticaraboloid before infarction to a hyperbolic paraboloidfter infarction.

ig 3. A representative rotational cross-sectional image from aostinfarction three-dimensional contrast echocardiogram data set.he yellow line represents the endocardial contour. The green lineepresents the epicardial contour. The red line encloses unperfused

yocardium.

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These complex changes in borderzone geometry asssessed by 2DCE were compared with a group of 4dditional sheep that were studied using 3DCE, as de-cribed above. Figure 3 demonstrates a representativeotational cross-sectional image from a postinfarctionDCE data set. For each sheep, 18 of these cross-sectionalmages were combined into a postinfarction wire-mesh

odel of the LV, as illustrated in Figure 4. Surfacesepresenting the endocardial and epicardial contoursere laid over the wire-mesh structure, as in Figure 5.Finally, the Gaussian curvature over spline surface fits

o both the endocardial and epicardial surface models.epresentative results of this geometric analysis areresented for a single postinfarction sheep LV in Figure. This figure confirms a regional heterogeneity in bothndocardial and epicardial surface curvature, in that theorderzone myocardium at the margin of the nonper-

used infarct assumes a deformed geometrical conforma-ion. Both endocardial and epicardial curvature wasound to be highly dependent on the location within theentricle. As one would have predicted from the priorDCE results, azimuthal (short axis) curvature tended toecrease in the area of the BZM that was closest to theeptum and base of the heart, while the paradoxicalhange in concavity (ie, negative curvature) in the direc-ion of zenith was consistently demonstrated in theateral and more apical segments of the BZM (Fig 6).

ommenthe incidence of heart failure has risen steadily in devel-ped countries during the last 50 years while 5-yearurvival after diagnosis has remained stubbornly around0% [18]. Infarction-induced remodeling is now respon-ible for nearly 70% of all cases of heart failure [1].

It has been recognized for nearly 3 decades [19] that theyocardium adjacent to an infarction is functionally

mpaired even though perfusion remains normal. Recent

ork by our group and others has identified the border- �

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one as a region of myocardium in which the impetus foremodeling is established and sustained. Studying theerturbation of regional myocardial mechanics and ge-metry that are initiated by a myocardial infarction has

Fig 4. (Left) A postinfarctionwire-mesh model of the left ven-tricle in one sheep. These modelswere generated by tracing theendocardial and epicardial con-tours, as well as the perfusiondefect, in the 18 cross-sectionalimages comprising a completerotational three-dimensionalecho data set. The green linesrepresent perfused epicardium,yellow lines represent perfusedendocardium, and red lines rep-resent the perfusion defect.(Right) The same ventricleviewed from its base, illustrat-ing the rotational nature of thedata set.

ig 5. A wire-mesh structure with surfaces representing the endocar-ial and epicardial contours overlaid. (Green area � perfused en-ocardium; dark red area � ischemic endocardium; dark purple

ischemic epicardium; LAD � left anterior descending artery.)

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he potential for an improved understanding of thisnsidious pathologic process as well as the developmentf better preventative and diagnostic strategies.A study of regional mechanics after MI is dependent

n a tool that allows precise registration of local perfu-ion status, geometry and function. While a combinationf marker imaging technology and microsphere injectionas provided valuable data that have helped to elucidate

he remodeling phenomenon [12, 20], they cannot bepplied clinically and provide, at best, two dimensionaltrain data that are laborious to analyze. Contrast echo-ardiography has the potential to overcome these defi-iencies with the added benefit of being portable andelatively inexpensive.

Although contrast echocardiography is currently theest clinically relevant imaging modality for identifyingnd following BZM acutely and chronically, the fewxisting studies using this technique to assess BZM haveeen limited to two-dimensional studies and have uni-

ormly focused on assessing contractile function, ignor-ng the analysis of geometric changes [21, 22].

Using an ovine model of acute anteroapical MI thatndergoes early expansion and results in adverse long-

erm remodeling, we have demonstrated the ability ofontrast echocardiography to identify and characterizeubtle but consistent changes in BZM geometry thatccur immediately after a MI. Early increases in BZMtress resulting from acute changes in the geometry ofhis region of myocardium have been implicated as anmportant inciting mechanism for the development ofdverse ventricular remodeling and the subsequent de-elopment of congestive heart failure [12, 14, 17]. Theesults of the 2DCE analysis in both long and short axisemonstrated a surprising complexity in borderzoneeometry immediately after an acute anteroapical infarc-ion. The short-axis data demonstrated decreased BZMurvature and wall thickness immediately after infarctionhich is consistent with increased regional stress. How-

ver, the analysis in the long-axis direction demonstratedseemingly paradoxical BZM thickening as well as a

ig 6. The left ventricle of a single postinfarc-ion sheep. Gaussian curvature, calculated frompline surface fits to the epicardial (left) andndocardial (right) surfaces, is indicated byseudocolor (medium blue � 1.5 cm-2; blueray � 0.5 cm-2; olive green � 0.0 cm-2; lightlive green � –0.5 cm-2; and yellow � –1.5m-2). The borderzone myocardium at the mar-in of the nonperfused infarct assumes a de-ormed geometrical conformation, confirming aegional heterogeneity in surface curvature.

