ATS
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

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

Ann Thorac Surg 2005;79:881-887
© 2005 The Society of Thoracic Surgeons

Original article: Cardiovascular

Early Ventricular Restraint After Myocardial Infarction: Extent of the Wrap Determines the Outcome of Remodeling

Yoshiharu Enomoto, MDa, Joseph H. Gorman, III, MDa, Sina L. Moainie, MDa, Benjamin M. Jackson, MDa, Landi M. Parish, SBa, Theodore Plappert, CVTb, Ahmad Zeeshan, MDa, Martin G. St. John-Sutton, MBBSb, Robert C. Gorman, MDa,*

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

Abbreviations and Acronyms AAanteroapical; AACanteroapical infarct control group; AAWanteroapical infarct wrap group; CHFcongestive heart failure; D2second diagonal branch of the left anterior descending artery; ECGechocardiogram; EFejection fraction; ESMCARend-systolic muscle to cavity area ratio; IMRischemic mitral regurgitation; IVintravenous; LADleft anterior descending artery; LVleft ventricle; LVEDVleft ventricular end-diastolic volume; LVESVleft ventricular end-systolic volume; MRmitral regurgitation; OM2second obtuse marginal branch of the circumflex artery; OM3third obtuse marginal branch of the circumflex artery; PBposterobasal; PBCposterobasal infarct control group; PBPposterobasal infarct patch group; PBWposterobasal infarct wrap group; PDAposterior descending coronary artery

* Address reprint requests to Dr Robert Gorman, Department of Surgery, 6 Silverstein Pavilion, Hospital of the University of Pennsylvania, 3400 Spruce St, Philadelphia, PA 19104 (E-mail: gormanr{at}uphs.upenn.edu).

Presented at the Fortieth Annual Meeting of The Society of Thoracic Surgeons, San Antonio, TX, Jan 26–28, 2004.


   Abstract
Top
 Abstract
Introduction
 Material and Methods
 Results
 Comment
 Discussion
 Acknowledgments
 References
 
BACKGROUND: Early infarct expansion initiates adverse remodeling, leads to left ventricular dilatation and portends a poor long-term outcome. Early mechanical prevention of infarct expansion has been proposed as a method to improve remodeling, but the extent of ventricular restraint necessary to optimize the salutary effect is not known. We tested the hypothesis that left ventricular restraint (wrap) is superior to infarct stiffening (patch).

METHODS: Infarction of 20% to 25% of the left ventricle was induced by coronary ligation in 69 sheep. Infarcts were either anteroapical (n = 33) or posterobasal (n = 36). Animals with each infarct received either no treatment (anteroapical, n = 26; posterobasal, n = 17), infarct stiffening with a localized Marlex mesh patch (posterobasal, n = 9) or left ventricular wrapping with Merseline mesh (anteroapical, n = 7; posterobasal, n = 10). End-systolic volume, end-diastolic volume, end-systolic muscle to cavity area ratio, left ventricular sphericity, ejection fraction, and degree of mitral regurgitation as determined by quantitative echocardiography were assessed before infarction and at 2, 5, and 8 weeks after infarction to evaluate the extent of left ventricular remodeling.

RESULTS: Control animals in both groups experienced adverse remodeling. Anteroapical infarct animals developed large left ventricular aneurysms and the posterobasal infarct animals developed severe mitral regurgitation. Early infarct stiffening did not significantly improve any aspect of remodeling due to the posterobasal infarct. Early left ventricular wrapping significantly improved remodeling after both types of infarctions.

CONCLUSIONS: Early left ventricular wrapping attenuates infarct expansion and has a salutary effect on remodeling. Simple infarct stiffening alone is not effective.


   Introduction
Top
 Abstract
 Introduction
Material and Methods
 Results
 Comment
 Discussion
 Acknowledgments
 References
 
Infarction-induced left ventricular (LV) remodeling is now responsible for almost 70% of the 4.9 million cases of heart failure in the United States [1]. Early infarct expansion (ie, stretching) has been identified as the inciting event that initiates adverse remodeling and leads to LV dilatation [2, 3, 4]. Once established, ventricular dilatation is difficult to reverse and portends a poor long-term outcome [5]. These data, in conjunction with the development of emerging devices suitable for providing LV restraint in patients, [6, 7] 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.

