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(Chest. 2000;117:636-642.)
© 2000 American College of Chest Physicians

Is Mitral Valve Prolapse Due to Cardiac Entrapment in the Chest Cavity?*

A CT View

Paolo Raggi, MD; Tracy Q. Callister, MD, FCCP; Nicholas J. Lippolis, MD and Donald J. Russo, MD

* From the EBT Research Foundation, Nashville, TN.

Correspondence to: Paolo Raggi, MD, Director, EBT Research Foundation, 64 Valleybrook Dr, Hendersonville, TN 37075; e-mail: praggi{at}ibm.net


   Abstract
TOP
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 References
 
Background: Mitral valve prolapse (MVP) is the most frequently diagnosed valvular disease, but its pathophysiology remains elusive. Its complete absence in 1,734 neonatal echocardiographic studies suggests that this may be an acquired rather than a congenital disease. We observed several patients with distorted cardiac and valvular anatomies on electron beam CT (EBCT) images of the chest who reported symptoms reminiscent of MVP. In these patients, the heart is compressed between the spine and the anterior chest wall and it appears trapped in a chest cavity that is too small for its size.

Methods: We performed EBCT in 66 patients with echocardiographically proven MVP and no clinical pectus excavatum (group A; 80% were women; mean age, 48 ± 12 years) and in 96 control patients without MVP by echocardiography (group B; 72% were women; mean age, 49 ± 10 years). EBCT alone was also performed on 200 patients who had reported atypical chest discomfort and palpitations to their physicians (group C) and on 200 asymptomatic patients (group D). The EBCT measurements included the following: anteroposterior chest diameter (APD); the angle formed by the confluence of the mitral valve ring with the interatrial septum (ANGLE); and the contact area between the posterior surface of the anterior chest wall and the myocardium (CA). Entrapment was considered present if the individual patient’s measurements varied by more than two SDs compared to measurements made in control subjects (group B).

Results: EBCT images demonstrated cardiac entrapment in 82% of group A patients and in 4.2% of group B patients (p < 0.001). ANGLE and CA were significantly larger in MVP patients than in group B patients (114 ± 9° vs 91 ± 5° and 6,230 ± 2,020 mm2 vs 476 ± 1,009 mm2, respectively; p < 0.001 for both comparisons), while APD was significantly smaller (91 ± 16 mm vs 128 ± 17 mm, respectively; p < 0.001). The prevalence of entrapment was significantly greater in group C patients than in group D patients (22% vs 6.5%; p < 0.001).

Conclusions: MVP may be an acquired condition caused by a growth disproportion between the heart and the chest cavity, with distortion of the mitral valve annulus and subsequent leaflet prolapse. A narrow APD, a wide ANGLE, and a large CA characterize this condition. Similar findings are found in a sizable proportion of patients with atypical chest pain symptoms and palpitations.

Key Words: electron beam computed tomography • mitral valve prolapse • thoracic radiography • thorax


   Introduction
TOP
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 References
 
Mitral valve prolapse (MVP) is currently the most commonly diagnosed form of valvular heart disease in the western countries,1 2 3 and yet its etiology and pathophysiology remain unknown. Some investigators have suggested that this condition is inherited as an autosomal dominant trait.4 5 However, the reported complete absence of MVP in 1,734 newborn echocardiographic studies seems to refute this opinion.6 Several other pathophysiologic explanations have been proposed, such as undetected rheumatic fever in childhood,7 8 myxomatous degeneration of valve leaflets and chordae tendinae,9 and valvular-ventricular disproportion.10 11 12 13 MVP has also been described in association with Marfan’s syndrome, straight back syndrome, scoliosis, and pectus excavatum.14 15 16 17 18 19 20 21 These associations indicate that chest deformities may play an important role in the pathophysiology of this condition or, alternatively, that these conditions are in some way developmentally related. We observed several patients with unusual anatomic cardiac features on electron beam CT (EBCT) images of the chest who reported symptoms reminiscent of the MVP syndrome. In the EBCT images, the heart appears trapped in the chest cavity and the mitral valve annulus undergoes a morphologic distortion that could predispose to the development of MVP. Therefore, we undertook this EBCT and echocardiographic comparative study to assess the relationship between echocardiographically proven MVP and cardiac entrapment on EBCT. Subsequently, we assessed the prevalence of cardiac entrapment in a subset of patients with chest discomfort and palpitations but no evidence of MVP and in a matched group of control subjects with no symptoms. This was done to verify the frequency with which the cardiothoracic morphologic abnormalities we describe in this study are found in the population at large and in a group of patients lamenting symptoms similar to those of MVP patients.


