(Circulation. 1999;99:135-142.)
© 1999 American Heart Association, Inc.
Basic Science Reports |
Restraining Infarct Expansion Preserves Left Ventricular Geometry and Function After Acute Anteroapical Infarction
From the Departments of Surgery and Medicine, School of Medicine and Department of Bioengineering, University of Pennsylvania, Philadelphia, Pa.
Correspondence to Dr L. Henry Edmunds, Jr, Department of Surgery, 6 Silverstein, Hospital of the University of Pennsylvania, Philadelphia, PA 19104. E-mail hedmunds{at}mail.med.upenn.edu
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Abstract |
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Background—Expansion of an acute myocardial infarction predicts progressive left ventricular (LV) dilatation, functional deterioration, and early death. This study tests the hypothesis that restraining expansion of an acute infarction preserves LV geometry and resting function.
Methods and Results—In 23 sheep, snares were placed around the distal left anterior descending and second diagonal coronary arteries. In 12 sheep, infarct deformation was prevented by Marlex mesh placed over the anticipated myocardial infarct. Snared arteries were occluded 10 to 14 days later. Serial hemodynamic measurements and transdiaphragmatic quantitative echocardiograms were obtained up to 8 weeks after anteroapical infarction of 0.23 of LV mass. In sheep with mesh, circulatory hemodynamics, stroke work, and end-systolic elastance return to preinfarction values 1 week after infarction and do not change subsequently. Ventricular volumes and ejection fraction do not change after the first week postinfarction. Control animals develop large anteroapical ventricular aneurysms, increasing LV dilatation, and progressive deterioration in circulatory hemodynamics and ventricular function. At week 8, differences in LV end-diastolic pressure, cardiac output, end-diastolic and end-systolic volumes, ejection fraction, stroke work, and end-systolic elastance are significant (P<0.01) between groups.
Conclusions—Preventing expansion of acute myocardial infarctions preserves LV geometry and function.
Key Words: ventricles • remodeling • myocardial infarction
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Many variables affect ventricular remodeling after acute myocardial infarction. Size, transmurality, and infarct location are major variables1–4; loading conditions, previous scar, revascularization of occluded vessels,5 and ACE inhibitors6 are among other important variables. Nearly 70% of all infarctions are transmural,7
54% are
anterior,7 and 35% to 42% of anterior
infarctions develop slippage between myocytes8 to
produce infarct expansion and thinning.1 2 3 4 8
Ventricular dilatation ceases after a few days in
well-compensated hearts with small, minimally expansive
infarcts.9 In patients with expanding infarctions
and more severe left ventricular (LV) dysfunction, the
prognosis is ominous,1 2 4 9 10 because
progressive LV dilatation and functional deterioration continue for
weeks, months, and even years.2 4 10 11 Little is known of the material properties of healing myocardial infarctions,12 yet relative stiffness of the healing infarct influences mechanical forces affecting ventricular remodeling and performance.13 14 On the basis of infarct fibrosis, hydroxyproline content, and uniaxial stress extension studies,15 clinicians generally conclude that infarcts stiffen. However, this conclusion is inconsistent with the natural history of expanding infarctions2 3 4 9 10 11 and is not confirmed by biaxial stress extension studies of ovine infarctions.12 Mathematical models predict preservation of LV shape and resting function by preventing infarct expansion,13 14 but this prediction has not been tested in sophisticated finite-element models or demonstrated by serial measurements of postinfarction ventricular function. This study tests the hypothesis that restraining infarct expansion preserves ventricular geometry and resting function in a sheep model of acute anteroapical infarction that consistently progresses to LV aneurysm.16
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Methods |
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Surgical Protocol
Twenty-three healthy, Dorsett hybrid sheep were induced, intubated, anesthetized with isoflurane 1.5% to 2%, and ventilated with oxygen (Drager anesthesia monitor, North American Drager). All animals received glycopyrrolate 0.4 mg IV and cefazolin 1 g IV. Animals were treated in compliance with the Guide for the Care and Use of Laboratory Animals (NIH publication No. 85-23) as revised in 1985.
