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):
Sunil K. Bhudia
Buu-Khanh Lam
Eugene H. Blackstone
Bruce W. Lytle
Lars G. Svensson
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 Bhudia, S. K.
Right arrow Articles by Svensson, L. G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bhudia, S. K.
Right arrow Articles by Svensson, L. G.
Related Collections
Right arrow Valve disease

Ann Thorac Surg 2006;81:843-848
© 2006 The Society of Thoracic Surgeons


Original article: Cardiovascular

Mitral Valve Surgery in the Adult Marfan Syndrome Patient

Sunil K. Bhudia, MD a , Richard Troughton, MD, PhD b , Buu-Khanh Lam, MD a , Jeevanantham Rajeswaran, MS c , William R. Mills, MD b , A. Marc Gillinov, MD a , Brian P. Griffin, MD c , Eugene H. Blackstone, MD a , c , Bruce W. Lytle, MD a , Lars G. Svensson, MD, PhD a , *

a Marfan Syndrome and Connective Tissue Disorder Clinic, Department of Thoracic and Cardiovascular Surgery, The Cleveland Clinic Foundation, Cleveland, Ohio
b Department of Cardiovascular Medicine, The Cleveland Clinic Foundation, Cleveland, Ohio
c Department of Quantitative Health Sciences, The Cleveland Clinic Foundation, Cleveland, Ohio

Accepted for publication August 29, 2005.

* Address correspondence to Dr Svensson, Aortic Surgery Center, Marfan Syndrome and Connective Tissue Disorder Clinic, Cleveland Clinic Foundation, 9500 Euclid Ave, Desk F24, Cleveland, OH 44195 (Email: svenssl{at}ccf.org).


    Abstract
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 References
 
BACKGROUND: Because mitral valve dysfunction in adults with Marfan syndrome is poorly characterized, this study compares mitral valve pathophysiology and morphology with that of myxomatous mitral disease, documents types of mitral valve operations, and assesses long-term survival and durability of mitral valve surgery in Marfan patients.

METHODS: From May 1975 to June 2000, 27 adults with Marfan syndrome underwent mitral valve surgery. Their valve pathophysiology and morphology was compared with that of 119 patients with myxomatous mitral disease undergoing surgery from September 1995 to March 1999. Survival and repair durability were assessed at follow-up.

RESULTS: Compared with myxomatous disease patients, Marfan patients had less posterior leaflet prolapse (44% versus 70%, p= 0.01), more bileaflet (44% versus 28%, p= 0.09) and anterior leaflet prolapse (11% versus 3%, p = 0.07), and presented earlier for surgery (age 41 ± 12 years versus 57 ± 13, p < 0.0001). Marfan patients had longer and thinner leaflets. Mitral valve repair was performed less frequently in Marfan (16 of 27, 59%) than myxomatous disease patients (112 of 119, 94%). There were no hospital deaths; at 10 years, survival was 80% and freedom from reoperation 96%, with only 1 reoperation among the 16 repairs.

CONCLUSIONS: Mitral valve pathophysiology and morphology differ between Marfan and myxomatous mitral valve diseases. Valve repair in Marfan patients is durable and gives acceptable long-term results, even in adults who present with advanced mitral valve pathology. With increasing use of the modified David reimplantation operation and sparing of the aortic valve, mitral valve repair is a greater imperative, particularly since we have not had to reoperate on any Marfan patients with reimplantations.


    Introduction
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 References
 
Marfan syndrome is an inherited autosomal dominant connective tissue disorder characterized by cardiovascular, skeletal, and ocular abnormalities [1]. Mitral valve dysfunction occurs in 80% of patients, and by age 30 years, 1 in 8 has moderate to severe mitral regurgitation [1, 2]. Mitral valve abnormalities in these patients have received little attention, however.

In general, mitral valve repair is preferable to replacement [3–9]. For mitral regurgitation, valve reconstruction is possible in as many as 90% of cases; and in patients with myxomatous mitral valve disease, repair is durable. Gross features of myxomatous mitral valve disease—chordal elongation, chordal rupture, and excess leaflet tissue—are also common in Marfan syndrome.

Although outcome of mitral valve surgery in Marfan patients has been reported [10, 11], those studies included both children and adults and failed to provide quantitative measurements of mitral valve morphology. Therefore, purposes of this study were to compare mitral valve pathophysiology and morphology of Marfan disease in adults with that of myxomatous mitral disease, document types of mitral valve operations performed, and assess long-term survival and durability of mitral valve surgery in Marfan patients.


