HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

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

Ann Thorac Surg 2004;78:1248-1255
© 2004 The Society of Thoracic Surgeons

---

Original article: cardiovascular

The Dynamic Anterior Mitral Annulus

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

Accepted for publication April 1, 2004.

^* Address reprint requests to Dr Joseph Gorman, Department of Surgery, 6 Silverstein, Hospital of the University of Pennsylvania, Philadelphia, PA 19104, USA
gormanj{at}uphs.upenn.edu

	Abstract

Top Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
BACKGROUND: The anterior mitral annulus is considered a fixed structure. Recent data suggest otherwise. This study tested the hypothesis that the size of the anterior annulus varies with hemodynamic loading and ventricular contractility.

METHODS: Sonomicrometry array localization measured annular area, total annular circumference, anterior circumference, and posterior circumference in 6 sheep before and after neosynephrine increased systolic blood pressure by at least 150% during atrial pacing at 120 beats/min. In 6 additional animals the same dimensions were measured during atrial pacing (at 120 and 150 beats/min) and during isoproteronol infusions to increase heart rate to 120 and 150 beats/min.

RESULTS: Neosynephrine increased systolic total annular circumference from 99.7 ± 5.5 mm to 106.9 ± 9.6 mm. Anterior circumference increased from 40.8 ± 4.0 mm to 45.3 ± 5.7 mm whereas posterior circumference only increased from 59.0 ± 5.5 mm to 61.6 ± 7.0 mm. Low isoproteronol infusion decreased systolic total annular circumference from 107.5 ± 8.3 mm to 101.9 ± 10.6 mm. Most of this change occurred in the posterior circumference. Higher infusions of isoproteronol decreased total annular circumference from 106.8 ± 8.3 mm to 98.3 ± 9.7 mm. At this higher inotropic state the decrease in annular size was similar in the anterior and posterior annulus.

CONCLUSIONS: In sheep, the anterior annulus is a dynamic structure that varies in size in response to changes in hemodynamic loading and ventricular contractility.

	Introduction

Top Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
It is clear from experimental and clinical data that the mitral annulus is a dynamic structure that undergoes substantial area change throughout the cardiac cycle, which is affected by inotropic state [1]. However, it has long been believed that the anterior portion of the mitral annulus is fixed in size. Accepted surgical dogma teaches that this anatomic structure is unresponsive to the phase of the cardiac cycle, hemodynamic loading, and ventricular remodeling [2–4]. Any change in annular size associated with these variables has been attributed to the ostensibly more dynamic posterior portion of the annulus [5]. This concept has become ingrained in surgeons and has influenced the development of valvuloplasty techniques as well as annuloplasty design for over three decades.

Recent pathologic studies of human heart specimens and in vivo animal studies have begun to challenge this belief. These reports have demonstrated that the anterior annulus changes in size throughout the cardiac cycle [6–9] and that it is stretched by postinfarction ventricular remodeling, thereby contributing to the mechanism of functional and ischemic mitral regurgitation [10–12].

Although these data have begun to cast doubt on the axiom of a rigid anterior annulus, the issue is not yet settled [13]. An understanding of the physiology of the anterior mitral annulus has important implications for valve repair techniques and annuloplasty ring design. This study was performed to test the hypothesis that the dimensions of the anterior mitral annulus are affected by variations in afterload and ventricular contractility.

	Material and Methods

Top Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Surgical Protocol
In compliance with guidelines for humane care (National Institutes of Health Publication No. 85 to 23, revised 1985) 12 male Dorsett sheep (6 for the afterload study and 6 for the contractility study; 35 to 45 kg) were induced with sodium thiopental (10 to 15 mg/kg intravenously), intubated, anesthetized, and ventilated with isofluorane (1.5% to 2%) and oxygen. The surface electrocardiogram (ECG) and arterial blood pressure (ABP) were continuously monitored.