By use of aseptic technique, polypropylene snares were placed around
the homonymous (designated LAD in this article) and second
diagonal (D2) coronary arteries 40% from the apex via left
anterolateral thoracotomy.16 An ultrasonic flow
probe (Transonic Systems, Inc) was placed around the aortic root. Two
epicardial pacemaker wires were sewn to the right atrium. Group
assignment was random; 11 animals served as controls (group 1). In 12
animals (group 2), Marlex mesh, a nondistensible, monofilament, knitted
polypropylene mesh used for hernia repair, was sutured over the precise
location of the expected anteroapical infarction of 0.23 of LV
mass.16 The wound was closed, and the animals
recovered.
Baseline Data
After 10 to 14 days, sheep were anesthetized with
isoflurane 1% to 2%, intubated, and placed supine. Surface ECGs and
arterial blood pressure were monitored continuously. A
Swan-Ganz catheter (131h-7Fr Baxter Healthcare Corp) was introduced via
the left internal jugular vein. A high-fidelity pressure transducer
(Spc-350, Millar Instruments Inc) was inserted from the femoral artery
into the LV (Hewlett-Packard 78534c monitor). Animals were disconnected
from the ventilator, and the heart was atrially paced at 120 bpm for
all measurements and echocardiograms.
Echocardiography
Subdiaphragmatic 2-dimensional echocardiographic
images were obtained through a sterile, midline laparotomy with a
5-MHz. probe (Hewlett Packard 77020A) and were recorded on 0.5-in
videotape at 30 Hz (Panasonic AG-6300 VHS Recorder, Matsushita
Electric Industries Co Ltd). LV short-axis images at 3 levels
(at the tips of the papillary muscles, at the bases of the papillary
muscles, and at the apex) and 2 orthogonal long-axis views were
obtained. As the LV aneurysm developed, the
ventricular long axis angulated; therefore, the apical
short-axis image was not always parallel to other short-axis images. LV
apical long-axis views were used to calculate LV cavity volumes by
biplane Simpson's rule.17
In addition, serial echocardiographic measurements were made of LV cavity diameter (at the tips of the papillary muscle) and LV long-axis cavity length to assess LV cavity shape (defined as the ratio of the short axis to long axis) at all time points in all animals. LV wall thickness was measured from short-axis images at the level of the papillary muscle bases at baseline and in infarct and remote zones at end diastole and end systole. Wall thickness was also measured in the apical short axis at 8 weeks. Myocardial infarct length was measured as the length of LV cavity perimeter that was either akinetic or dyskinetic (A/D); this A/D length as a percentage of the total cavity perimeter was calculated.9 Last, the length of cavity perimeter from the insertion of the aortic valve leaflets to the edge of the A/D segment in the anterior wall was measured immediately after infarction through 8 weeks.
Stroke Work
LV stroke work (SW) was measured from simultaneous
measurements of stroke volume and LV pressure18:
SW (ergs)=LVA (mm Hg–beat)xSV (mL/beat)x1330, where LVA is the area
under the LV pressure trace, SV is stroke volume as determined by the
aortic flow probe, and beat is time in seconds. Measurements were
repeated 5 times; means were used for subsequent analyses.
Slope of the Stroke Work–LV End-Diastolic
Pressure Relationship
A 50-mL Fogarty catheter (US Catheter and Instrument Co) was
placed via the jugular vein into the inferior vena cava
under fluoroscopic guidance and inflated to decrease
ventricular preload. LV pressure and stroke volume were
measured over the subsequent 10 beats, and stroke work was plotted
against left ventricular end diastolic pressure
(LVEDP).18 The relationship was plotted for all
10 beats; correlation coefficients were calculated; all were >0.94,
and most were 0.99. Caval occlusions were repeated 5 times, and mean
slopes were recorded.