   Materials and Methods
TOP
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 References
 
Patients
The study was approved by the Internal Review Board of our institution, and all patients signed an informed consent form prior to participating in the study. For the first part of the study, we enrolled 66 patients with echocardiographically proven MVP (group A) and 96 control patients (group B) with no evidence of MVP on echocardiography. None of these patients showed evidence of pectus excavatum on physical examination, and they all underwent echocardiography followed by EBCT imaging. Of the 66 patients in group A, 53 were women (80%; mean ± SD age, 48 ± 12 years). Of the 96 patients in group B, 69 were women (72%; mean ± SD age, 49 ± 10 years). For the second part of the study, EBCT scanning was performed on 200 patients who had reported atypical chest discomfort and palpitations to their physicians (group C; 50% were women; mean ± SD age, 50 ± 11 years) and on 200 asymptomatic patients (group D, 50% were women; mean ± SD age, 52 ± 12 years).

Imaging Protocols
Electron Beam CT: Electron beam CT is a radiologic imaging technique that allows the acquisition of accurate images of the heart and coronary arteries at very high speed to perform their computerized tomographic reconstruction.22 23 24 The fast imaging speed is necessary to prevent blurring of the images due to the continuous motion of the heart. The high quality of the images obtained allows for a detailed analysis of the cardiothoracic structures included in the field of view. All study patients underwent EBCT imaging (Imatron C-100 scanner; Imatron; San Francisco, CA). Scanning was performed with the patients lying in a supine position on a radiologic cradle during two 30- to 40-s breath-holding periods at end-inspiration. In these conditions, the respiratory motion artifacts and the area of contact between the myocardium and the anterior chest wall are reduced to a minimum. Images were obtained with 100-ms scan time and 3-mm single-slice thickness, with a total of 36 slices starting at the level of the carina and proceeding to the level of the diaphragm. Tomographic imaging was electrocardiographically triggered to 80% of the R-R interval. Off-line analysis of chest images was performed on a NetraMD workstation (ScImage; Los Altos, CA) with fly-through, calipers, and three-dimensional reconstruction capabilities. Interpretation of the EBCT images was performed by two expert investigators blinded to the results of the echocardiographic studies performed in patients in groups A and B. The following measurements were performed on all EBCT images (Fig 1 , top, A and bottom, B): (1) The anteroposterior chest diameter (APD), as measured between the posterior surface of the anterior chest wall and the anterior border of a vertebral body. The measurement was made at the level of the narrowest thoracic point still including all four cardiac chambers. (2) The angle formed by the confluence of the mitral valve ring with the interatrial septum (ANGLE; Fig 2 , top, A and bottom, B ). The mitral valve ring plane lies along the atrioventricular groove, and it can be identified by drawing a line joining the proximal segments of the left circumflex and right coronary artery. The interatrial septum plane can then be easily identified by scrolling through multiple cranial-to-caudal axial images of the heart. (3) The contact area between the posterior surface of the anterior chest wall and the myocardium (CA). To calculate this area, we multiplied the maximum contact lengths between chest wall and myocardium measured in the axial and sagittal views of the chest. The EBCT measurements made in the 96 control patients enrolled in group B were used as reference measurements. For the patients in groups A, C, and D, cardiac entrapment was considered present if their EBCT measurements differed by more than two SDs compared to those made in group B patients. We developed these computed tomographic criteria from a cohort of asymptomatic control subjects with echocardiographically proven absence of MVP (group B patients), since there are no pertinent published criteria in the current radiologic literature.



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  		Figure 1.. Top, A: An axial CT view of the chest in a patient without MVP. Note the spherical shape of the heart and the absence of contact between the myocardium and the anterior chest wall. Bottom, B: An axial CT view of the chest in a patient with echocardiographically proven MVP. Note the narrow APD, the obtuse ANGLE, and the large CA. The chest configuration appears similar to a horizontally placed "figure eight." AP = APD.

 


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  		Figure 2.. An electron beam CT image showing the reference markers used for the identification of the mitral valve plane and the interatrial septum. Top, A: the image is shown without the lines identifying the AV groove and the septum. Bottom, B: the same image is now shown after the addition of the lines used to define the ANGLE.