Through a sterile left lateral thoracotomy, six 2-mm hemispherical PZT-5A piezoelectric transducers (Sonometrics Corp., London, Ontario, Canada) were implanted in each sheep during cardiopulmonary bypass, as described previously [12, 14]. Figure 1 illustrates the relationship of the annular transducers to leaflet and annular anatomy. The posterior commissure (PC) and the anterior commissure (AC) transducers were placed at the cleft between the anterior and posterior leaflets. The aortic crystal (Ao) was placed on the aortic-mitral continuity. The annular transducers, marked P1, P2, and P3, were centered over the anterior, middle, and posterior scallops of the posterior leaflet. An aortic flow probe was implanted to measure cardiac output (CO). The chest was closed and the animal recovered.

View larger version (130K): [in this window] [in a new window]   Fig 1. The relationship of the sonomicrometry transducers to mitral annular and leaflet anatomy. (AC = anterior commissure; Ao = aortic; PC = posterior commissure; P1 = anterior portion of posterior annulus; P2 = mid-portion of posterior annulus; P3 = posterior portion of posterior annulus.) (Reprinted from Gorman JH, et al, Ann Thorac Surg; 2004; 77:852–7 [16], with permission.)

Animals were ß blocked with esmolol (mean infusion rate 5.3 ± 4.4 mg/min) to a heart rate (HR) of 90 beats/min. Atrial pacing (AP) was initiated to a HR of 120 and 150 beats/min. Sonomicrometry and simultaneous hemodynamic data were recorded for both conditions (AP = 120 and AP = 150, respectively). Ventilation was suspended during all measurements. Esmolol and atrial pacing were stopped and the animals were allowed to return to the steady state. After 10 minutes, an isoproterenol infusion was titrated to produce heart rates of 120 beats/min (mean infusion rate 4.0 ± 3.8 µg/min) and 150 beats/min (5.5 ± 4.1 µg/min). Sonomicrometry array localization (SAL) and simultaneous hemodynamic data were recorded for both conditions (Iso120 and Iso150, respectively). This experimental construction was designed to isolate the effect of inotropy from chronotropy.

Afterload
Six days to 2 weeks after instrumentation, the other 6 of 12 sheep were prepared for data collection as described for the contractility animals. Transducer wires were connected to a Sonometrics Series 5001 Digital Sonomicrometer (Sonometrics Corp.). Animals were ß blocked with esmolol (mean infusion rate 4.4 ± 3.1 mg/min) to a HR of 90 beats/min. Atrial pacing to 120 beats/min was then initiated. SAL and simultaneous hemodynamic data were collected as described above. Pacing and esmolol infusion were continued while a neosynephrine infusion was titrated to produce a systolic ABP of at least 150% of baseline. SAL and simultaneous hemodynamic data were again collected. At the completion of these experiments, animals were euthanized with 1 g of thiopental and 80 mEq of KCl. Hearts were removed and opened to verify the placement of the sonomicrometry transducers.

Data analysis
As described previously [14], SAL was used to determine the three-dimensional coordinates of each transducer every 5 ms throughout the cardiac cycle. From these data, four measures of annular size (area, total circumference, anterior circumference, and posterior circumference) were calculated at each time point. Annular area was calculated as described previously [14]. Anterior circumference was the distance between transducers AC, Ao, and PC. Posterior circumference was defined as the distance defined by transducers PC, P3, P2, P1, and AC. Total circumference (TC) was calculated as the sum of the anterior and posterior circumferences. End diastole (ED), end isovolemic contraction (EIVC), end systole (ES), and end isovolemic relaxation (EIVR) time points were determined as previously described [14]. To facilitate comparison, all datasets collected at 120 beats/min were normalized in time by means of linear interpolation to the average cardiac cycle for these data, that is, isovolemic contraction (from ED to EIVC) = 100 ms, ejection (EIVC to ES) = 205 ms, isovolemic relaxation (ES to EIVR) = 55 ms, and diastolic filling (EIVR to ED) = 155 ms. These values represent the average cardiac cycle for these data. All datasets collected at 150 beats/min were normalized by the same method to the average cardiac cycle for these data, that is, isovolemic contraction (from ED to EIVC) = 85 ms, ejection (EIVC to ES) = 175 ms, isovolemic relaxation (ES to EIVR) = 55 ms, and diastolic filling (EIVR to ED) = 105 ms.