End-Systolic Elastance
End-systolic elastance (Ees) was
measured by use of an occlusive balloon in the ascending aorta as
previously described and validated.19 A
custom-made 50-mL intra-aortic balloon (Datascope, Inc) was placed
during fluoroscopy in the aortic root from the femoral artery and was
connected to a System 90-T intra-aortic balloon pump (Datascope Inc).
The balloon was triggered to inflate during diastole and to
remain inflated during the following contraction. The balloon produced
an isovolumic contraction (verified by flow probe). Using custom
software, we constructed a pair of pressure-volume relationships from
simultaneous pressure and flow tracings of the last
ejecting and first isovolumic contraction19 and
assumed no change in end-diastolic
volume.19 The end-systolic
pressure-volume relationship (ESPVR) or Ees was
drawn from the peak isovolumic pressure-volume point tangential to the
left upper corner of the pressure-volume loop of the ejecting
contraction. Balloon inflation was repeated 5 times; absolute LV volume
was not measured.
Ees values obtained from 2 pressure-volume relationships (nonoccluded and completely occluded) were compared with mean values obtained from families of 4 partially occlusive pressure-volume loops created by varying volume in the ascending aortic balloon for 6 sheep at baseline and 2 sheep throughout the entire 8-week study (n=14). Results showed that average Ees values obtained by both methods differed by 3.4±1.3%, and slopes were not significantly different by paired t test (P=0.69). Thereafter, all Ees measurements were made by the complete occlusion method described above.
Infarction
After baseline data had been obtained, the previously placed
exteriorized subcutaneous snares were tightened sequentially.
Arrhythmias were rigorously monitored and controlled by an
infusion of lidocaine 2 mg/min and bolus doses of bretylium 5 mg/kg and
magnesium 0.5 g before infarction and esmolol 0.5 to 2.0 mg/kg
after infarction. When hemodynamic measurements
stabilized (1 hour), postinfarction measurements were made. The
laparotomy was closed.
Follow-Up Studies
Identical measurements were made at 1, 2, 5, and 8 weeks after
infarction. Only 9 measurements (5 mesh, 4 controls) were made at 1
week; all surviving sheep had measurements at the other time intervals.
After week 8, the animal was euthanized (potassium chloride 80 mEq).
The heart was excised, and the LV was opened in the long axis and
photographed. Sections were taken for histology.
Statistics
Measurements are reported as mean±SD. Differences between
groups are compared by 2-way MANOVA (group, time) with Bonferroni
adjustment for repeated measures (SPSS 6.0). When the group effect is
significant, 1-way ANOVA is used to determine significant differences
at different times in each group separately. If the time effect is
significant by 1-way ANOVA, differences between before-infarction
measurements and measurements at subsequent times are compared by the
paired t statistic. When the group effect is significant,
differences between groups at specific times are compared by the
unpaired t statistic. Significance is accepted at the
P<0.05 probability.
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Results |
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Fifteen sheep (9 control, 6 mesh) completed the 8-week protocol. Two animals in the control group died early after infarction, and 2 in group 2 died between 2 and 5 weeks of arrhythmias. Four sheep in group 2 died after 4 weeks of pneumonia, embolic stroke, or euthanasia for wound complications.2 At week 8, all control animals had evidence of heart failure (rales, lethargy); no mesh animal had evidence of heart failure.
Histological sections of mesh-covered infarcts 2 and 8
weeks after infarction show a nonspecific fibrous reaction surrounding
mesh fibers without new vessel ingrowth (Figure 1
). The epicardial fibrotic reaction does
not progress after 2 weeks (Figure 1).
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Echocardiograms in sheep with mesh show normal wall thickness and systolic wall thickening beneath the mesh before infarction. Diastolic wall thickness is similar in both groups (8.9±0.3 [SEM] mm, mesh; 9.2±0.4 mm, control) (P=0.47). At week 8, wall thickness near the infarcted apex was 4.8±0.3 (SEM) mm in group 1 and 6.6±0.2 mm in group 2 sheep (P=0.0004).
Hemodynamic measurements are presented in Table 1. The data indicate progressive
deterioration in circulatory function over 8 weeks in group 1 sheep and
no significant changes in resting hemodynamics in group
2 sheep except immediately after infarction (Figure 2, Table 1).
