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):
Thorsten Kramm
Eckhard Mayer
Juergen Meyer
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 Menzel, T.
Right arrow Articles by Meyer, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Menzel, T.
Right arrow Articles by Meyer, J.
Related Collections
Right arrow Great vessels

Ann Thorac Surg 2002;73:756-761
© 2002 The Society of Thoracic Surgeons

Original article: cardiovascular

Improvement of tricuspid regurgitation after pulmonary thromboendarterectomy

Thomas Menzel, MD*a, Thorsten Kramm, MDb, Stephan Wagner, MDa, Susanne Mohr-Kahaly, MDa, Eckhard Mayer, MDb, Juergen Meyer, MDa

a Second Medical Clinic (Department of Cardiology), Johannes Gutenberg-University, Mainz, Germany
b Clinic for Cardiothoracic and Vascular Surgery, Johannes Gutenberg-University, Mainz, Germany

Accepted for publication November 19, 2001.

* Address reprint requests to Dr Menzel, Weichselstrasse 14, D-81677 Munich, Germany
e-mail: menzel{at}mail.uni-mainz.de


   Abstract
Top
 Abstract
Introduction
 Material and methods
 Results
 Comment
 Acknowledgments
 References
 
Background. For patients with chronic thromboembolic pulmonary hypertension who undergo pulmonary thromboendarterectomy (PTE) it has not yet been systematically investigated how operation affects the severity of tricuspid regurgitation (TR). This study sought (1) to evaluate the extent of TR reversibility after operation, (2) to identify potential predictors of the reversibility of TR, and (3) to investigate the influence of geometric and hemodynamic alterations on the extent of TR severity.

Methods. Thirty-nine patients (55 ± 12 years) undergoing PTE without tricuspid valve repair were investigated before and 13 ± 8 days after operation by Doppler color flow mapping. Geometry of the tricuspid valve as well as right ventricular size and function were determined with echocardiography. Mean pulmonary arterial pressure was determined invasively.

Results. After PTE, mean pulmonary arterial pressure was significantly lower (48 ± 10 versus 25 ± 7 mm Hg, p < 0.05). Most of the patients had a distinct reduction of TR, and the improvement trend showed on the severity scale: number of patients with 4+TR (23 -> 4), 3+TR (12 -> 12), 2+TR (2 -> 13), and 1+TR (2 -> 10). Examination after PTE revealed profound reduction of right ventricular size and annulus diameter, with a normalization of the valvular geometry. However, none of the study variables were useful as indicators of the postoperative outcome.

Conclusions. After PTE without additional valve repair most patients show significantly reduced severity of TR soon afterward; the very few cases in which TR does not improve remain unidentifiable before operation. Our recommendation is consequently to refrain from additional tricuspid repair in patients undergoing PTE.


   Introduction
Top
 Abstract
 Introduction
Material and methods
 Results
 Comment
 Acknowledgments
 References
 
In most patients with chronic thromboembolic pulmonary hypertension undergoing pulmonary thromboendarterectomy (PTE), moderate to severe tricuspid regurgitation (TR) can be detected preoperatively [1]. In case of chronic thromboembolic pulmonary hypertension, the primary morphologic abnormality is right ventricular (RV) dilatation, which is associated with both tricuspid annulus dilatation and the apical and lateral displacement of papillary muscles. As a result of the malposition of the papillary muscles and annulus dilatation, leaflet area available for coaptation decreases [2]. If TR develops in chronic thromboembolic pulmonary hypertension, the preexisting increased RV afterload is further augmented by an increased preload, and a vicious cycle that further worsens the RV function can be established. Therefore it is of great interest to know whether TR may diminish or disappear after PTE, as could be shown with left-side repair, lung transplantation, and after lysis therapy for acute pulmonary embolism [3–5]. Although several studies on PTE have been published, none of them has systematically investigated the preoperative to postoperative changes of TR.

Thus the aim of the present study was to answer these questions:

  1. Is there a significant reduction of TR (ie, improvement by at least one degree) after PTE without additional valve repair?
  2. Is the severity of preoperative TR correlated with morphologic or functional alterations of the heart, age of the patient, or duration of the disease?
  3. Are there any preoperative predictors of postoperative reduction of TR?
  4. Which patients might have a benefit from additional valve surgical procedures?
  5. Is there a point of no return for the reversibility of TR?