The normalized measures (area, total circumference, anterior circumference, and posterior circumference) were averaged within each condition at each time point to form composite measures. For the afterload group, composite base line measures and composite neosynephrine measures were plotted against time and compared by paired Student's t test. For the contractility group, the composite data from the Iso120 condition was compared to the AP120 condition by the same method; the composite data from the Iso150 condition was compared to the AP150 condition by the same method. Hemodynamic data were compared in parallel with SAL data; significance was determined by paired Student's t test. Error ranges are presented as standard deviations. Significance is defined as p less than 0.05.

Subdiaphragmatic color-flow Doppler echocardiography (model 77020A; Hewlett-Packard Inc.) was performed through a midline laparotomy after each pharmacologic or pacing intervention to assess valve competency [15].

	Results

Top Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Effects of Afterload
A mean neosynephrine infusion rate of 386 ± 214 µg/min was required to increase systolic blood pressure by 182% ± 20% from a baseline of 98 ± 15 mm Hg to 184 ± 23 mm Hg. LV diastolic pressure and pulmonary artery pressures also increased significantly (p < 0.05). Cardiac output was not affected (Table 1).

View larger version (39K): [in this window] [in a new window]   Fig 2. (Top left) Average annular area, (bottom left) total circumference, (top right) anterior circumference, and (bottom right) posterior circumference for two afterload conditions. The lower traces are continuous p values by paired Student's t test. Both control and neosynephrine groups were atrial paced to 120 beats/min. (ED = end diastole; EIVC = end isovolemic contraction; EIVR = end isovolemic relaxation; ES = end systole; ME = mid-ejection.)

The diastolic effect of afterload on TC was less dramatic, approaching statistical significance only during early and late diastole (Fig 2). With increased afterload the anterior annular segment increased by 10.8% (p < 0.07) at ES and 9.4% (p < 0.03) at ED. Despite an increasing trend, at no time during diastole did the effects of increased afterload on the length of the posterior annulus reach statistical significance.

Effects of Contractility
This portion of the experiment was designed to isolate the inotropic effect of isoproterenol from its chronotropic effect [16]. At lower inotropic stimulation (comparison of the AP120 and Iso120 groups) CO increased significantly (p < 0.05) from 2.8 ± 0.5 L/min to 4.5 ± 1.0 L/min and LV diastolic pressure decreased significantly (p < 0.05) from 12 ± 6 mm Hg to 6 ± 4 mm Hg. The remaining hemodynamic factors where unchanged (Table 3). Higher levels of inotropic stimulation (comparison of the AP150 and Iso150 groups) increased cardiac output significantly (p < 0.05) from 3.2 ± 0.5 L/min to 5.8 ± 1.5 L/min and decreased LV diastolic pressure from 10 ± 6 mm Hg to 6 ± 5 (Table 3). The mitral valve remained competent under all conditions.

View larger version (39K): [in this window] [in a new window]   Fig 3. (Top left) Average annular area, (bottom left) total circumference, (top right) anterior circumference, and (bottom right) posterior circumference for the two contractility conditions at 120 beats/min (low isoproterenol infusion) throughout the cardiac cycle. The control group was atrial paced to 120 beats/min. The study group was achieved by titrating isoproterenol infusion to 120 beats/min. The lower traces are continuous p values by paired Student's t test. (ED = end diastole; EIVC = end isovolemic contraction; EIVR = end isovolemic relaxation; ES = end systole; ME = mid-ejection.)

View larger version (40K): [in this window] [in a new window]   Fig 4. (Top left) Average annular area, (bottom left) total circumference, (top right) anterior circumference, and (bottom right) posterior circumference for the two contractility conditions at 150 beats/min (high isoproterenol infusion) throughout the cardiac cycle. The control group was atrial paced to 150 beats/min. The study group was achieved by titrating isoproterenol infusion to 150 beats/min. The lower traces are continuous p values by paired Student's t test. (ED = end diastole; EIVC = end isovolemic contraction; EIVR = end isovolemic relaxation; ES = end systole; ME = mid-ejection.)