    Patients and Methods
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 References
 
Patients
From May 1, 1975, to June 1, 2000, 27 patients with Marfan syndrome underwent mitral valve surgery at The Cleveland Clinic Foundation. Charts were reviewed for the correct diagnosis of Marfan syndrome and for excluding other connective tissue disorders in the myxomatous group of patients. Preoperative, intraoperative, and postoperative variables were retrieved from the prospective Cardiovascular Information Registry, which has been approved for use in research by the Institutional Review Board.

Age of patients ranged from 20 to 69 years, and 13 (48%) were men. Their presentation, surgical management, and mitral valve pathophysiology and morphometrics were compared with those of 119 patients with myxomatous mitral disease who had undergone mitral valve surgery from September 1995 to March 1999 and had echocardiograms available for measurements. Age of patients with myxomatous disease ranged from 26 to 82 years, and 91 (76%) were men.

Mitral Valve Pathophysiology and Morphometrics
Echocardiograms of both groups were reviewed by a cardiologist (B.G., R.T., or W.M.) to obtain mitral valve leaflet and anular dimensions. Echocardiographic procedures were performed in standard fashion and were recorded on videotape for analysis [12]. Transesophageal echocardiography was performed with either multiplane or, rarely, biplane transducers. Gain settings were not evaluated for comparisons.

All measurements were made offline using standard echocardiographic measurement software and techniques [12]. Leaflet length was measured from the anular hinge point to the free edge, excluding chordae. Thickness of each leaflet was measured just distal to the hinge point, at the approximate midpoint (near the rough zone–clear zone junction), and at the tip [13]. Mean thickness for each leaflet was obtained by averaging these measurements. All measurements were indexed to body surface area.

Principles of Operative Repair
In Marfan patients who underwent mitral valve repair, the Cosgrove-Edwards anuloplasty band was increasingly used after 1996. As a general principle, when the height of the posterior leaflet exceeded 1.5 cm, a posterior leaflet sliding repair was used. It was used more frequently in Marfan patients than in those with myxomatous valves because their posterior leaflets were larger (Table 1). Also, calcification, which was not a contraindication to repair versus replacement, was more frequently debrided in the posterior anulus. Because anterior leaflet prolapse was also more frequent in Marfan syndrome patients, chordal transfer or artificial chordae were more often used. Of note, when Marfan patients received a mechanical aortic valve, their mitral valve was usually replaced rather than repaired. It should be noted, however, that since the closing date of this study, we try to do a modified David reimplantation operation for all aortic root procedures; thus, we also perform mitral valve repair if needed in these patients. Because myxomatous valve patients did not usually require aortic valve replacement, repair was more frequently performed. In addition, leaflet pathology was less complex (see Table 1).


View this table:
[in this window]
[in a new window]
 
Table 1. Mitral Valve Leaflet Pathophysiology and Morphometrics in Marfan Syndrome and Myxomatous Mitral Valve Disease
 
Outcome of Operation
Patients were followed up routinely every 2 years after operation, and this information was supplemented by the Social Security Death Index to determine vital status. Two hundred eighteen patient-years of follow-up were available for analysis. Among survivors, median follow-up was 6 years (mean, 7 ± 4), with 25% followed up for more than 9 years.

Estimates of survival and freedom from mitral valve reoperation were obtained by the Kaplan-Meier method [14] and by a parametric method that resolves the number of phases of instantaneous risk and estimates shaping parameters [15]. (For additional details, go to: http://www.clevelandclinic.org/heartcenter/hazard.)

Presentation
Continuous variables are summarized using mean ± SD, and categorical variables using frequencies and percentages. Comparison of continuous variables utilized Student's t test, and categorical variables, Fisher's exact test. Survival estimates are presented with 68% confidence limits (CL), equivalent to ± 1 standard error (SE).


    Results
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 References
 
Mitral Valve Pathophysiology and Morphometrics
Patients with Marfan syndrome presented at a younger age than those with myxomatous disease (41 ± 12 versus 57 ± 13 years, p< 0.0001) and were less likely to be male (13 of 27 [48%] versus 91 of 119 [76%], p = 0.008) (Table 1). In both Marfan syndrome and myxomatous disease, posterior leaflet prolapse (88% versus 98%) was the most common pathophysiologic finding. However, isolated posterior leaflet prolapse was less common in Marfan syndrome and bileaflet prolapse more typical (see Table 1).