   Material and methods
Top
 Abstract
 Introduction
 Material and methods
Results
 Comment
 Acknowledgments
 References
 
Patients
Thirty-nine patients undergoing PTE (16 female, 23 male; mean age, 55 ± 12 years; age range, 25 to 71 years) were included. The mean duration of symptomatic pulmonary hypertension was 39 ± 39 months (range, 4 to 170 months). Patients were investigated 12 ± 8 days before and 13 ± 8 days after operation.

A patent foramen ovale was found in 6 of 39 patients and was closed during the rewarming period, in five cases by direct suture and with a polyethylene terephthalate fiber (Dacron) patch in one case. None of the patients underwent additional tricuspid valve repair. Four patients had coronary artery disease. Two of these underwent additional coronary artery bypass grafting. None of the patients had previous or experienced a perioperative myocardial infarction. In 1 patient a mitral valve replacement was necessary because of mitral valve prolapse with severe mitral regurgitation.

Surgical procedure
The criteria for offering PTE were a pulmonary vascular resistance (PVR) of greater than 300 dynes · sec · cm-5, thromboembolic lesions considered surgically accessible (main, lobar, or segmental arteries), New York Heart Association functional class II, III and IV, and unsuccessful anticoagulation therapy for a 6-month period.

The endarterectomy of pulmonary arteries was performed with a standardized technique [6–8] as follows:

  1. Intrapericardial central incision of both pulmonary arteries.
  2. Endarterectomy performed exclusively under circulatory arrest, with a mean circulatory arrest time of 39 minutes (range, 14 to 55 minutes).
  3. Prolonged reperfusion to 37°C body temperature, resulting in a mean total operation time of 5.6 hours (range, 2.1 to 10.5 hours).
  4. Pressure-controlled high positive end-expiratory pressure (10 cm H2O) ventilation.
  5. Nitric oxide inhalation for persistent pulmonary hypertension in the early postoperative phase.
  6. Modified vasopressor therapy with low-dose dobutamine and arterenol through the left atrial catheter, and maintenance of cardiac index between 2.0 and 3.0 L · min-1 · m-2.
  7. Early extubation with a mean postoperative ventilation time of 11 hours (range, 6.5 to 26 hours).

Echocardiographic evaluation
Examinations were performed by two experienced echocardiographers using standard techniques on commercially available equipment (Hewlett-Packard, Sonos 2500 [2.0-MHz or 2.5-MHz transducer] or Sonos 5500 [S4 Ultraband 2- to 4-MHz transducer]; Hewlett-Packard Co, Andover, MA). Images were obtained with the patient in the left lateral position. Measurements were performed in end-expiration.

Tricuspid valve morphology was evaluated from the apical four-chamber and two-chamber views, the parasternal short-axis view, and the subcostal view. Functional TR was defined as failure of the tricuspid leaflets to reach the annulus level during systole, without evidence of structural abnormalities. Tricuspid regurgitation was defined as organic if any of the following were present: (1) valve, chordae tendinea, or papillary muscle thickening or calcification; or (2) doming or restricted motion of the leaflets.

The systolic configuration of the tricuspid valve was evaluated in the four-chamber view. The linear apical displacement of the coaptation point of the leaflets into the RV from the line connecting the annulus hinge points toward the RV was measured at the time of maximal systolic closure. The area between the atrial surface of the leaflets and the tricuspid annulus was traced at the same time [2]. The minimal systolic and maximal diastolic annulus diameter were measured in the same beat from the insertion of the septal leaflet to the insertion of the anterior leaflet [9].

The severity of TR was assessed by color Doppler echocardiography. According to Miyatake and associates [10], the area of the regurgitant jet was planimetrically determined in the apical four-chamber view (4+TR: jet area > 10 cm2; 3+TR: jet area > 4 <= 10 cm2; 2+TR: jet area > 2 <= 4 cm2; 1+TR: jet area > 0 <= 2 cm2). Care was taken to use optimal gain setting for each study. The maximal regurgitant jet area was chosen for measurement. This area included the aliased signals as well as immediately contiguous nonturbulent velocities in the same direction as the jet.

The RV end-diastolic (RV-EDA) and end-systolic (RV-ESA) cavity areas were determined planimetrically in the apical four-chamber view. Fractional area change of the ventricle (RV-FAC) was calculated as follows: RV-FAC = (RV-EDA - RV-ESA)/RV-EDA x 100 [11].