Recent laboratory studies have, indeed, suggested that mechanical infarct restraint initiated soon after infarction can influence outcome of remodeling [8–11]. The extent of ventricular restraint required to optimally affect remodeling remains to be determined. In this study using two ovine models of infarction-induced remodeling we compared localized infarct stiffening with a Marlex mesh patch to Merseline mesh wrapping of the exposed LV on the outcome of remodeling.


   Material and Methods
Top
 Abstract
 Introduction
 Material and Methods
Results
 Comment
 Discussion
 Acknowledgments
 References
 
Animals and Infarction Models
We used two well-characterized models of infarction-induced adverse remodeling and CHF in sheep.

An anterioapical (AA) infarction involving 22% ± 3% of the LV mass was created in 33 animals by ligating the left anterior descending artery (LAD) and its second diagonal branch (D2) 40% of the distance from the apex to the base of the heart. This infarction reproducibly results in large LV aneurysms after 8 weeks of remodeling [12]. Twenty-six animals acted as untreated controls (AAC group). These control animals were created as part of several experimental protocols over a 5-year period since our laboratory began performing quantitative echocardiograms in sheep in 1998. Seven animals had an appropriately sized piece of Merseline mesh wrap sutured in place over the LV from base to apex and from the LAD to posterior descending coronary artery (PDA) 14 days before infarction (AAW group).

A posterobasal (PB) infarction involving 24% ± 4% of the LV mass was induced in 36 animals by ligating the second (OM2) and third (OM3) obtuse marginal branches of the circumflex artery [13, 14]. This infarction routinely results in adverse remodeling and moderate to severe ischemic mitral regurgitation after 8 weeks. Seventeen animals acted as untreated controls (PBC). Again, these control animals were created over a 5-year period since our laboratory began performing quantitative echocardiograms. Nine animals had infarct stiffening with a localized Marlex mesh patch sutured over the infarct area 14 days before infarction (PBP group). Six of these animals were included in a recent report by Moainie and colleagues [9]. Ten animals had Merseline mesh ventricular wrapping (PBW) as described for the AA infarct. These animals have been previously reported by Guy and colleagues [10].

Surgical Protocol
Dorset male sheep (Animal Biotech Industries, Doylestown, PA) 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 (IACUC) and in compliance with National Institutes of Health publication No. 85 to 23 as revised in 1985. Animals were induced with thiopental sodium (10 to 15 mg/kg intravenously [IV]) and intubated. Anesthesia was maintained with isofluorane (1.5% to 2%) and oxygen. All animals received glycopyrrolate (0.4 mg IV) and enrofloxin (10 mg/kg IV) on induction. Under aseptic conditions, animals underwent left thoracotomy and polypropylene snares were loosely placed around the appropriate coronary arteries. Control group animals (AAC and PBC) then underwent chest closure with the coronary snares left subcutaneously. Patch treated animals (PBP) had a piece of Marlex mesh (Ethicon, Somerset, NJ) fashioned to cover the area of intended infarction only (Fig 1). This patch was sewn in place using multiple 4-0 sutures. Wrap group animals (AAW and PBW) had a piece of Merseline mesh (Ethicon) appropriately tailored and sutured to the accessible LV from base to apex and from LAD to PDA (Fig 2). After placement of either restraining mechanism animals had chest closures with snares left subcutaneously. No attempt to close the pericardium was made in any animal.



View larger version (149K):
[in this window]
[in a new window]
  		Fig 1. Intraoperative photograph demonstrating placement of Marlex mesh restraint patch over posterolateral infarct territory. The base of the heart is at the bottom of the photograph, the posterior descending artery is at the left and the apex is at the top.

 


View larger version (81K):
[in this window]
[in a new window]
  		Fig 2. Intraoperative photograph demonstrating placement of the Merseline mesh ventricular wrap from anterior (left) and posterior (right) views. Wrap extends from base to apex and from left anterior descending artery to the posterior descending artery. The right ventricle is not covered by the wrap.