Anterior and posterior leaflets were longer and thinner in patients with Marfan syndrome than in those with myxomatous disease (see Table 1). After indexing leaflet dimensions to body surface area, Marfan syndrome patients had longer anterior leaflets (p = 0.03) and thinner anterior (p = 0.002) and posterior (p = 0.0007) leaflets compared with myxomatous disease patients.

Mitral Valve Operation
Mitral valve repair was performed in 16 patients (59%) and replacement in 11 (41%). Marfan patients were less likely to undergo repair than were those with myxomatous disease (16 of 27 [59%] versus 112 of 119 [94%], p < 0.0001). Distribution of mitral valve repair compared with replacement over the 25-year period is shown in Table 2. Most patients undergoing valve repair had no concomitant procedure, whereas more than half of those undergoing replacement did (Table 3).


View this table:
[in this window]
[in a new window]
 
Table 2. Number of Mitral Valve Repairs Versus Replacements During the Study Period
 

View this table:
[in this window]
[in a new window]
 
Table 3. Characteristics of Marfan Syndrome Patients
 
Among patients undergoing repair, posterior mitral leaflet pathology was most common, whereas in patients who had replacement, bileaflet pathology was most often seen (Table 4). More Marfan syndrome patients who underwent mitral valve repair had anular calcification than those undergoing mitral valve replacement (see Table 4). A Cosgrove-Edwards anuloplasty band was placed in 14 patients (86%) undergoing repair, with 34 mm the most common size. In patients undergoing replacement, a bileaflet mechanical prosthesis was utilized in 8 (74%), a porcine xenograft in 2 (18%), and a ball-and-cage valve in 1 (9%).


View this table:
[in this window]
[in a new window]
 
Table 4. Mitral Valve Pathophysiology in Marfan Syndrome Patients at Operation
 
Outcome of Operation
Survival
There were no hospital deaths (0 of 27; CL: 0% to 6.9%). Survival at 1, 3, 5, and 10 years was 100%, 97%, 94%, and 80%, respectively (Fig 1). No patient undergoing mitral valve repair died during follow-up.


Figure 1
View larger version (11K):
[in this window]
[in a new window]
 
Fig 1. Survival after mitral valve surgery in patients with Marfan syndrome. Symbols represent Kaplan-Meier estimates, and vertical bars are 68% confidence limits. Numbers in parentheses represent patients at risk. Solid line shows parametric estimates enclosed within dashed 68% confidence limits.

 
Reoperation
During 12 years of follow-up, there were two mitral valve reoperations. One occurred 2 weeks after mitral valve repair (for torn posterior leaflet), and the other occurred 12 years after mitral valve replacement (for cardiomyopathy). Overall actuarial freedom from mitral valve reoperation at 1 month and 10 years was 96% (Fig 2).


Figure 2
View larger version (7K):
[in this window]
[in a new window]
 
Fig 2. Freedom from reoperation after mitral valve surgery in patients with Marfan syndrome. Symbol represents Kaplan-Meier estimate, and vertical bar is 68% confidence limits. Numbers in parentheses represent patients at risk.

 

    Comment
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 References
 
Marfan syndrome is the most common heritable connective tissue disorder with multisystem manifestations [1]. Cardiovascular manifestations include aneurysmal dilatation of the ascending aorta, aortic valvar regurgitation, aortic dissection, floppy mitral valve with mitral valve prolapse, mitral valvar regurgitation, and mitral anular dilatation [1, 16–19]. If untreated, cardiovascular manifestations account for as high as 50% mortality during the first 4 decades of life [18, 20]. Aortic root dilatation and aortic complications account for most of these deaths [18].

Mitral valve abnormalities have received little attention in the past, despite 80% of patients with Marfan syndrome having mitral valve dysfunction [2, 11, 21]. In the pediatric Marfan population, mitral valve dysfunction is the most common cause of mortality and morbidity [18, 20]. On clinical examination and echocardiographic investigation, 60% to 80% of pediatric Marfan patients have mitral prolapse [2, 11, 21]. This is progressive: by the age of 30 years, 1 in 8 patients has moderate to severe mitral regurgitation [2]. Once the mitral valve is regurgitant, pathologic findings include fibromyxomatous changes of the leaflets and chordae, anular dilatation, calcium deposits, and elongation and rupture of the chordae [2, 21].