hange in curvature from concave toward the ventricular A

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avity before infarction to convex toward the ventriclefter infarction. The three-dimensional analysis con-rmed these findings, and provided a better and moreomplete understanding of the regional heterogeneity ofZM geometry.This study confirms the dynamic nature of BZM geom-

try early after an acute MI and the probable importancef this region to the phenomenon of infarction-inducedemodeling. However, the data suggest that explanationshich attribute the initiation and progression of ventric-lar remodeling to increased regional BZM wall stressay be overly simplistic. For the first time we have

emonstrated the ability of 3DCE to assess the complexature of the geometric changes that affect the BZM afterI. Our data strongly support the use of 3DCE over

DCE for studies attempting to elucidate the mechanismf infarction-induced LV remodeling.New pharmacologic, cell-based, and surgical therapies

old promise for improving the outcome of infarction-nduced remodeling; however, it is becoming increas-ngly apparent that results will be optimized when treat-

ent is instituted early after MI with the intent ofreventing rather than reversing remodeling.Determination of efficacy and ultimate clinical accep-

ance of such innovative therapies will be greatly poten-iated by an imaging technique that can reliably assesshe long-term risk for adverse remodeling when per-ormed early after MI. Such a tool would also greatlymprove the cost effectiveness of such therapy by allow-ng only those patients at significant risk for adverseemodeling to undergo prophylactic treatment.

Thus, there is a growing need to develop a reliablemaging modality that is capable of identifying patients atigh risk for left ventricular dilatation early after MI. Weelieve that contrast-enhanced three-dimensional echo-ardiography can be developed to address this criticalnd expanding, yet unmet clinical need.Although our results are encouraging, there are, how-

ver, important technical issues in this study that limithe immediate application of this modality to patients.

ll the three-dimensional data were collected with a

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otational three-dimensional probe that required longcquisition times and necessitated data acquisition over8 cardiac cycles. This weakness will be greatly mitigatedy the use of the new Phillips iE33 system and xMatrixeal-time three-dimensional echocardiographic probe.

The use of contrast in three-dimensional echocardiog-aphy is itself a nascent field. In spite of this fact, we wereble to achieve excellent delineation between infarctednd perfused myocardium using direct coronary injec-ion of contrast media. Further work will be required toevelop a clinically applicable technique for contrastdministration (ie, intravenous delivery).Finally, all the work presented here was obtained in a

ighly idealized model of a large, transmural, apicalnfarction that is known to adversely remodel. The effec-iveness of 3DCE in assessing BZM geometry will need toe studied in models in which infarct size, location, andeperfusion status are varied to replicate clinically real-stic scenarios.

upported by HL63954, HL71137, HL73021 and HL76560 fromhe National Heart Lung Blood Institute, National Institutes of

ealth, Bethesda, Maryland, by a grant from the Mary L. Smithharitable Trust, Newtown Square, Pennsylvania, and by the.W. Smith Charitable Trust, Newtown Square, Pennsylvania.

eferences

1. Gheorghiade M, Bonow RO. Chronic heart failure in theUnited States: a manifestation of coronary artery disease.Circulation 1998;97:282–9.

2. Stone PH, Raabe DS, Jaffe AS, et al. Prognostic significanceof location and type of myocardial infarction: independentadverse outcome associated with anterior location. J Am CollCardiol 1988;11:453–63.

3. Berger CJ, Murabito JM, Evans JC, Anderson KM, Levy D.Prognosis after first myocardial infarction: comparison ofQ-wave and non–Q-wave myocardial infarction in the Fra-mingham Heart Study. JAMA 1992;268:1545–51.

4. Chareonthaitawee P, Christian TF, Hirose K, Gibbons RJ,Rumberger JA. Relation of initial infarct size to extent of leftventricular remodeling in the year after acute myocardialinfarction. J Am Coll Cardiol 1995;25:567–73.

5. Bolognese L, Cerisano G, Buonamici P, et al. Influence ofinfarct-zone viability on left ventricular remodeling follow-ing acute myocardial infarction. Circulation 1997;96:3353–9.

6. Weisman HF. Healy B. Myocardial infarct expansion, infarctextension, and reinfarction: pathophysiologic concepts. Prog

Cardiovasc Dis 1987;30:73–110.

hanges inducing and perpetuating LV remodeling, and

es

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2005 by The Society of Thoracic Surgeonsublished by Elsevier Inc

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7. St John Sutton MG, Pfeffer MA, Plappert T, et al. Quantita-tive two-dimensional echocardiographic measurements aremajor predictors of adverse cardiovascular events after acutemyocardial infarction. The protective effects of captopril.Circulation 1994;89:68–75.