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) and mesh-treated (
) sheep at each time point. Error bars
represent SEM. *P<0.05;
P<0.01 by unpaired t test between
groups.
LV end-diastolic and end-systolic volumes increase
progressively over 8 weeks in control sheep but do not progress after
week 1 postinfarction in mesh-treated sheep (Figure 3). At week 8, end-systolic and
end-diastolic volumes are significantly smaller in sheep
with restrained infarcts (Table 2).
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, 
) volumes for control and
mesh-treated animals at each time point.
P<0.01 within groups vs baseline value. Other
symbols as in Figure 2
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In control sheep, ejection fraction, stroke volume, stroke work,
the stroke work–LVEDP relationship, and Ees and
stroke volume progressively decrease after infarction, and all values
except Ees are significantly less than
preinfarction measurements at week 8 (Figure 4, Table 2
). In group 2 sheep, stroke
volume, stroke work, the stroke work–LVEDP relationship, and
Ees do not differ significantly from baseline
measurements at any time after infarction. Ejection fraction decreases
early after infarction but does not decrease further after the first
week (Table 2).
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Figures 5 and 6 illustrate long-axis echocardiograms
before infarction and at 1 and 8 weeks after infarction in control and
mesh-treated sheep. The mesh-restrained infarct does not expand,
whereas the unrestrained infarct expands asymmetrically into an
anteroapical aneurysm.
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MANOVA with adjustment for repeated measures showed a significant
time effect (P<0.05) for 25 of 34
echocardiographic variables measured; however, only
5 variables were significantly different between groups when
analyzed without baseline measurements (Table 3). Differences in LV
diastolic cavity shape between groups approached
statistical significance at 8 weeks (P=0.055) (Table 3). In
mesh-treated sheep, infarct expansion was less over time in control
animals and the contractile segment of the anterior wall was greater
(Table 3).
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Figure 7 is a photograph of a normal
ovine heart, a mesh-constrained anteroapical infarction, and an
untreated anteroapical infarction at week 8. The shapes of the
mesh-constrained infarcted heart and the uninfarcted normal heart are
similar.
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Discussion |
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A patch of Marlex mesh applied before infarction overcomes the technical obstacle of restraining infarct expansion. The ensuing fibrosis prevents infarct expansion, does not change baseline wall thickness, and has minimal impact on surrounding myocardium. Consistency of ovine coronary arterial anatomy between sheep and lack of preformed collateral vessels20 permit accurate prediction of infarct size and location.16 Although the method has no therapeutic value, mesh permits a test of our hypothesis.
Prevention of infarct expansion attenuates a decrease in ejection fraction, prevents aneurysm formation, and preserves resting ventricular function. The ventricle retains its normal conical shape despite loss of 0.23 of LV mass.16 In the mesh group, dimensional, hemodynamic, and functional consequences of the infarct do not progress after 1 or 2 weeks. Exercise reserve may be reduced, but resting ventricular geometry and function are preserved and progressive ventricular deformation is aborted.
Expanding acute anterior infarctions produce progressive deterioration in ventricular function, dilatation, and eventually heart failure in both patients and sheep.1 3 9 10 11 16 The sheep model may exaggerate and accelerate this scenario, but in both species, there is little evidence that either the size or function of the ventricle stabilizes or that the remodeling process ends until regional expansion ends.10 11 16 21
The progressive deterioration in ventricular function is best explained by ongoing involvement of viable, border-zone myocardium. Ischemia rapidly reduces end-systolic wall thickness22 and, by LaPlace's law, increases end-systolic circumferential and meridional wall stresses. Increased regional wall stresses favor infarct expansion, but the amount of expansion also depends on material properties of the new infarction. If the infarct expands, the radius of curvature of infarct and adjacent border zone also increases15; elevated wall stresses in both regions cause progressive wall thinning. Border-zone thinning decreases myocyte contractility,23 increases segmental length, and pulls myocardium toward the expanding infarct. Mature scar may stabilize the center of the infarct,15 but in the border zone, the process may continue until expansion stops or heart failure and death intervene.