The effect of inotropy on all portions of the annular circumference was amplified at the higher dose of isoproterenol (comparison of the AP150 and Iso150 groups). At these higher infusion rates TC decreased by 8.0% from 106.8 ± 8.3 mm to 98.3 ± 9.7 mm at ME (p < 0.05). At this higher inotropic state the decrease in annular size was more symmetric, affecting the anterior annulus as much as the posterior. At ME the posterior annulus decreased by 6.6% from 58.7 ± 7.5 mm to 54.9 ± 6.1 mm (p < 0.05), although the anterior annulus decreased by 9.7% from 48.2 ± 6.4 mm to 43.4 ± 5.7 mm (p < 0.05).

	Comment

Top Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Since the pioneering work of Tsakiris and coworkers [5] in the early 1970s, several groups have documented the complex dynamic nature of the mitral valve annulus in animals [6, 14, 15, 17, 18] and humans [19, 20]. Until recently, it has been accepted that the dynamic nature of the mitral annulus was largely attributable to its posterior intercommisural portion. It has long been considered axiomatic that the anterior annulus (the segment between the commissures along the aorta) is rigid because of its close association with the fibrous trigone of the base of the heart [2, 3]. This belief has lead to the idea of an unchanging anterior annulus, a structure that can be used as a reference to size annuloplasty rings and neglected during valve repair. This view remained unchallenged until Glasson and associates demonstrated some variability in the anterior annulus during the cardiac cycle in dogs [6]. However, recent reviews on mitral annular function still minimize [1] or question [13] the contribution of the anterior portion of the annulus to the dynamic nature of the mitral valve. Subsequent work by other groups has demonstrated the susceptibility of the anterior portion of the annulus to ventricular remodeling in both humans and experimental animals [10–12]. The effect of hemodynamic loading and contractile state on the anterior annulus has, however, remained poorly elucidated until the completion of this study.

The finding that increased afterload stretches the anterior annulus more than the posterior is consistent with the report of Lansac and associates [9], and likely is the result of aortic root distention. This phenomenon may, at least, partially explain the known positive correlation between afterload and the degree of functional or ischemic mitral regurgitation.

The contractility experiments presented here illustrate that at lower levels of inotropy the posterior annulus is in fact more dynamic than the anterior annulus but as inotropic state increases anterior annular contraction becomes quantitatively quite similar. The exact mechanism by which adrenergic stimulation affects the anterior annulus remains difficult to explain but does imply that there is a muscular component. It is likely that the anterior annulus is inhomogeneous in its material properties; being more fibrous (and less flexible) anteriorly and more muscular towards the posterior commissure. The spatial resolution of the sonomicrometry transducer array used in this study did not allow us to definitively comment on this point. But in previous work, using the same array to study the annular deformations associated with ischemic mitral regurgitation in an ovine model, we showed the potentially more fibrous portion of the anterior annulus stretched as much as any other segment as the ventricle remodeled [12].

Although the results presented here along with several other well done reports [5, 6, 9, 11, 12, 21] demonstrate that the anterior annular dimension often varies to the same extent as the posterior annulus the clinical implications are still not completely clear. How this relatively new information should affect the type of annuloplasty ring used during mitral valve repair is still difficult to determine. Despite this, complete ring annuloplasty is likely more appropriate in the treatment of functional and ischemic MR since in these disease states the entire annulus is distorted by the remodeling process. What can be said more definitively is that on an anatomic and physiologic basis the concept of a fixed, rigid and unchanging anterior annulus should be abandoned.