Principal Findings
Pathophysiology and morphometrics
Unlike myxomatous mitral valve disease that leads predominantly to posterior leaflet prolapse, mitral valve disease in Marfan patients leads to nearly equal anterior and posterior leaflet prolapse. Leaflets were longer and thinner than in myxomatous disease. This information adds to what is already known about the histopathologic distinctions between the two disease processes [22].

Mutations in the fibrillin-1 (FBN1) locus on chromosome 15, the gene that encodes for fibrillin-1, are responsible for the syndrome [23]. Fibrillin-1 monomers form complex extracellular macroaggregates called microfibrils. These are important for the integrity and homeostasis of both elastic and nonelastic tissues [24, 25]. Microfibrils serve as an anchoring scaffold in the construction of the elastin network. Mutations of fibrillin-1 result in a wide range of phenotypes that show considerable variation in timing of onset, tissue distribution, and severity of clinical manifestation [26]. Microfibrils may also play a role in clinical manifestation by modulating expression of various cytokines [27].

Although Marfan syndrome and myxomatous mitral valves share some characteristics, there are few data comparing them directly. In mitral valve leaflets and aortic valve cusps of Marfan syndrome patients, fibrillin density is reduced and other fibers are partially or completely fragmented [28]. Myxomatous mitral valve tissue is thicker than normal tissue, but the additional thickness does not contribute mechanical strength [29], perhaps owing to an increase in glycosaminoglycan in the tissue, which binds with water and causes tissue swelling and disruption of collagen fibers, resulting in reduced mechanical strength [30].

Fornes and colleagues [22] compared mitral valves of Marfan patients with those of myxomatous disease patients and found that the former had more elastic fiber alteration. Conversely, myxomatous valves had more myxoid infiltration than Marfan syndrome valves. These two findings are consistent with the echocardiographic morphometrics found in our study.

Outcome of operation
Mitral valve surgery is a safe procedure in Marfan syndrome patients, as evidenced by 0% hospital mortality in our group as well as in the series reported by Gillinov and colleagues [11]. Long-term survival was almost 80% at 10 years, which compares well with previous reports, despite our older patient population [10].

Mitral valve operation
In mitral valve surgery, repair is the preferred option when possible [3–9]. A previous study showed that the majority of Marfan patients requiring mitral valve operation could be treated successfully with repair [11]. In that report, however, mean age was 26 ± 2.6 years, and 7 of the 29 patients were under age 18 years. Furthermore, many had mild to moderate regurgitation, and the mitral valve was repaired concurrently with aortic root and ascending aorta replacement. In our study, mean age was 41 years (youngest age was 20 years), mitral valve disease was more advanced, and only 16 of the 27 patients had valve repair.

Mitral valve repair was performed in 86% of patients who did not require a concomitant procedure, compared with only 30% of those who did. Clearly, the older practice of aortic valve replacement influenced the decision to replace the mitral valve as well. Since this series, based on increasing experience with aortic-valve–sparing and root-preserving procedures in 389 patients through December 2004, 73 using the David reimplantation operation [11], we have performed 24 David reimplantations in Marfan patients, including mitral valve repair in 6. Thus, with increasing preservation of the aortic valve, avoiding anticoagulation by repairing the mitral valve has become increasingly important. Furthermore, our freedom from reoperation for David reimplantation is 97% at 10 years, similar to the 96% for mitral valve procedures in this series of Marfan patients.

Limitations
Limitations of this study include the small number of patients; moreover, we do not know what proportion of all Marfan syndrome patients who had cardiac surgery are represented by our sample. Also, the study period extended from 1975 to 2000, and during this time, medical and surgical management evolved and understanding of the disease process improved. Imaging methods have also improved. There may have been a bias toward mitral valve replacement in Marfan syndrome patients in the earlier years. An implicit assumption is that indications for operation for Marfan syndrome and myxomatous disease patients are sufficiently similar to allow valid comparison of mitral valve morphometrics. We appreciate that there is a spectrum of heritable connective tissue disorders that may present with mitral valve disease; however, every effort was made to identify presence of a heritable disorder before categorizing a patient as having noninherited mitral valve prolapse. Nevertheless, we based this categorization on limited genomic data. Finally, we have limited longitudinal echocardiographic data to assess repair durability, in part, because of HIPAA regulations that limit our ability to obtain echocardiograms from outside referring cardiologists.