 
Baseline Data and Infarction
Fourteen days after initial instrumentation, the sheep were again anesthetized. The surface electrocardiogram (ECG) and arterial blood pressure were continuously monitored. Echocardiographic data were recorded as described below. The subcutaneous snares were exposed, tightened, and tied to produce a myocardial infarction. Each animal received magnesium sulfate (1g IV), amiodarone (150 mg IV), and lidocaine (3 mg/kg IV bolus, then 2 mg/min infusion) before infarction. Echocardiographic data were collected 30 minutes after infarction.

Echocardiography
Quantitative two-dimensional subdiaphragmatic echocardiograms were obtained before infarction and at 30 minutes, 2, 5, and 8 weeks after infarction. A sterile midline laparotomy (or a right or left subcostal incision) was made and subdiaphragmatic quantitative two-dimensional echocardiographic images were obtained using a 5-MHz probe (77020A; Hewlett Packard, Palo Alto, CA). Images were recorded on VHS videotape at 30 Hz (Panasonic AG-6300 VHS recorder). Left ventricular short-axis images at three levels (the tips of the papillary muscles, the bases of the papillary muscles, and the apex) and two orthogonal long axis views were recorded. Previous reports have validated the reproducibility and effectiveness of this technique for evaluating LV remodeling in sheep [8–10]. Left ventricular volumes at end-systole (LVESV) and end-diastole (LVEDV) were calculated using Simpson's rule. Ejection fraction (EF) was calculated from LVESV and LVEDV. End-systolic muscle to cavity area ratio (ESMCAR) was also determined at each time point. Ventricular sphericity at end systole was assessed as the ratio of LVESV to the volume of a sphere with a diameter equal to the LV long-axis dimension. This ratio approaches unity as the ventricle becomes more spherical. All the measured echocardiographic indexes of remodeling were normalized to their base line values. The degree of mitral regurgitation (MR) was determined quantitatively in PB infarct animals by assessing the area of the regurgitant jet as a percentage of left atrial area in the apical four-chamber view. The following grading was used: grade 1 less than 20%; grade 2 = 20% to 40%; grade 3 = 40% to 60%; and, grade 4 greater than 60% [15].

Follow-Up Studies
Echocardiographic data were collected at 30 minutes and 2, 5, and 8 weeks after infarction. Following the 8-week study, the animals were euthanized (80 mEq potassium chloride IV bolus). The heart was excised, opened, and inspected to confirm infarction size and location.

Statistics
Measurements are reported as means ± standard errors of the mean. For each dependent variable differences between groups are compared by analysis of variance (SPSS, Chicago, IL); significance was established at p < 0.05. Post hoc comparisons at each time point are performed with a Student's t tests with Bonferroni correction. Differences in degree of MR were compared using the Mann-Whitney test.


   Results
Top
 Abstract
 Introduction
 Material and Methods
 Results
Comment
 Discussion
 Acknowledgments
 References
 
Echocardiographic data are summarized in Tables 1 and 2. In the AA infarct groups all animals had significant (p < 0.05) increases in LVESV (AAC = 2.38 ± 0.12, AAW = 1.74 ± 0.35), and LVEDV (AAC = 1.78 ± 0.07, AAW = 1.32 ± 0.13) by 8 weeks after infarction (Fig 3). However, both of these parameters of remodeling were significantly less in the AAW group (p < 0.05). Normalized sphericity increased and ESCMAR decreased significantly (p < 0.05) at 8 weeks in the AAC group (respectively; 1.20 ± 0.06 and 0.86 ± 0.06) but were maintained at base line values in the AAW group (respectively; 1.01 ± 0.14 and 1.01 ± 0.07) at 8 weeks after infarction (Fig 4).


View this table:
[in this window]
[in a new window]
  		Table 1. Anterior Apical Infarct
 


View larger version (19K):
[in this window]
[in a new window]
  		Fig 3. (A) Normalized left ventricular end-systolic volume (LVESV) during remodeling in anteroapical infarct animals. (B) Normalized LVESV during remodeling in posterobasal infarct animals.