Right atrial cavity area was traced in the four-chamber view at end-systole.

Right heart catheterization
Hemodynamic studies using a Swan-Ganz catheter to determine the mean pulmonary artery pressure (mPAP), PVR, central venous pressure, and cardiac index were performed preoperatively and postoperatively in all patients.

Statistical analysis
Data processing was performed using the Statistical Analysis System (SAS, Version 6.12; SAS Institute, Cary, NC). Continuous variables were averaged from three consecutive measurements (five in case of atrial fibrillation). Preoperative and postoperative continuous variables were compared by the Wilcoxon signed-rank test. Correlation between preoperative values of Doppler-derived area of TR and other preoperative study variables and between postoperative values of Doppler-derived area of TR and other postoperative study variables, as well as correlation between the change of Doppler-derived TR and study variables, were investigated using Spearman’s correlation coefficient. A p value less than 0.05 was considered to be statistically significant.

Two analyses were undertaken with the following objectives: (1) to identify preoperative predictors of postoperative severity of TR, the influence of study variables on postoperative TR was tested using a linear regression analysis with adjustment for preoperative TR; and (2) to determine variables that identify those patients with preoperatively severe TR that did not improve after PTE. For the second analysis, we divided the group of patients with a preoperative 3+TR or 4+TR into two subgroups: group 1, patients with 4+TR and 3+TR that did not change after PTE (n = 6); and group 2, patients with 4+TR and 3+TR in whom TR severity decreased postoperatively (n = 29).

Differences regarding preoperative study variables between groups 1 and 2 were investigated by the Wilcoxon rank sum test.

The following variables were investigated in both analyses: systolic and diastolic annulus diameter, shortening of annulus diameter, linear apical displacement of the coaptation point of the leaflets from the annulus, area of displacement between the leaflets and the annulus, right atrial end-systolic area, RV-EDA, RV-ESA, RV-FAC, age of the patient, duration of the disease, central venous pressure, mPAP, and PVR.


   Results
Top
 Abstract
 Introduction
 Material and methods
 Results
Comment
 Acknowledgments
 References
 
Invasively determined variables
After PTE, a marked decrease could be shown for PVR and mPAP (895 ± 317 versus 282 ± 155 dynes · sec · cm-5, p < 0.05; 48 ± 10 versus 25 ± 7 mm Hg, p < 0.05). Cardiac index increased after operation (2.3 ± 0.5 versus 3.4 ± 0.6 L · min-1 · m-2, p < 0.05). Central venous pressure (8.5 ± 3.9 versus 9.2 ± 1.7 mm Hg) and heart rate (84 ± 15 versus 87 ± 13 beats/min) did not change significantly.

The 6 patients (group 1) with 4+ and 3+ TR that did not improve immediately after PTE did show a marked decrease in PVR and mPAP (1126 ± 475 versus 368 ± 251 dynes · sec · cm-5 and 53 ± 8 versus 29 ± 8 mm Hg).

Echocardiographic data
In 1 of 39 patients, tracing of RV areas was not possible, whereas color Doppler investigation of TR was successful. No patient originally included in the study had to be excluded because of a technically unsatisfactory echocardiogram. The results of echocardiographic determined variables can be seen in Table 1.


View this table:
[in this window]
[in a new window]
  		Table 1. Echocardiographic Variables

 
Changes of severity of tricuspid regurgitation
Preoperative tricuspid valve regurgitation was classified as follows: 23 patients 4+TR, 12 patients 3+TR, 2 patients 2+TR, and 2 patients 1+TR. After operation, severity decreased in most patients and TR was then classified as follows: 4 patients 4+TR, 12 patients 3+TR, 13 patients 2+TR, and 10 patients 1+TR.

In patients with preoperative 4+TR, severity decreased to 3+TR in 10, to 2+TR in 6, and to 1+TR in 3 cases. Four remained unchanged. In patients with preoperative 3+TR, severity decreased to 2+TR in 7 and to 1+TR in 3, and 2 remained unchanged. Two patients with 2+TR showed a decrease to 1+TR, and 2 patients with 1+TR showed no postoperative change in severity. An increase in regurgitation severity could not be observed among the patients investigated (Fig. 1).