In conclusion, the pathophysiology and morphometrics of mitral valves in Marfan syndrome and myxomatous disease are different. Mitral valve surgery in Marfan syndrome patients can be performed safely despite multisystem involvement. Mitral valve repair is durable and gives acceptable long-term results, even for adults who may present with advanced valve pathology.


    References
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 References
 

  1. Pyeritz RE. The Marfan syndrome Annu Rev Med 2000;51:481-510.[Medline]
  2. Pyeritz RE, Wappel MA. Mitral valve dysfunction in the Marfan syndrome. Clinical and echocardiographic study of prevalence and natural history Am J Med 1983;74:797-807.[Medline]
  3. Carpentier A. Cardiac valve surgery—the "French correction." J Thorac Cardiovasc Surg 1983;86:323-337.[Medline]
  4. Chauvaud S, Fuzellier JF, Houel R, Berrebi A, Mihaileanu S, Carpentier A. Reconstructive surgery in congenital mitral valve insufficiency (Carpentier's techniques)long-term results. J Thorac Cardiovasc Surg 1998;115:84-93.[Abstract/Free Full Text]
  5. Cohn LH, Couper GS, Aranki SF, Rizzo RJ, Kinchla NM, Collins Jr JJ. Long-term results of mitral valve reconstruction for regurgitation of the myxomatous mitral valve J Thorac Cardiovasc Surg 1994;107:143-151.[Abstract/Free Full Text]
  6. Cosgrove DM, Chavez AM, Lytle BW, et al. Results of mitral valve reconstruction Circulation 1986;74(Suppl):I82-I87.
  7. Cosgrove DM, Stewart WJ. Mitral valvuloplasty Curr Probl Cardiol 1989;14:359-415.[Medline]
  8. Gillinov AM, Cosgrove DM, Blackstone EH, et al. Durability of mitral valve repair for degenerative disease J Thorac Cardiovasc Surg 1998;116:734-743.[Abstract/Free Full Text]
  9. Yun KL, Miller DC. Mitral valve repair versus replacement Cardiol Clin 1991;9:315-327.[Medline]
  10. Fuzellier JF, Chauvaud SM, Fornes P, et al. Surgical management of mitral regurgitation associated with Marfan's syndrome Ann Thorac Surg 1998;66:68-72.[Abstract/Free Full Text]
  11. Gillinov AM, Hulyalkar A, Cameron DE, et al. Mitral valve operation in patients with the Marfan syndrome J Thorac Cardiovasc Surg 1994;107:724-731.[Abstract/Free Full Text]
  12. Otto CM. The practice of clinical echocardiography2nd ed.. Philadelphia: WB Saunders; 2002.
  13. Weissman NJ, Pini R, Roman MJ, Kramer-Fox R, Andersen HS, Devereux RB. In vivo mitral valve morphology and motion in mitral valve prolapse Am J Cardiol 1994;73:1080-1088.[Medline]
  14. Kaplan EL, Meier P. Nonparametric estimation from incomplete observations J Am Stat Assoc 1958;53:457-481.
  15. Blackstone EH, Naftel DC, Turner Jr ME. The decomposition of time-varying hazard into phases, each incorporating a separate stream of concomitant information J Am Stat Assoc 1986;81:615-624.
  16. Savolainen A, Savolainen H, Savunen T, et al. Results of cardiovascular surgery in the Marfan syndrome. A retrospective study of 49 patients Scand J Thorac Cardiovasc Surg 1995;29:11-15.[Medline]
  17. el Habbal MH. Cardiovascular manifestations of Marfan's syndrome in the young Am Heart J 1992;123:752-757.[Medline]
  18. van Karnebeek CD, Naeff MS, Mulder BJ, Hennekam RC, Offringa M. Natural history of cardiovascular manifestations in Marfan syndrome Arch Dis Child 2001;84:129-137.[Abstract/Free Full Text]
  19. Svensson LG, Crawford ES, Coselli JS, Safi HJ, Hess KR. Impact of cardiovascular operation on survival in the Marfan patient Circulation 1989;80(Suppl):I233-I242.
  20. Murdoch JL, Walker BA, Halpern BL, Kuzma JW, McKusick VA. Life expectancy and causes of death in the Marfan syndrome N Engl J Med 1972;286:804-808.
  21. Hirata K, Triposkiadis F, Sparks E, Bowen J, Boudoulas H, Wooley CF. The Marfan syndromecardiovascular physical findings and diagnostic correlates. Am Heart J 1992;123:743-752.[Medline]
  22. Fornes P, Heudes D, Fuzellier JF, Tixier D, Bruneval P, Carpentier A. Correlation between clinical and histologic patterns of degenerative mitral valve insufficiencya histomorphometric study of 130 excised segments. Cardiovasc Pathol 1999;8:81-92.[Medline]
  23. Montgomery RA, Geraghty MT, Bull E, et al. Multiple molecular mechanisms underlying subdiagnostic variants of Marfan syndrome Am J Hum Genet 1998;63:1703-1711.[Medline]
  24. Sakai LY, Keene DR, Engvall E. Fibrillin, a new 350-kD glycoprotein, is a component of extracellular microfibrils J Cell Biol 1986;103:2499-2509.[Abstract/Free Full Text]
  25. Pereira L, Andrikopoulos K, Tian J, et al. Targetting of the gene encoding fibrillin-1 recapitulates the vascular aspect of Marfan syndrome Nat Genet 1997;17:218-222.[Medline]
  26. Dietz HC, Pyeritz RE. Mutations in the human gene for fibrillin-1 (FBN1) in the Marfan syndrome and related disorders Hum Mol Genet 1995;4:1799-1809.[Abstract]
  27. Ng CM, Cheng A, Myers LA, et al. TGF-beta-dependent pathogenesis of mitral valve prolapse in a mouse model of Marfan syndrome J Clin Invest 2004;114:1586-1592.[Medline]
  28. Fleischer KJ, Nousari HC, Anhalt GJ, Stone CD, Laschinger JC. Immunohistochemical abnormalities of fibrillin in cardiovascular tissues in Marfan's syndrome Ann Thorac Surg 1997;63:1012-1017.[Abstract/Free Full Text]
  29. Barber JE, Ratliff NB, Cosgrove III DM, Griffin BP, Vesely I. Myxomatous mitral valve chordae. I: Mechanical properties J Heart Valve Dis 2001;10:320-324.[Medline]
  30. Grande-Allen KJ, Griffin BP, Calabro A, Ratliff NB, Cosgrove III DM, Vesely I. Myxomatous mitral valve chordae. II: Selective elevation of glycosaminoglycan content J Heart Valve Dis 2001;10:325-333.[Medline]