 


View larger version (18K):
[in this window]
[in a new window]
  		Fig 4. (A) Normalized end-systolic muscle to cavity area ratio (ESMCAR) during remodeling in anteroapical infarct animals. (B) Normalized ESMCAR during remodeling in posterobasal infarct animals.

 
In the PB infarct groups all animals underwent remodeling as demonstrated by significant changes in LVESV (PBC = 2.09 ± 0.17, PBP = 2.09 ± 0.18, PBW = 1.73 ± 0.17), LVEDV (PBC = 1.74 ± 0.12, PBP = 1.52 ± 0.14, PBW = 1.52 ± 0.19), sphericity (PBC = 1.44 ± 0.12, PBP = 1.55 ± 0.17, PBW = 1.33 ± 0.17), and ESMCAR (PBC = 0.67 ± 0.04, PBP = 0.67 ± 0.05, PBW = 0.91 ± 0.12) by 8 weeks after infarction (Figs 3 and 4, p < 0.05). However, LVESV, LVEDV, ESMCAR were all significantly improved by ventricular wrapping when compared to the control and patch groups (p < 0.05). The PBP group was not significantly different from PBC group with respect to any variable of remodeling. MR was significantly reduced in both the PBP and PBW groups compared with the PBC group (Fig 5, p < 0.05).



View larger version (16K):
[in this window]
[in a new window]
  		Fig 5. Degree of mitral regurgitation (MR) graded on a scale of 0 to 4 (0 = no MR, 4 = severe MR) in posterobasal infarct animals.

 

   Comment
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
Discussion
 Acknowledgments
 References
 
All animals in this study experienced adverse remodeling as demonstrated by increased ventricular volumes and changes in ventricular shape. These data indicate the powerful stimulus for remodeling that a 20% to 25% transmural infarct imposes on the LV. In spite of this stimulus to remodel, extensive LV mesh wrapping significantly attenuated the remodeling process in both anteroapical and posterobasal infarcts. Patch infarct stiffening, however, did not produce a significant improvement in remodeling when compared to controls. Moainie and colleagues had previously reported a nonsignificant trend toward improved remodeling with mesh infarct stiffening in the posterobasal infarct model [9]. This trend was, however, lost in the current study with the addition of three additional animals to the treatment group and subsequent comparison of these treatment animals to a larger historical control group.

The results of the current experiment confirm and extend the findings of Guy and colleagues [10], which demonstrated a benefit on remodeling of ventricular wrapping in the posterobasal ovine infarct model. Pilla and colleagues [11] have reported a beneficial effect of early postinfarction circumferential heart wrapping (ie, including the right ventricle) in an ovine model of dilated ischemic cardiomyopathy not associated with LV aneurysm or IMR. All these studies considered together suggest that extensive ventricular wrapping can significantly reduce infarction-induced remodeling, but that simple infarct stiffening is insufficient.

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, 16]. The stretch-induced myopathic process has been associated with myocyte apoptosis [17] and disruption of the extracellular matrix secondary to activation of matrix metalloproteinases [18]. The failure of surgical reshaping operations and interventions for IMR to improve survival in ischemic cardiomyopathy patients strongly suggests that infarct-induced myopathy is very difficult to reverse once established [19–22].

Merseline mesh was chosen for the ventricular wrapping procedures for technical reasons. This mesh is more pliable and more readily conforms to the shape of the ventricle than does Marlex. After handling the two types of mesh it is obvious that Marlex is far less distensible than is Merseline; however we have not precisely characterized the properties of either mesh. Future studies will be needed to determine the optimum material properties for ventricular restraining devices.

Although the type and extent of ventricular restraint had no significant effects on right or left ventricular filling pressures we did not precisely assess diastolic function. This is a potential complication of ventricular wrapping therapy for acute MI that requires further evaluation in future studies.

Using contrast echocardiography, Jackson and coworkers [23] demonstrated that geometric changes consistent with increased regional wall stress occur in the border zone region adjacent to infarcts undergoing early expansion and subsequent remodeling. A finite element analysis by Guccione and colleagues [24] confirms these findings and also demonstrates that once the myopathic process is fully developed, contractile function in nonischemic myocardium is impaired beyond what would be expected due to changes in LV geometry and stress distribution. The salutary affect of ventricular wrapping demonstrated in this study is likely due to its ability to attenuate early infarct expansion thereby reducing adverse remodeling.