View larger version (14K):
[in this window]
[in a new window]
  		Fig 1. Preoperative (black bars) to postoperative (white bars) changes of the severity grade of tricuspid regurgitation. (TR = tricuspid regurgitation.).

 
All 6 patients with unimproved 3+ to 4+TR were reexamined postoperatively in other hospitals (on average after 1.5 years). In two cases, severe TR was seen to persist, whereas postoperative examination showed 2+TR and 1+TR in two cases each.

Tricuspid valve and annulus morphology
Organic TR was found in none of the patients. In 1 patient, two-dimensional echocardiography showed an increased echogenicity of the papillary muscle.

Linear apical displacement of the coaptation point of the leaflets from the tricuspid annulus and the area of displacement between the leaflets and the annulus were elevated in preoperative measurements, whereby there was a statistically significant decrease in postoperative findings. Preoperative measurements of the systolic and diastolic annulus diameter were elevated and decreased, respectively, after operation (Table 1).

Right heart measurements
Before operation, all of the patients showed enlargement of the RV cavity area (both end diastolic and end systolic), and systolic function was impaired. On examination after operation, both area measurements were smaller, and systolic function had improved (Table 1).

Determinants of preoperative tricuspid regurgitation
Preoperative severity of TR was correlated with RV-EDA and RV-ESA (r = 0.41 and r = 0.43, respectively), with systolic and diastolic tricuspid annulus diameter (r = 0.37 and r = 0.41, respectively), with apical and area displacement of the leaflets (r = 0.46 and r = 0.41, respectively), and with the area of the right atrium (r = 0.58). A weak correlation could be shown with PVR (r = 0.32). All these correlations were statistically significant (p < 0.05).

No correlation could be shown between preoperative TR and either age, duration of disease, mPAP, RV-FAC (ie, RV systolic function), or systolic annulus shortening.

Determinants of postoperative tricuspid regurgitation
Postoperative severity of TR was correlated with RV-EDA and RV-ESA (r = 0.32 and r = 0.44, respectively), with systolic and diastolic tricuspid annulus diameter (r = 0.46 and r = 0.40, respectively), with apical and area displacement of the leaflets (r = 0.40 and r = 0.6, respectively), with mPAP (r = 0.49), and with PVR (r = 0.41). All these correlations were statistically significant (p < 0.05).

Reversed correlations could be shown for postoperative severity of TR with RV-FAC (r = -0.43; p < 0.05) and with systolic shortening of tricuspid annulus (r = -0.39; p < 0.05).

No correlation could be shown between the postoperative TR and age, duration of disease, area of the right atrium, or central venous pressure.

Perioperative changes of tricuspid regurgitation and study variables
Only with the postoperative change of RV-EDA could a significant albeit weak correlation (r = 0.36; p < 0.05) be observed.

Predictors of postoperative outcome
None of the study variables was an independent predictor of TR regression. Nor did any of the variables in question show a statistically significant difference between patients with severe TR that did or did not improve postoperatively.


   Comment
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
Acknowledgments
 References
 
The aim of this study was to investigate the relationship between RV afterload reduction and the severity of associated TR in patients with severe chronic thromboembolic pulmonary hypertension. The influence of decreasing RV pressure overload on pathophysiologic aspects of functional TR was examined by preoperative and postoperative determination of contributive factors to the severity of TR. Right ventricular afterload reduction was achieved by PTE [1, 12–20]. The possibility of a preoperative evaluation of expected postoperative improvement of TR was examined in this study in which we also endeavored to identify the particular cases in which tricuspid repair should have been undertaken together with PTE because RV afterload reduction did not result in a significant improvement of TR.

Although several studies on PTE have been published, none of them has systematically investigated the preoperative and postoperative severities of TR. Jamieson and coworkers [1] point out that in the setting of pulmonary hypertension even severe cases of TR do not require valve surgical procedures, as PTE induces substantial improvement of valvular function; but they do not provide data on this topic. Two studies dealing with lung transplantation describe the severity of TR measured preoperatively and postoperatively. Ritchie and colleagues [4] found moderate to severe TR in 10 of 13 patients before operation, whereas there was only trivial postoperative TR in 6 of 13 of these patients. In four preoperative measurements Kramer and associates [21] reported 3+TR in 3 patients and 4+TR in 1 patient, whereas in all 4 patients postoperative investigation showed no more than 1+TR.