This article has been cited by other articles:


Home page
CirculationHome page
S. Goland and U. Elkayam
Cardiovascular Problems in Pregnant Women With Marfan Syndrome
Circulation, February 3, 2009; 119(4): 619 - 623.
[Full Text] [PDF]


Home page
CirculationHome page
G. D. Pearson, R. Devereux, B. Loeys, C. Maslen, D. Milewicz, R. Pyeritz, F. Ramirez, D. Rifkin, L. Sakai, L. Svensson, et al.
Report of the National Heart, Lung, and Blood Institute and National Marfan Foundation Working Group on Research in Marfan Syndrome and Related Disorders
Circulation, August 12, 2008; 118(7): 785 - 791.
[Full Text] [PDF]


Home page
CirculationHome page
M. G. Keane and R. E. Pyeritz
Medical Management of Marfan Syndrome
Circulation, May 27, 2008; 117(21): 2802 - 2813.
[Full Text] [PDF]


Home page
Ann. Thorac. Surg.Home page
L. G. Svensson, E. H. Blackstone, J. Feng, D. de Oliveira, A. M. Gillinov, M. Thamilarasan, R. A. Grimm, B. Griffin, D. Hammer, T. Williams, et al.
Are Marfan Syndrome and Marfanoid Patients Distinguishable on Long-Term Follow-Up?
Ann. Thorac. Surg., March 1, 2007; 83(3): 1067 - 1074.
[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):
Sunil K. Bhudia
Buu-Khanh Lam
Eugene H. Blackstone
Bruce W. Lytle
Lars G. Svensson
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 Bhudia, S. K.
Right arrow Articles by Svensson, L. G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bhudia, S. K.
Right arrow Articles by Svensson, L. G.
Related Collections
Right arrow Valve disease


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