A secondary result of the analysis performed here has to do with contribution of ischemic MR (IMR) to the remodeling process. It is interesting to note that the significant reduction in IMR seen in the PBP group was not associated with a significant improvement in remodeling. These data suggest that IMR is not an important component of the stimulus that drives postinfarction ventricular remodeling. Careful review of the echocardiographic data from the control groups provides further evidence that IMR has a minimal effect on postinfarction remodeling. Both control groups (AAC and PBC) had similar-size infarcts and even though the PBC group developed severe IMR, the outcome of remodeling as assessed by echocardiographic factors was very similar (Fig 6). These data strongly suggest that IMR is a manifestation rather than a contributing factor to postinfarction remodeling [10].



View larger version (17K):
[in this window]
[in a new window]
  		Fig 6. Comparison of normalized left ventricular end-systolic volume (LVESV) between anteroapical and posterobasal infarct control groups during remodeling. Even though the posterobasal animals developed moderate to severe mitral regurgitation there was no statistical difference between the groups in the extent of ventricular dilatation 8 weeks after infarction.

 
The pre-emptive and prophylactic surgical interventions used in this study cannot, obviously, be directly applied clinically. They were used to simplify the experiment by eliminating the need for a second operation after infarction had been induced. However, the results of the study have important clinical implications. Our findings provide further support for infarct restraint as an early intervention intended to prevent rather than reverse infarction-induced remodeling. Because of the theoretical risk of constrictive pericarditis and the potential difficultly with re-operative surgery associated with ventricular wrapping we had hoped that simple infarct stiffening would be sufficient. However, this work strongly suggests that extensive ventricular wrapping is necessary to significantly influence remodeling.

A great deal of work is still required to optimize the implementation this preventative strategy before it can be clinically applied. Future experiments will need to determine the best timing for restraint placement and if complete heart wrapping (including the right ventricle) adds any benefit. The effect of infarct location and the material properties of the restraining device on remodeling will also need to be studied. In addition to these technical details, more precise studies to assess the effect of ventricular wrapping on ventricular diastolic function will need to be performed. Finally, it will be important to develop an imaging modality to assess the risk of adverse remodeling early after infarction to permit intervention only in high risk patients.


   Discussion
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Discussion
Acknowledgments
 References
 
DR JOHN CONTE (Baltimore, MD): Do you have any sense as to what the impact would be if your wrap was done at 2 weeks, 4 weeks, 6 weeks? Can you hypothesize what might be a time period for a therapeutic intervention in the future?

DR MOAINIE: One of the issues with this study is that we do a prophylactic wrap, thus eliminating timing as an issue. Further studies are necessary to determine at what exact timepoint we lose that beneficial effects of restraint and the heart has become irreversibly damaged due to adverse remodeling.


View this table:
[in this window]
[in a new window]
  		Table 2. Posterobasal Infarct Echocardiographic Data
 

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


   References
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Discussion
 Acknowledgments
 References
 