 
In two patients, 125 mL of IV iodine contrast were injected at a rate of 5 mL/s to perform a noninvasive contrast cineangiogram for visualization of the cardiac chambers and valvular structures (Fig 3 ). In these patients, images were acquired using the multislice scanning mode and a slice thickness of 8 mm.22



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  		Figure 3.. An electron beam CT systolic angiographic frame demonstrating prolapse of the posterolateral leaflet of the mitral valve inside the left atrium (arrow) in a patient with cardiac entrapment. LA = left atrium; LV = left ventricle; RA = right atrium; RV = right ventricle.

 
Echocardiography: Echocardiographic measurements were made using commercially available phased-array echocardiographic systems (CFM750; VingMed Sound A/S; Horten, Norway and Sonos 2000; Hewlett-Packard; Palo Alto, CA) equipped with 2.5- and 3.5-MHz transducers. Comprehensive two-dimensional and M-mode scanning, as well as Doppler interrogation and color flow analysis were performed in the parasternal long-axis and apical 2, 4 and 5 chamber views. All studies were recorded on one-half inch VHS-format videotapes and reviewed off-line by an expert investigator independent of the EBCT investigator and unaware of the results of the EBCT imaging procedures. MVP was diagnosed by the following standard echocardiographic criteria: (A) two-dimensional mode, the posterior-superior displacement of one or both leaflets above the mitral valve annulus in the parasternal long-axis view; and (B) M-mode, the systolic posterior displacement of a mitral leaflet of >= 3 mm.

Statistical Analysis
The two-tailed t test was used to compare continuous variables between patient groups. The {chi}2 and test-on-proportions were utilized for comparison of categorical variables. All variables were expressed as mean ± SD. A p value < 0.05 was considered statistically significant.


   Results
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 References
 
Group A vs Group B Subjects
The clinical characteristics and EBCT measurements for the patients with echocardiographically proven MVP and for the respective age-matched control subjects are presented in Table 1 . As shown, the mean ANGLE and CA were significantly greater, while the mean APD was significantly smaller in patients with echocardiographically proven MVP than in group B patients (114 ± 9° vs 91 ± 5° and 6,230 ± 2,020 mm2 vs 476 ± 1,009 mm2, and 91 ± 16 mm vs 128 ± 17 mm, respectively; p < 0.001 for all comparisons). All group A patients presented measurements of ANGLE and CA above the mean of the normal control subjects, and all had APD measurements below the mean for the control subjects. Cardiac entrapment, as defined by a difference of more than two SDs from expected values, was present in 82% of group A patients and in 4.2% of group B patients (p < 0.001).


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  		Table 1.. Clinical Characteristics and Chest CT Measurements*

 
No significant differences in APD, ANGLE, and CA measurements were found between male patients and female patients in group A, although there was a tendency for female patients to show a smaller APD than male patients (89 ± 16 mm vs 98 ± 16 mm; p = not significant [NS]). This tendency is known to occur in the general population as well.25 Indeed, the APD was significantly smaller in female patients than in male patients in group B (122 ± 12 vs 144 ± 17; p < 0.001). The APD measurements made on EBCT images for group A and B patients compared statistically well with measurements made on plain chest roentgenograms in patients with straight back syndrome and normal control subjects by Twigg et al25 (p = NS for comparison of means).

Figure 1 shows a comparison of a tomographic chest image of a normal subject (top, A) with that of a patient with echocardiographically proven MVP (bottom, B). The deformed cardiac anatomy in the MVP patient is clearly demonstrated with a wide ANGLE, a narrow APD, and a large CA. Figure 3 shows an EBCT angiographic frame from a patient with echocardiographically proven MVP. The posterolateral leaflet of the mitral valve is showing prolapsing inside the left atrium during systole (black arrow). Figure 4 is an M-mode echocardiographic image obtained in the parasternal long-axis view in a patient with MVP and cardiac entrapment on EBCT. In this image, systolic posterior displacement of the posterior mitral valve leaflet is clearly visible (arrow).



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  		Figure 4.. M-mode systolic frame obtained in a patient with entrapment on EBCT showing classical displacement of the posterior mitral leaflet (arrow).

 
In patients with echocardiographically proven MVP, we identified two types of chest deformities causing cardiac entrapment. In the first type, the chest is shaped in the semblance of a horizontally placed "figure eight" (Fig 1 , bottom, B); in the second type, the thoracic cage is shaped as a reversed letter "C" (Fig 5 ). In the "figure eight" shape type of deformity, the sternum is sunken into the rib cage and the thoracic spine shows an accentuated lordotic curvature. In the second type of deformity, the accentuated lordotic curvature of the spine is the only noticeable skeletal abnormality. The actual pathophysiologic significance of these different phenotypes is unclear at this time.