8. Bolognese L, Neskovic AN, Parodi G, et al. Left ventricularremodeling after primary coronary angioplasty: patterns ofleft ventricular dilation and long-term prognostic implica-tions. Circulation 2002;106:2351–7.

9. Giannuzzi P, Temporelli PL, Bosimini E, et al. Heterogeneityof left ventricular remodeling after acute myocardial infarc-tion: results of the Gruppo Italiano per lo Studio dellaSopravvivenza nell’Infarto Miocardico-3 Echo Substudy. AmHeart J 2001;141:131–8.

0. Moulton MJ, Downing SW, Creswell LL, et al. Mechanicaldysfunction in the border zone of an ovine model of leftventricular aneurysm. Ann Thorac Surg 1995;60:986–98.

1. Kramer CM, Lima JA, Reichek N, et al. Regional differencesin function within noninfarcted myocardium during leftventricular remodeling. Circulation 1993;88:1279–88.

2. Jackson BM, Gorman JH III, Moainie S, et al. Extension ofborderzone myocardium in postinfarction dilated cardiomy-opathy. J Am Coll Cardiol 2002;40:1160–7.

3. Lima JA, Becker LC, Melin JA, et al. Impaired thickening ofnonischemic myocardium during acute regional ischemia inthe dog. Circulation 1985;71:1048–59.

4. Guccione JM, Moonly SM, Moustakidis P, et al. Mechanismunderlying mechanical dysfunction in the borderzone of leftventricular aneurysm: a finite element model study. AnnThorac Surg 2001;71:654–62.

5. Markovitz LJ, Savage EB, Ratcliffe MB, et al. Large animalmodel of left ventricular aneurysm. Ann Thorac Surg 1989;48:838–45.

6. Kelley ST, Malekan R, Gorman JH III, et al. Restraininginfarct expansion preserves left ventricular geometry andfunction after acute anteroapical infarction. Circulation 1999;99:135–42.

7. Jackson BM, Gorman JH III, Salgo I, et al. Altered border-zone geometry increases wall stress after anteroapical myo-cardial infarction: a contrast echocardiographic assessment.Am J Physiol Heart Circ Physiol 2003;284:H475–9.

8. Levy D, Kenchaiah S, Larson MG, et al. Long-term trends inthe incidence of and survival with heart failure. N EnglJ Med 2002;347:1397–402.

9. Eaton LW, Weiss JL, Bulkley BH, et al. Regional cardiacdilatation after acute myocardial infarction. N Engl J Med1979;300:57–62.

0. Moainie SL, Gorman JH III, Guy TS, et al. An ovine model ofpostinfarction dilated cardiomyopathy. Ann Thorac Surg2002;74:753–60.

1. Scherrer-Crosbie M, Liel-Cohen N, Otsuji Y, et al. Myocar-dial perfusion and wall motion in infarction border zone:assessment by myocardial contrast echocardiography. J AmSoc Echocardiogr 2000;13:353–7.

2. Sakai K, Kozo W, Millard RW. Defining the mechanicalborderzone: a study in the pig heart. Am J Physiol

1985;249:H88–94.

NVITED COMMENTARY

urgeons are increasingly challenged by the sequelae ofeft ventricular remodeling secondary to ischemic heartisease. Current therapeutic options in ischemic end-tage heart failure surgery (ie, surgical ventricular resto-ation, restrictive mitral annuloplasty, and application ofardiac support devices) are empirically implementednd evaluated. Although steady progress is made, veryittle is known about the underlying pathophysiologic

ven less knowledge exists as to which factors determineuccessful reverse remodeling.

With their ovine model, Jackson and colleagues [1]ave already provided many valuable contributions to-ard understanding the remodeling changes that occur

n the infarcted ventricle. In this study, they evaluate thebility of three-dimensional contrast enhanced echocar-iography (3DCE) to assess geometric changes in the

orderzone myocardium, the normally perfused but hy-

0003-4975/05/$30.00doi:10.1016/j.athoracsur.2005.07.006

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DOI: 10.1016/j.athoracsur.2005.05.103 2005;80:2250-2255 Ann Thorac Surg

C. Gorman RobertHiroaki Sakamoto, Theodore Plappert, Martin G. St. John Sutton, Ivan Salgo and

Benjamin M. Jackson, Landi M. Parish, Joseph H. Gorman, III, Yoshiharu Enomoto, Contrast Enhanced Echocardiographic Study

Borderzone Geometry After Acute Myocardial Infarction: A Three-Dimensional

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