  1. Gheorghiade M, Bonow RO. Chronic heart failure in the United States: a manifestation of coronary artery disease Circulation 1998;97:282-289.[Free Full Text]
  2. Aweisman HF, Healy B. Myocardial infarct expansion, infarct extension, and reinfarction: pathophysiologic concepts Prog Cardiovasc Dis 1987;30:73-109.[Medline]
  3. Jackson BM, Gorman III JH, Moainie S, et al. Extension of borderzone myocardium in postinfarction dilated cardiomyopathy J Am Coll Cardiol 2002;40:1160-1167.[Abstract/Free Full Text]
  4. Pfeffer MA, Braunwald E. Ventricular remodeling after myocardial infarction: experimental observations and clinical implications Circulation 1990;81:1161-1172.[Abstract/Free Full Text]
  5. St John Sutton MG, Pfeffer MA, Plappert T, et al. Quantitative two-dimensional echocardiographic measurements are major predictors of adverse cardiovascular events after acute myocardial infarction: the protective effects of captopril Circulation 1994;89:68-75.[Abstract/Free Full Text]
  6. Raman JS, Hata M, Storer M, et al. The mid-term results of ventricular containment (ACORN WRAP) for end-stage ischemic cardiomyopathy Ann Thorac Cardiovasc Surg 2001;7:278-281.[Medline]
  7. Oz MC, Konertz WF, Kleber FX, et al. Global surgical experience with theAcorn cardiac support device J Thorac Cardiovasc Surg 2003;126:983-991.[Abstract/Free Full Text]
  8. Kelley ST, Malekan R, Gorman III JH, et al. Restraining infarct expansion preserves left ventricular geometry and function after acute anteroapical infarction Circulation 1999;99:135-142.[Abstract/Free Full Text]
  9. Moainie SL, Guy TS, Gorman III JH, et al. Infarct restraint attenuates remodeling and reduces chronic ischemic mitral regurgitation after posterolateral infarction Ann of Thorac Surg 2002;74:444-449.[Abstract/Free Full Text]
  10. Guy TS, IV, Moainie SL, Gorman JH III, et al. Prevention of ischemic mitral regurgitation does not influence the outcome of remodeling after posterolateral myocardial infarction. J Am Coll Cardiol 2004;43:377–83..
  11. Pilla JJ, Blom AS, Brockman DJ, et al. Ventricular constraint using the acorn cardiac support device reduces myocardial akinetic area in an ovine model of acute infarction Circulation 2002;106(Supplement 1):I207-I211.
  12. Markovitz LJ, Savage EB, Ratcliffe MB, et al. Large animal model of left ventricular aneurysm Ann Thorac Surg 1989;48:838-845.[Abstract]
  13. Llaneras MR, Nance ML, Streicher JT, et al. Large animal model of ischemic mitral regurgitation Ann Thorac Surg 1994;57:432-439.[Abstract]
  14. Gorman III JH, Gorman RC, Jackson BM, Enomoto Y, St John-Sutton MG, Edmunds Jr LH. Annuloplasty ring selection for chronic ischemic mitral regurgitation: lessons from the ovine model Ann Thorac Surg 2003;76:1556-1563.[Abstract/Free Full Text]
  15. Miyatake K, Izumi S, Okamoto M, et al. Semiquantitative grading of severity of mitral regurgitation by real-time two-dimensional Doppler flow imaging technique J Am Coll Cardiol 1986;7:82-88.[Abstract]
  16. Narula J, Dawson MS, Singh BK, et al. Noninvasive characterization of stunned, hibernating, remodeled and nonviable myocardium in ischemic cardiomyopathy J Am Coll Cardiol 2000;36:1913-1919.[Abstract/Free Full Text]
  17. Cheng W, Li B, Kajstura J, et al. Stretch-induced programmed myocyte cell death J Clin Invest 1995;96:2247-2259.
  18. Wilson EM, Moainie SL, Baskin JM, et al. Region- and type- specific induction of matrix metalloproteinases in post-myocardial infarction remodeling Circulation 2003;107:2857-2863.[Abstract/Free Full Text]
  19. Couper GS, Bunton RW, Birjiniuk V, et al. Relative risks of left ventricular aneurysmectomy in patients with akinetic scars versus true dyskinetic aneurysms Circulation 1990;82(Suppl IV):IV248-IV256.
  20. Batista RJV, Verde J, Nery P, Bocchino L, et al. Partial left ventriculectomy to treat end-stage heart disease Ann Thorac Surg 1997;64:634-638.[Abstract/Free Full Text]
  21. Dor V, Sabatier M, DiDonato M, et al. Efficacy of endoventricular patch plasty in large post infarction akinetic scar and severe left ventricular dysfunction: comparison with a series of large dyskinetic scars J Thorac Cardiovasc Surg 1998;116:50-59.[Abstract/Free Full Text]
  22. Gillinov AM, Wierup PN, Blackstone EH, et al. Is repair preferable to replacement for ischemic mitral regurgitation? J Thor Cardiovasc Surg 2001;122:1125-1141.[Abstract/Free Full Text]
  23. Jackson BM, Gorman III JH, Salgo I, et al. Altered borderzone geometry increases wall stress after anteroapical myocardial infarction: A contrast echocardiographic assessment Am J Physiol Heart Circ Physiol 2003;284:H475-H479.[Abstract/Free Full Text]
  24. Guccione JM, Moonly SM, Moustakidis P, et al. Mechanism underlying mechanical dysfunction in the borderzone of left ventricular aneurysm: A finite element model study Ann Thorac Surg 2001;71:654-662.[Abstract/Free Full Text]