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  		Figure 5.. The configuration of the chest in this patient with cardiac entrapment and MVP by echocardiography resembles a reversed letter "C." Note the morphologic difference compared to the patient in Figure 1 , bottom, B.

 
Group C vs Group D Subjects
The prevalence of cardiac entrapment on EBCT images was statistically greater in symptomatic patients (group C) than in asymptomatic patients (group D; 28% vs 6.5%; p < 0.001). The prevalence of cardiac entrapment did not differ between male patients and female patients in group D (4% vs 9%; p = NS). On the contrary, in group C there was a statistically greater proportion of women than men with entrapment on EBCT images of the chest (41% vs 17%; p = 0.002).


   Discussion
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
References
 
Our study shows that there is a close correlation between MVP and a structural chest anomaly not readily discernible by visual inspection, but easily detected with high-quality chest CT imaging. In this condition, the heart appears trapped in a chest cavity too small for its size, and its anatomic architecture is seemingly altered in an attempt to accommodate these insufficient dimensions. Our findings, along with the complete absence of MVP in 1,734 consecutive neonates reported by Nascimento et al,6 argue in favor of an acquired etiology of this frequently diagnosed valvular condition.

Other authors have previously reported the association of pectus excavatum and the straight back syndrome with MVP and physiologic mitral regurgitation,18 19 20 21 26 and have suggested that flattening of the thorax during growth may cause morphologic abnormalities of the left atrium and ventricle. The association of MVP with the straight back syndrome has been reported to be due to an autosomal dominant inheritance,27 and Chen et al19 proposed that these associated conditions might be features of a more generalized disorder with incomplete penetrance. However, no prior study clearly demonstrated the presence of a distorted cardiac anatomy in association with skeletal abnormalities, as we have shown in this chest CT analysis.

Murakami et al28 studied the mechanisms responsible for mitral valve malcoaptation in patients with the straight back syndrome. They concluded that anteroposterior flattening of the left ventricle predisposes to asynchronous motion of the papillary muscles at end-systole, causing leaflet malcoaptation and mitral regurgitation. Lee et al29 maintained that the cause of MVP is excessive papillary muscle traction with superior displacement of the mitral leaflets due to the presence of a valvular-ventricular disproportion, the mitral annulus being dilated compared to the size of the left ventricle. In this condition, continuing papillary muscles and chordal stretching eventually causes valvular prolapse. However, in others authors’ views, the prolapse should be considered primary and the chordal stretching secondary.10 13 30 31

Because of the presence of myxoid degenerative changes and redundancy of the mitral leaflets sometimes found in this condition, MVP has been considered a forme fruste of Marfan’s syndrome,14 32 33 although this opinion is disputed by some investigators.17

Palpitations are almost ubiquitous in patients with MVP,2 34 35 and atypical chest discomfort is reported very frequently.2 36 37 Some of the proposed dysrhythmic mechanisms include traction of the papillary muscles, preexcitation, focal cardiomyopathic changes, increased QRS complex dispersion, and long QT syndrome.38 Though lethal arrhythmias have been associated with the MVP syndrome, the arrhythmias in MVP are usually benign. Interestingly, in our study, cardiac entrapment was not only seen in the large majority of patients with echocardiographically proven MVP, but also in a sizeable proportion of non-MVP patients reporting chest discomfort and palpitations, particularly women.

Finally, presyncope and orthostatic hypotension are often reported by patients with MVP and are thought by some investigators to be pathophysiologically linked to the small size of the left ventricular cavity and the subsequent underfilling during times of hyperdynamic function.2 11

We believe that our findings offer an opportunity to develop a unifying theory for the morphogenesis of MVP, its symptoms and hemodynamic findings. If an inherited disorder were truly the cause of this condition, MVP might be the consequence of a congenital predisposition to cardiothoracic growth disproportion. Compression of the left ventricle in a small space could effectively cause valvular-ventricular disproportion due to distortion and enlargement of the mitral valve annulus. The probable subsequent stretching of the papillary muscles and of the prolapsing leaflets could provoke palpitations and chest discomfort as proposed by Slovut and Lurie.37 On the other hand, prolonged traction and friction of the prolapsing leaflets and chordae may conceivably cause myxoid-like degeneration of these structures.