Material properties of the normal, beating heart are heterogeneous, anisotropic, and time-dependent and are affected by numerous variables, including alignment of layered collagen and muscle fibers.24 The material properties of myocardial infarctions are also heterogeneous, anisotropic, and possibly even time-dependent.12 25 Compliance of the infarct initially decreases after infarction because of edema and necrotic myocytes12 26 but often increases later.2 15 27 Late changes in infarct compliance vary with infarct size, location, transmurality, and other factors2 3 7 11 and reflect changes in infarct material properties and regional wall stresses in the remodeling ventricle.2 3 7 11 15 In sheep28 and perhaps in humans, differences in infarct expansion between anterior and posterior infarctions of similar sizes may be explained by differences in material properties rather than initial differences in systolic wall stress. Stable ventricular geometry requires a balance between myocardial material properties resisting expansion and ventricular wall stresses and strains. It follows that when regional wall stresses increase, myocardium must either stiffen to prevent or minimize strain or, alternatively, deform in the direction of applied stresses.
The clinical benefit of preventing infarct deformation and preserving ventricular geometry shown in this study focuses attention on the extracellular matrix of healing infarctions.29 Late reperfusion (6 to 12 hours after onset of chest pain) attenuates infarct expansion and improves survival but does not rescue myocytes.5 30 Initially, hemorrhage and edema may stiffen the infarct; later, revascularization may alter the molecular and cellular responses in the extracellular matrix. At present, no surgical procedures exist to limit expansion of acute infarctions, but given the need, operations can be developed.
Limitations of This Study
The relevance of the sheep model to transmural anteroapical
infarctions in humans cautions against extrapolation of these
conclusions to patients. The sheep model avoids many confounding
variables associated with human anteroseptal infarctions, but these
variables may be relevant to clinical care.
Mesh applied before infarction may stimulate an inflammatory reaction within the underlying myocardium and alter the remodeling process independently of external restraint. At this time, this possibility lacks supportive evidence. It is acknowledged that the mesh also covered some border-zone tissue, but the amount is small and logically should reduce rather than enhance LV performance.
This study raises but does not address the issue of how best to prevent expansion of acute myocardial infarctions.
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Acknowledgments |
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This study was supported by grant HL-36308 from the NHLBI, NIH, Bethesda, Md. The authors thank Priscilla Hillyer and Dr Carol Reynolds for their help in this study.
Received March 27, 1998; revision received August 21, 1998; accepted August 31, 1998.
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T. Yano, T. Miura, P. Whittaker, T. Miki, J. Sakamoto, Y. Nakamura, Y. Ichikawa, Y. Ikeda, H. Kobayashi, K. Ohori, et al. Macrophage Colony-Stimulating Factor Treatment After Myocardial Infarction Attenuates Left Ventricular Dysfunction by Accelerating Infarct Repair J. Am. Coll. Cardiol., February 7, 2006; 47(3): 626 - 634. [Abstract] [Full Text] [PDF]
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B. M. Jackson, L. M. Parish, J. H. Gorman III, Y. Enomoto, H. Sakamoto, T. Plappert, M. G. St. John Sutton, I. Salgo, and R. C. Gorman Borderzone Geometry After Acute Myocardial Infarction: A Three-Dimensional Contrast Enhanced Echocardiographic Study Ann. Thorac. Surg., December 1, 2005; 80(6): 2250 - 2255. [Abstract] [Full Text] [PDF]