This article has been cited by other articles:


Home page
 Ann. Thorac. Surg.Home page
J. J. Pilla, J. H. Gorman III, and R. C. Gorman
Theoretic impact of infarct compliance on left ventricular function.
Ann. Thorac. Surg., March 1, 2009; 87(3): 803 - 810.
[Abstract] [Full Text] [PDF]

Home page
 Ann. Thorac. Surg.Home page
L. P. Ryan, K. Matsuzaki, M. Noma, B. M. Jackson, T. J. Eperjesi, T. J. Plappert, M. G. St. John-Sutton, J. H. Gorman III, and R. C. Gorman
Dermal Filler Injection: A Novel Approach for Limiting Infarct Expansion
Ann. Thorac. Surg., January 1, 2009; 87(1): 148 - 155.
[Abstract] [Full Text] [PDF]

Home page
 Eur J Heart FailHome page
T. Wang, D.-Q. Wu, X.-J. Jiang, X.-Z. Zhang, X.-Y. Li, J.-F. Zhang, Z.-B. Zheng, R. Zhuo, H. Jiang, and C. Huang
Novel thermosensitive hydrogel injection inhibits post-infarct ventricle remodelling
Eur J Heart Fail, January 1, 2009; 11(1): 14 - 19.
[Abstract] [Full Text] [PDF]

Home page
 Ann. Thorac. Surg.Home page
A. S. Blom, J. J. Pilla, J. Arkles, L. Dougherty, L. P. Ryan, J. H. Gorman III, M. A. Acker, and R. C. Gorman
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
Ann. Thorac. Surg., December 1, 2007; 84(6): 2004 - 2010.
[Abstract] [Full Text] [PDF]

Home page
 J Am Coll CardiolHome page
K. L. Christman and R. J. Lee
Biomaterials for the Treatment of Myocardial Infarction
J. Am. Coll. Cardiol., September 5, 2006; 48(5): 907 - 913.
[Abstract] [Full Text] [PDF]

Home page
 CirculationHome page
A. Cheng, T. C. Nguyen, M. Malinowski, F. Langer, D. Liang, G. T. Daughters, N. B. Ingels Jr, and D. C. Miller
Passive Ventricular Constraint Prevents Transmural Shear Strain Progression in Left Ventricle Remodeling
Circulation, July 4, 2006; 114(1_suppl): I-79 - I-86.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
B. G. Leshnower, H. Sakamoto, A. Zeeshan, L. M. Parish, R. Hinmon, T. Plappert, B. M. Jackson, J. H. Gorman III, and R. C. Gorman
Role of acetaminophen in acute myocardial infarction
Am J Physiol Heart Circ Physiol, June 1, 2006; 290(6): H2424 - H2431.
[Abstract] [Full Text] [PDF]

Home page
 Ann. Thorac. Surg.Home page
J. J. Pilla, A. S. Blom, J. H. Gorman III, D. J. Brockman, J. Affuso, L. M. Parish, H. Sakamoto, B. M. Jackson, M. A. Acker, and R. C. Gorman
Early Postinfarction Ventricular Restraint Improves Borderzone Wall Thickening Dynamics During Remodeling
Ann. Thorac. Surg., December 1, 2005; 80(6): 2257 - 2262.
[Abstract] [Full Text] [PDF]

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

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
ANN THORAC SURG ASIAN CARDIOVASC THORAC ANN EUR J CARDIOTHORAC SURG
J THORAC CARDIOVASC SURG ICVTS ALL CTSNet JOURNALS