Although the present study offers only observational data and no cause-and-effect link can be established between the morphologic findings described on EBCT and MVP, it suggests that a developmental mechanism may be responsible for this frequently diagnosed valvular abnormality. Our study also offers an apparent explanation for the higher prevalence of MVP in women. In fact, women on the average tend to have smaller APDs than men, and a myocardial-chest disproportion may occur more easily under these conditions. Furthermore, a smaller chest cavity may predispose women to the more frequent development of atypical chest pain symptoms than men, as was seen in our group of patients with nonanginal chest discomfort and palpitations in the absence of true MVP.

The morphologic anomalies of the heart and rib cage seen on a high-quality chest CT as described in this study should alert the interpreting physician to the possible presence of underlying MVP. Moreover, this abnormality can help the specialist using chest CT imaging to explain some of the nonanginal symptoms reported by patients without overt coronary artery disease.


   Footnotes
 
Abbreviations: ANGLE = angle formed by the confluence of the mitral valve ring with the interatrial septum; APD = anteroposterior chest diameter; CA = contact area between the posterior surface of the anterior chest wall and the myocardium; EBCT = electron beam CT; MVP = mitral valve prolapse; NS = not significant

Presented at the XIXth World Congress on Diseases of the Chest and the 64th Chest Annual Scientific Assembly, Toronto, Ontario, Canada, November 8–12, 1998.

Received for publication April 1, 1999. Accepted for publication August 13, 1999.