	Acknowledgments

Top Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Supported by 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 Acknowledgments References

 

1. Timek TA, Miller DC. Experimental and clinical assessment of mitral annular area and dynamics: what are we actually measuring? Ann Thorac Surg. 2001;72:966–974[Abstract/Free Full Text]
2. Choo SJ, Olomon J, Bowles C, et al. An in vivo study of the correlation between aortic valve diameter and mitral intertrigonal distance: a simple method to select the correct mitral annuloplasty ring size. J Heart Valve Dis. 1998;7:593–597[Medline]
3. Cosgrove DM, Arcidi JM, Rodriguez L, Stewart WJ, Powell K, Thomas JD. Initial experience with the Cosgrove-Edwards annuloplasty system. Ann Thorac Surg. 1995;60:499–504[Abstract/Free Full Text]
4. Oki T, Fukuda N, Luchi A, et al. Possible mechanisms of mitral regurgitation in dilated hearts: a study using transesophageal echocardiography. Clin Cardiol. 1996;19:639–643[Medline]
5. Tsakiris AG, von Bernuth G, Rastelli GS, Bourgeois MJ, Titus JL, Wood EG. Size and motion of the mitral valve annulus in anesthesized intact dogs. J Appl Physiol. 1971;30:611–618[Free Full Text]
6. Glasson JR, Komeda M, Daughters GT, et al. Three-dimensional regional dynamics of the normal mitral anulus during left ventricular ejection. J Thorac Cardiovasc Surg. 1996;111:574–585[Abstract/Free Full Text]
7. Komoda T, Hetzer R, Oellinger J, et al. Mitral annular flexibility. J Card Surg. 1997;12:102–109[Medline]
8. Flachskampf FA, Chandra S, Gadipatti A, et al. Analysis of shape and motion of the mitral annulus in subjects with and without cardiomyopathy by echocardiographic 3-dimensional reconstruction. J Am Soc Echocardiogr. 2000;13:277–287[Medline]
9. Lansac E, Lim KH, Shomura Y, et al. Dynamic balance of the aortamitral junction. J Thorac Cardiovasc Surg. 2002;123:911–918[Abstract/Free Full Text]
10. Hueb AC, Jatene FB, Moreira LFP, Pomerantzeff PM, Kallás E, De Oliveira SA. Ventricular remodeling and mitral valve modifications in dilated cardiomyopathies: new insights from anatomic study. J Thorac Cardiovasc Surg. 2002;124:1216–1224[Abstract/Free Full Text]
11. Tibayan FA, Rodriguez F, Langer F, et al. Annular geometric remodeling in chronic ischemic mitral regurgitation. Ann Thorac Surg. 2003;76:1549–1555[Abstract/Free Full Text]
12. Gorman JH III, Gorman RC, Jackson BM, Enomoto Y, St John-Sutton MG, Edmunds LH Jr. Annuloplasty ring selection for chronic ischemic mitral regurgitation: lessons from the ovine model. Ann Thorac Surg. 2003;76:1556–1563[Abstract/Free Full Text]
13. McCarthy PM. Does the intertrigonal distance dilate? Never say never. J Thorac Cardiovasc Surg. 2002;124:1078–1079[Free Full Text]
14. Gorman JH III, Gupta KB, Streicher JS, et al. Dynamic three-dimensional imaging of the mitral valve using rapid sonomicrometry array localization. J Thorac Cardiovasc Surg. 1996;112:712–725[Abstract/Free Full Text]
15. Gorman RC, McCaughan J, Ratcliffe MB, et al. Pathogenesis of acute ischemic mitral regurgitation in three dimensions. J Thorac and Cardiovasc Surg. 1995;109:684–693[Abstract/Free Full Text]
16. Gorman JH III, Jackson BM, Moainie SL, Enomoto Y, Gorman RC. The influence of inotropy and chronotropy on the mitral valve sphincter mechanism. Ann Thorac Surg. 2004;77:852–858[Abstract/Free Full Text]
17. Glasson JR, Komeda KM, Daughters GT, et al. Three dimensional dynamics of the canine mitral annulus during ischemic mitral regurgitation. Ann Thorac Surg. 1996;62:1059–1067[Abstract/Free Full Text]
18. Gorman JH, Jackson BM, Gorman RC, Kelley ST, Gikakis N, Edmunds LH Jr. Papillary muscle discoordination rather than increased annular area facilitates mitral regurgitation after acute posterior myocardial infarction. Circulation. 1997;96(Suppl II):124–127
19. Flachskampf FA, Chandra S, Gaddipatti A, et al. Analysis of shape and motion of the mitral annulus in subjects with and without cardiomyopathy by echocardiographic 3-dimensional reconstruction. J Am Soc Echocardiogr. 2000;13:277–287
20. Levine RA, Handschumacher MD, Sanfilippo AJ, et al. Three dimensional echocardiographic reconstruction of the mitral valve, with implications for the diagnosis of mitral valve prolapse. Circulation. 1989;80:589–598[Abstract/Free Full Text]
21. Hueb AC, Jatene FB, Moreira LFP, et al. Ventricular remodeling and mitral valve modifications in dilated cardiomyopathy: new insights from anatomic study. J Thorac Cardiovasc Surg. 2002;124:1216–1224