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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]
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 I. A. Memon, Y. Sawa, N. Fukushima, G. Matsumiya, S. Miyagawa, S. Taketani, S. K. Sakakida, H. Kondoh, A. N. Aleshin, T. Shimizu, et al. Repair of impaired myocardium by means of implantation of engineered autologous myoblast sheets J. Thorac. Cardiovasc. Surg., November 1, 2005; 130(5): 1333 - 1341. [Abstract] [Full Text] [PDF]
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R. A. Levine and E. Schwammenthal Ischemic Mitral Regurgitation on the Threshold of a Solution: From Paradoxes to Unifying Concepts Circulation, August 2, 2005; 112(5): 745 - 758. [Full Text] [PDF]
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F. Rodriguez, F. Langer, K. B. Harrington, A. Cheng, G. T. Daughters, J. C. Criscione, N. B. Ingels, and D. C. Miller Alterations in transmural strains adjacent to ischemic myocardium during acute midcircumflex occlusion J. Thorac. Cardiovasc. Surg., April 1, 2005; 129(4): 791 - 803. [Abstract] [Full Text] [PDF]
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Y. Enomoto, J. H. Gorman III, S. L. Moainie, B. M. Jackson, L. M. Parish, T. Plappert, A. Zeeshan, M. G. St. John-Sutton, and R. C. Gorman Early Ventricular Restraint After Myocardial Infarction: Extent of the Wrap Determines the Outcome of Remodeling Ann. Thorac. Surg., March 1, 2005; 79(3): 881 - 887. [Abstract] [Full Text] [PDF]
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Y. Enomoto, J. H. Gorman III, S. L. Moainie, T. S. Guy, B. M. Jackson, L. M. Parish, T. Plappert, A. Zeeshan, M. G. St. John-Sutton, and R. C. Gorman Surgical treatment of ischemic mitral regurgitation might not influence ventricular remodeling J. Thorac. Cardiovasc. Surg., March 1, 2005; 129(3): 504 - 511. [Abstract] [Full Text] [PDF]
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M. Cirillo, A. Amaducci, F. Brunelli, M. Dalla Tomba, P. Parrella, G. Tasca, G. Troise, and E. Quaini Determinants of postinfarction remodeling affect outcome and left ventricular geometry after surgical treatment of ischemic cardiomyopathy J. Thorac. Cardiovasc. Surg., June 1, 2004; 127(6): 1648 - 1656. [Abstract] [Full Text] [PDF]
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T. S. Guy IV, S. L. Moainie, J. H. Gorman III, B. M. Jackson, T. Plappert, Y. Enomoto, M. G. St. John-Sutton, L. H. Edmunds Jr, and R. C. Gorman Prevention of ischemic mitral regurgitation does not influence the outcome of remodeling after posterolateral myocardial infarction J. Am. Coll. Cardiol., February 4, 2004; 43(3): 377 - 383. [Abstract] [Full Text] [PDF]
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J. H. Gorman III, B. M. Jackson, Y. Enomoto, and R. C. Gorman The effect of regional ischemia on mitral valve annular saddle shape Ann. Thorac. Surg., February 1, 2004; 77(2): 544 - 548. [Abstract] [Full Text] [PDF]
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J. H. Gorman III, R. C. Gorman, B. M. Jackson, Y. Enomoto, M. G. St. John-Sutton, and L. H. Edmunds Jr Annuloplasty ring selection for chronic ischemic mitral regurgitation: lessons from the ovine model Ann. Thorac. Surg., November 1, 2003; 76(5): 1556 - 1563. [Abstract] [Full Text] [PDF]
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F. J. Villarreal, M. Griffin, J. Omens, W. Dillmann, J. Nguyen, and J. Covell Early Short-Term Treatment With Doxycycline Modulates Postinfarction Left Ventricular Remodeling Circulation, September 23, 2003; 108(12): 1487 - 1492. [Abstract] [Full Text] [PDF]
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K. Matsubayashi, P. W.M. Fedak, D. A.G. Mickle, R. D. Weisel, T. Ozawa, and R.-K. Li Improved Left Ventricular Aneurysm Repair With Bioengineered Vascular Smooth Muscle Grafts Circulation, September 9, 2003; 108(90101): II-219 - 225. [Abstract] [Full Text] [PDF]