Simon and coworkers [3] reported on 20 patients with pulmonary hypertension and various degrees of TR who were investigated after mitral valve operation. They found TR unequivocally decreased in 6 patients, unchanged in 13 patients, and worsened in the case of 1 patient. Duran and coworkers [22] also investigated the reversibility of functional TR in patients with left-side-repair. They stated that functional TR can be ignored, but only in patients with predictable and significant reduction of PVR. In our study, moderate to 3+ to 4+TR could be detected preoperatively in 35 of 39 patients investigated. After operation, moderate to severe TR was present in 16 of 39 patients, whereas TR was 1+ to 2+ in 23 of 39 patients. The greater preoperative TR severity had been, the more TR declined after PTE.

The results of this study indicate strongly that TR does prove to be at least partially reversible immediately on attaining afterload reduction by PTE. Although it has not been documented here, we expect further positive remodeling of the RV and reduction of TR severities to occur with time.

We followed 6 exemplary patient cases with moderate to severe TR in which PTE did not reduce the severity of valve incompetence and which were reexamined in other hospitals at an average interim of 1.5 years after operation. Severe TR persisted in 2 of these patients, whereas it was graded 2+ in 2 cases, and 1+ in 2 cases.

The usual concept of TR is that pressure overload increases RV volume and tricuspid annulus size, reducing the overlap of tricuspid leaflet tips. In surgical and postmortem studies, annular dilatation has been reported to be a cause of functional TR [23]. Ubago and associates [24] stated that in addition to annulus dilation, an impairment in the percentage of annulus shortening during systole causes severe TR. Sagie and colleagues [2] identified the displacement of the coaptation points of the leaflets as a predictor of TR. Changes in RV shape rather than size are what alter the annulus or papillary muscle geometry and create incomplete leaflet closure.

Corresponding to the findings of Sagie and colleagues [2], apical and area displacement of the leaflet tips, annulus diameter, and the RV as well as right atrial cavity areas correlated with the preoperative severity of TR. Interestingly, systolic annulus shortening, RV-FAC, and mPAP did not. As opposed to preoperative investigation, postoperative measurements showed there was a positive correlation to be found between TR severity and PVR as well as mPAP. The postoperative results showed an inverse correlation between TR severity and both RV-FAC and systolic annulus shortening.

Thus, we conclude the increase of TR severity related to functional changes of the tricuspid valve and the RV is caused by elevation of mPAP, but increasing TR severity exists only up to a certain point from which further increment of RV afterload does not result in further alteration of RV and tricuspid valve geometry.

In PTE, preoperative factors that can potentially predict irreversible, severe TR—and therefore the need for tricuspid valve operation—are necessary because significant TR persisting postoperatively seems to be a marker for adverse outcome [25]. None of the preoperatively determined variables could independently predict postoperative severity of TR. In a second analysis we compared the group of patients with preoperative, severe TR that did not improve (6 patients) with the group of patients whose preoperative, severe TR did improve (29 patients). No significant differences of study variables could be identified.

Limitations
The main problem with conclusions from this study is that we cannot present long-term results as yet. Further improvement of TR can be expected, as shown for 6 patients with 3+ to 4+TR, the severity of which was not immediately reduced, but on examination by other specialists 1.5 years later was found clearly improved in the majority of cases. How conclusive this evidence is remains to be seen.

In this study, invasive and echocardiographic examinations were not performed simultaneously. However, heart rate and mean arterial blood pressure did not differ significantly in these examinations. Determination of TR severity using color Doppler technique has several limitations. Thus, care was taken to use the optimal gain setting for each study; and only investigations with a reasonable image quality were included.

Conclusions
Approximately 2 weeks after PTE an improvement of at least one or two degrees in TR severity could be observed in most of the individuals who have been investigated. The very few patients in whom severe TR did not improve immediately after PTE in our clinic could not have been identified preoperatively. However, follow-up of those patients 1.5 years after operation showed conspicuous improvement by then.

We subsequently recommend refraining from additional tricuspid repair in patients undergoing PTE.


   Acknowledgments
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 Acknowledgments
References
 
The authors thank R. Meinert, PhD, Institute for Statistics and Documentation, Johannes-Gutenberg-University, Mainz, Germany, for statistical data processing. We also thank Joy Christensen, InternationalMeetingPoint (joysuechr@get2net.dk), for English language advice.