This article has been cited by other articles:

				P. G. Bruno, C. Leva, L. Santambrogio, I. Lazzarini, G. Musazzi, G. Del Rosso, and G. Di Credico Early Clinical Experience and Echocardiographic Results With a New Semirigid Mitral Annuloplasty Ring: The Sorin Memo 3D. Ann. Thorac. Surg., November 1, 2009; 88(5): 1492 - 1498. [Abstract] [Full Text] [PDF]

				A. Itoh, D. B. Ennis, W. Bothe, J. C. Swanson, G. Krishnamurthy, T. C. Nguyen, N. B. Ingels Jr., and D. C. Miller Mitral annular hinge motion contribution to changes in mitral septal-lateral dimension and annular area J. Thorac. Cardiovasc. Surg., November 1, 2009; 138(5): 1090 - 1099. [Abstract] [Full Text] [PDF]

				P. Ferrazzi, A. Iacovoni, S. Pentiricci, M. Senni, M. Iascone, N. Borenstein, L. Behr, A. Borghi, R. Balossino, and E. Quaini Toward the development of a fully elastic mitral ring: preliminary, acute, in vivo evaluation of physiomechanical behavior. J. Thorac. Cardiovasc. Surg., January 1, 2009; 137(1): 174 - 179. [Abstract] [Full Text] [PDF]

				L. P. Ryan, B. M. Jackson, H. Hamamoto, T. J. Eperjesi, T. J. Plappert, M. St. John-Sutton, R. C. Gorman, and J. H. Gorman III The Influence of Annuloplasty Ring Geometry on Mitral Leaflet Curvature Ann. Thorac. Surg., September 1, 2008; 86(3): 749 - 760. [Abstract] [Full Text] [PDF]

				W. Y. Szeto, R. C. Gorman, J. H. Gorman III, and M. A. Acker Ischemic Mitral Regurgitation Card. Surg. Adult, January 1, 2008; 3(2008): 785 - 802. [Full Text]

				L. P. Ryan, B. M. Jackson, L. M. Parish, H. Sakamoto, T. J. Plappert, M. St. John-Sutton, J. H. Gorman III, and R. C. Gorman Mitral Valve Tenting Index for Assessment of Subvalvular Remodeling Ann. Thorac. Surg., October 1, 2007; 84(4): 1243 - 1249. [Abstract] [Full Text] [PDF]

				L. P. Ryan, B. M. Jackson, L. M. Parish, T. J. Plappert, M. G. St. John-Sutton, J. H. Gorman III, and R. C. Gorman Regional and Global Patterns of Annular Remodeling in Ischemic Mitral Regurgitation Ann. Thorac. Surg., August 1, 2007; 84(2): 553 - 559. [Abstract] [Full Text] [PDF]

				H. Sakamoto, L. M. Parish, H. Hamamoto, Y. Enomoto, A. Zeeshan, T. Plappert, B. M. Jackson, M. G. St. John-Sutton, R. C. Gorman, and J. H. Gorman III Effects of hemodynamic alterations on anterior mitral leaflet curvature during systole J. Thorac. Cardiovasc. Surg., December 1, 2006; 132(6): 1414 - 1419. [Abstract] [Full Text] [PDF]

				M. T. Spoor, A. Geltz, and S. F. Bolling Flexible Versus Nonflexible Mitral Valve Rings for Congestive Heart Failure: Differential Durability of Repair Circulation, July 4, 2006; 114(1_suppl): I-67 - I-71. [Abstract] [Full Text] [PDF]

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