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 B. M. Jackson, J. H. Gorman III, I. S. Salgo, S. L. Moainie, T. Plappert, M. St. John-Sutton, L. H. Edmunds Jr., and R. C. Gorman Border zone geometry increases wall stress after myocardial infarction: contrast echocardiographic assessment Am J Physiol Heart Circ Physiol, February 1, 2003; 284(2): H475 - H479. [Abstract] [Full Text] [PDF]
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 R. C. Gorman, J. H. Gorman III, and L. H. Edmunds Jr. Ischemic Mitral Regurgitation Card. Surg. Adult, January 1, 2003; 2(2003): 751 - 769. [Full Text]
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B. M. Jackson, J. H. Gorman III, S. L. Moainie, T. S. Guy, N. Narula, J. Narula, M. G. St. John-Sutton, L. H. Edmunds Jr, and R. C. Gorman Extension of borderzone myocardium in postinfarction dilated cardiomyopathy J. Am. Coll. Cardiol., September 18, 2002; 40(6): 1160 - 1167. [Abstract] [Full Text] [PDF]
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M. B. Ratcliffe Non-ischemic infarct extension: A new type of infarct enlargement and a potential therapeutic target J. Am. Coll. Cardiol., September 18, 2002; 40(6): 1168 - 1171. [Full Text] [PDF]
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S. L. Moainie, T. S. Guy, J. H. Gorman III, T. Plappert, B. M. Jackson, M. G. St. John-Sutton, L. H. Edmunds Jr, and R. C. Gorman Infarct restraint attenuates remodeling and reduces chronic ischemic mitral regurgitation after postero-lateral infarction Ann. Thorac. Surg., August 1, 2002; 74(2): 444 - 449. [Abstract] [Full Text] [PDF]
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R. C. Gorman and J. H. Gorman III Cellular myoplasty: What are we really trying to achieve? J. Thorac. Cardiovasc. Surg., March 1, 2002; 123(3): 582 - 583. [Full Text] [PDF]
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R. C. Gorman and J. H. Gorman III Cellular myoplasty: what are we really trying to achieve? Ann. Thorac. Surg., January 1, 2002; 73(1): 342 - 343. [Full Text] [PDF]
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F. W. Bowen, S. C. Jones, N. Narula, M. G. St. John Sutton, T. Plappert, L. H. Edmunds Jr, and I. M.C. Dixon Restraining acute infarct expansion decreases collagenase activity in borderzone myocardium Ann. Thorac. Surg., December 1, 2001; 72(6): 1950 - 1956. [Abstract] [Full Text] [PDF]
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F. W. Bowen, T. Hattori, N. Narula, I. S. Salgo, T. Plappert, M. G. St. John Sutton, and L. H. Edmunds Jr Reappearance of myocytes in ovine infarcts produced by six hours of complete ischemia followed by reperfusion Ann. Thorac. Surg., June 1, 2001; 71(6): 1845 - 1855. [Abstract] [Full Text] [PDF]
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M. Jain, H. DerSimonian, D. A. Brenner, S. Ngoy, P. Teller, A. S. B. Edge, A. Zawadzka, K. Wetzel, D. B. Sawyer, W. S. Colucci, et al. Cell Therapy Attenuates Deleterious Ventricular Remodeling and Improves Cardiac Performance After Myocardial Infarction Circulation, April 10, 2001; 103(14): 1920 - 1927. [Abstract] [Full Text] [PDF]
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 Q.-G. Xia, O. Chung, H. Spitznagel, S. Illner, G. Janichen, B. Rossius, P. Gohlke, and T. Unger Significance of timing of angiotensin AT1 receptor blockade in rats with myocardial infarction-induced heart failure Cardiovasc Res, January 1, 2001; 49(1): 110 - 117. [Abstract] [Full Text] [PDF]
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R. J. Edwards, M. S. Marber, S. T. Kelley, R. Malekan, J. H. Gorman III, B. M. Jackson, R. C. Gorman, Y. Suzuki, T. Plappert, D. K. Bogen, et al. Restraining Infarct Expansion Preserves Left Ventricular Geometry and Function After Acute Anteroapical Infarction • Response Circulation, December 21, 1999; 100 (25): e152 - e152. [Full Text] [PDF]
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