   References
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 Acknowledgments
 References
 

  1. Jamieson S.W., Auger W.R., Fedullo P.F., et al. Experience and results with 150 pulmonary thromboendarterectomy operations over a 29-month period. J Thorac Cardiovasc Surg 1993;106:116-127.[Abstract]
  2. Sagie A., Schwammenthal E., Padial L.R., et al. Determinants of functional TR in incomplete tricuspid valve closure: Doppler flow study of 109 patients. J Am Coll Cardiol 1994;24:446-453.[Abstract]
  3. Simon R., Oelert H., Borst H.-G., Lichtlen P.R. Influence of mitral valve surgery on tricuspid incompetence concomitant with mitral valve surgery. Circulation 1980;62(Suppl 1):I52-I57.
  4. Ritchie M., Waggoner A.D., Davila-Roman V.G., Barzilai B., Trulock E.P., Eisenberg P.R. Echocardiographic characterization of the improvement in RV function in patients with severe pulmonary hypertension after single-lung transplantation. J Am Coll Cardiol 1993;22:1170-1174.[Abstract]
  5. Come P.C., Kim D., Parker A., et al. Early reversal of RV dysfunction in patients with acute pulmonary embolism after treatment with intravenous tissue plasminogen activator. J Am Coll Cardiol 1987;10:971-978.[Abstract]
  6. Daily P.O., Dembitsky W.P., Peterson K.L., Moser K.M. Modifications of techniques and early results of pulmonary thromboendarterectomy for chronic pulmonary embolism. J Thorac Cardiovasc Surg 1987;93:221-233.[Abstract]
  7. Iversen S., Mayer E., Schmiedt W., Oelert H. Das chirurgische Konzept der pulmonalen Thrombendarteriektomie [Early results of pulmonary thromboendarterectomy in chronic thromboembolic pulmonary hypertension]. Z Herz Thorax Gefasschir 1993;7:23-28.
  8. Mayer E., Kramm T., Dahm M., et al. Aktuelle Frühergebnisse nach pulmonaler Thrombendarteriektomie bei chronischer thromboembolischer pulmonaler Hypertonie. Z Kardiol 1997;86:920-927.[Medline]
  9. Gibson T.C., Foale R.A., Guyer D.E., Weymann A.E. Clinical significance of incomplete tricuspid valve closure seen on two-dimensional echocardiography. J Am Coll Cardiol 1984;4:1052-1057.[Abstract]
  10. Miyatake K., Okamoto M., Kinoshita N., et al. Evaluation of tricuspid regurgitation by pulsed Doppler and two-dimensional echocardiography. Circulation 1982;66:777-789.[Abstract/Free Full Text]
  11. Kaul S., Tei C., Hopkins J.M., Shah P.M. Assessment of RV function using two-dimensional echocardiography. Am Heart J 1984;107:526-531.[Medline]
  12. Moser K.M., Spragg R.G., Utley J., Daily P.O. Chronic thrombotic obstruction of major pulmonary arteries. Ann Intern Med 1983;99:299-305.
  13. Moser K.M., Auger W.R., Fedullo P.F. Chronic major-vessel thromboembolic pulmonary hypertension. Circulation 1990;81:1735-1743.[Free Full Text]
  14. Mayer E., Dahm M., Hake U., et al. Thromboendarterectomy in CTEPH: hemodynamics, and right-heart function over the long term. Dtsch med Wochenschr 1996;121:9-15.[Medline]
  15. Iversen S. Surgical treatment of thromboembolism-induced pulmonary hypertension. Z Kardiol 1994;83(Suppl 6):193-199.
  16. Simonneau G., Azaria R., Brenot F., Dartevelle P.G., Musset D., Duroux P. Surgical management of unresolved pulmonary embolism. Chest 1995;107(Suppl):52S-55S.[Medline]
  17. Klepetko W., Moritz A., Burghuber O.C., et al. Die chronisch-thromboembolische pulmonale Hypertension und ihre Behandlung mit der pulmonalen Thrombendarteriektomie [Chronic thromboembolic pulmonary hypertension and its treatment with pulmonary thrombendarerectomy]. Wien Klin Wochenschr 1995;107:396-402.[Medline]
  18. Hartz R.S., Byrne J.G., Levitsky S., Park J., Rich S. Predictors of mortality in pulmonary thromboendarterectomy. Ann Thorac Surg 1996;62:1255-1260.[Abstract/Free Full Text]
  19. Chow L.C., Dittrich H.C., Hoit B.D., Moser K.M., Nicod P.H. Doppler assessment in right-sided cardiac hemodynamics after pulmonary thromboendarterectomy. Am J Cardiol 1988;61:1092-1097.[Medline]
  20. Dittrich H.C., Chow L.C., Nicod P.H. Early improvement in left ventricular diastolic function after relief of chronic right ventricular pressure overload. Circulation 1989;80:823-830.[Abstract/Free Full Text]
  21. Kramer M.R., Valantine H.A., Marshall S.E., Starnes V.A., Theodore J. Recovery of the right ventricle after single-lung transplantation in pulmonary hypertension. Am J Cardiol 1994;73:494-500.[Medline]
  22. Duran C.M.G., Pomar J.L., Colman T., Figueroa A., Revuelta J.M., Ubago J.L. Is tricuspid valve repair necessary?. J Thorac Cardiovasc Surg 1980;80:849-860.[Abstract]
  23. Carpentier A., Deloche A., Hanania G., et al. Surgical management of acquired tricuspid valve disease. J Thorac Cardiovasc Surg 1974;67:53-65.[Medline]
  24. Ubago L.J., Figueroa A., Ochoteco A., Colman T., Duran R.M., Duran C.G. Analysis of the amount of tricuspid valve anular dilatation required to produce functional tricuspid regurgitation. Am J Cardiol 1983;52:155-158.[Medline]
  25. Sagie A., Schwammenthal E., Newell J.B., et al. Significant tricuspid regurgitation is a marker for adverse outcome in patients undergoing percutaneous balloon mitral valvuloplasty. J Am Coll Cardiol 1994;24:696-702.[Abstract]