   References
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

  1. Levy, D, Savage, DD (1987) Prevalence and clinical features of mitral valve prolapse. Am J Med 113,1281-1290
  2. Devereux, RB (1994) Mitral valve prolapse. J Am Med Womens Ass 49,192-197
  3. Rose, AG (1996) Etiology of valvular heart disease. Curr Opin Cardiol 11,98-113[CrossRef][ISI][Medline]
  4. Devereux, RB, Brown, WT, Kramer-Fox, R, et al (1982) Inheritance of mitral valve prolapse: effect of age and sex on gene expression. Ann Intern Med 97,826-832
  5. Strahan, NV, Murphy, EA, Fortuin, NJH, et al (1983) Inheritance of the mitral valve prolapse syndrome: discussion of a three-dimensional penetrance model. Am J Med 74,967-972[CrossRef][ISI][Medline]
  6. Nascimento, R, Freitas, A, Teixeira, F, et al (1997) Is mitral valve prolapse a congenital or acquired disease? Am J Cardiol 79,226-227[CrossRef][ISI][Medline]
  7. Zuppiroli, A, Favill, S, Mori, F, et al (1994) Relationship between rheumatic disease and mitral valve prolapse: an ethiopathogenetic connection or the results of a semiologic confusion? G Ital Cardiol 24,35-39[Medline]
  8. Steinfeld, L, Dimich, I, Rappaport, H, et al (1975) Late systolic murmur of rheumatic mitral insufficiency. Am J Cardiol 35,397-401[CrossRef][ISI][Medline]
  9. Tamura, K, Fukuda, Y, Ishizaki, M, et al (1995) Abnormalities in elastic fibers and other connective-tissue components of floppy mitral valve. Am Heart J 129,1149-1158[CrossRef][ISI][Medline]
  10. Chen, TO (1976) The click-murmur syndrome: a medical pendulum and a unifying concept. Chest 70,569-572[Free Full Text]
  11. Sloman, G, Duffield, A, Hunt, D, et al (1979) Mitral valve prolapse. Med J Aust 1,39-45[ISI][Medline]
  12. Malcolm, AD (1985) Mitral valve prolapse associated with other disorders: casual coincidence, common link, or fundamental genetic disturbance? Br Heart J 53,353-362[Free Full Text]
  13. Chen, TO (1989) Mitral valve prolapse: an overview. J Cardiol 19(suppl XXI),3-20
  14. Read, RC, Thal, AP, Wendt, VE (1965) Symptomatic valvular myxomatous transformation (the floppy valve syndrome): a possible forme fruste of Marfan’s syndrome. Circulation 32,897-910[Abstract/Free Full Text]
  15. Bowen, J, Boudoulas, H, Wooley, C (1987) Cardiovascular disease of connective tissue origin. Am J Med 82,481-488[CrossRef][Medline]
  16. Brown, OR, DeMots, H, Kloster, FE, et al (1975) Aortic root dilatation and mitral valve prolapse in Marfan’s syndrome. Circulation 52,651-657[Abstract/Free Full Text]
  17. Roman, MJ, Devereux, RB, Kramer-Fox, R, et al (1989) Comparison of cardiovascular and skeletal features of primary mitral valve prolapse and Marfan syndrome. Am J Cardiol 36,317-321
  18. Salomon, J, Shah, PM, Heinle, RA (1975) Thoracic skeletal abnormalities in idiopathic mitral valve prolapse. Am J Cardiol 36,32-36[CrossRef][ISI][Medline]
  19. Chen, WWC, Chan, FL, Wong, PHC, et al (1983) Familial occurrence of mitral valve prolapse: is this related to the straight back syndrome? Br Heart J 50,97-100[Abstract/Free Full Text]
  20. Udoshi, MB, Shah, A, Fisher, VJ, et al (1979) Incidence of mitral valve prolapse in subjects with skeletal abnormalities: a prospective study. Am Heart J 97,303-311[CrossRef][ISI][Medline]
  21. Davies, MK, Mackintosh, P, Cayton, RM, et al (1980) The straight back syndrome. Q J Med 49,443-460[Abstract/Free Full Text]
  22. Stanford W, Rumberger JA, eds. Ultrafast computed tomography in cardiac imaging: principles and practice. Mount Kisko, NY: Futura Publishing, 1992
  23. Galvin, JR, Gingrich, RD, Hoffman, E, et al (1994) Ultrafast computed tomography of the chest. Radiol Clin North Am 32,775-793[ISI][Medline]
  24. Ritchie, CJ, Godwin, JD, Crawford, CR, et al (1992) Minimum scan speeds for suppression of motion artifacts in CT. Radiology 185,37-42[Abstract/Free Full Text]
  25. Twigg, HL, de Leon, AC, Perloff, JK, et al (1967) The straight-back syndrome: radiographic manifestation. Radiology 88,274-277[ISI][Medline]
  26. Mishiro, Y, Oki, T, Iuchi, A, et al (1997) Echocardiographic characteristics and casual mechanism of physiologic mitral regurgitation in young normal subjects. Clin Cardiol 20,850-855[ISI][Medline]
  27. Weiss, An, Mimbs, JW, Ludbrook, PA, et al (1975) Echocardiographic detection of mitral valve prolapse: exclusion of false positive diagnosis and determination of inheritance. Circulation 52,1091-1096[Abstract/Free Full Text]
  28. Murakami, H, Iwakura, M, Ogawa, S, et al (1987) The systolic slipping mechanism of the anterior mitral leaflet in patients the straight back syndrome. J Cardiol 17,531-539[Medline]
  29. Lee, TM, Su, SF, Huang, TY, et al (1996) Excessive papillary muscle traction and dilated mitral annulus in mitral valve prolapse without mitral regurgitation. Am J Cardiol 78,482-485[CrossRef][ISI][Medline]
  30. Cheng, TO (1997) Papillary muscle traction in mitral valve prolapse: the hen or the egg [letter]? Am J Cardiol 79,845
  31. Sanfilippo, AJ, Harrigan, P, Popovic, AD, et al (1992) Papillary muscle traction in mitral valve prolapse: quantitation by two-dimensional echocardiography. J Am Coll Cardiol 19,564-571[Abstract]
  32. Pomerance, A (1969) Ballooning deformity (mucoid degeneration) of atrioventricular valves. Br Heart J 31,343-351[Free Full Text]
  33. Rizzon, P, Biasco, G, Brindicci, G, et al (1973) Familial syndrome of midsystolic click and late systolic murmur. Br Heart J 35,245-259[Free Full Text]
  34. Duren, DR, Becker, AE, Dunning, AJ (1988) Long-term follow-up of idiopathic mitral valve prolapse in 300 patients: a prospective study. J Am Coll Cardiol 11,42-47[Abstract]
  35. Zimetbaum, P, Josephson, ME (1998) Evaluation of patients with palpitations. N Engl J Med 338,1369-1373[Free Full Text]
  36. Rokicki, W, Krzystolik-Ladzinska, J, Goc, B (1995) Clinical characteristics of primary mitral valve prolapse syndrome in children. Acta Cardiol 50,147-153[ISI][Medline]
  37. Slovut, DP, Lurie, KG (1998) A potential mechanism for mitral valve prolapse. J Cardiovasc Electrophysiol 9,100-102[ISI][Medline]
  38. Oakley, CM (1992) Mitral valve palpitations. Aust N Z J Med 22,562-565[ISI][Medline]



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