This article has been cited by other articles:


Home page
 Ann. Thorac. Surg.Home page
H. Ogino, M. Ando, H. Matsuda, K. Minatoya, H. Sasaki, N. Nakanishi, S. Kyotani, H. Imanaka, and S. Kitamura
Japanese Single-Center Experience of Surgery for Chronic Thromboembolic Pulmonary Hypertension
Ann. Thorac. Surg., August 1, 2006; 82(2): 630 - 636.
[Abstract] [Full Text] [PDF]

Home page
 J. Thorac. Cardiovasc. Surg.Home page
P. A. Thistlethwaite, A. Kemp, L. Du, M. M. Madani, and S. W. Jamieson
Outcomes of pulmonary endarterectomy for treatment of extreme thromboembolic pulmonary hypertension
J. Thorac. Cardiovasc. Surg., February 1, 2006; 131(2): 307 - 313.
[Abstract] [Full Text] [PDF]

Home page
 PerfusionHome page
L. Puis, E. Vandezande, L. Vercaemst, P. Janssens, Y. Taverniers, M. Foulon, R. Demeyere, M. Delcroix, and W. Daenen
Pulmonary thromboendarterectomy for chronic thromboembolic pulmonary hypertension
Perfusion, March 1, 2005; 20(2): 101 - 108.
[Abstract] [PDF]

Home page
 J Am Coll CardiolHome page
H. M. Sadeghi, B. J. Kimura, A. Raisinghani, D. G. Blanchard, E. Mahmud, P. F. Fedullo, S. W. Jamieson, and A. N. DeMaria
Does lowering pulmonary arterial pressure eliminate severe functional tricuspid regurgitation?: Insights from pulmonary thromboendarterectomy
J. Am. Coll. Cardiol., July 7, 2004; 44(1): 126 - 132.
[Abstract] [Full Text] [PDF]

Home page
 J Am Coll CardiolHome page
N. Galie, A. L. Hinderliter, A. Torbicki, T. Fourme, G. Simonneau, T. Pulido, N. Espinola-Zavaleta, G. Rocchi, A. Manes, R. Frantz, et al.
Effects of the oral endothelin-receptorantagonist bosentan on echocardiographicand doppler measures in patients with pulmonary arterial hypertension
J. Am. Coll. Cardiol., April 16, 2003; 41(8): 1380 - 1386.
[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):
Thorsten Kramm
Eckhard Mayer
Juergen Meyer
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 Menzel, T.
Right arrow Articles by Meyer, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Menzel, T.
Right arrow Articles by Meyer, J.
Related Collections
Right arrow Great vessels

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