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(Chest. 2000;117:643-648.)
© 2000 American College of Chest Physicians

Partial Improvement in Pulmonary Function After Successful Percutaneous Balloon Mitral Valvotomy*

Joan A. Gómez-Hospital, MD; Angel Cequier, MD; Pablo V. Romero, MD; Concepción Cañete, MD; Carmen Ugartemendia, MD; Josepa Mauri, MD and Enrique Esplugas, MD

* From the Division of Cardiology (Drs. Gómez-Hospital, Cequier, Ugartemendia, Mauri, and Esplugas) and Division of Pulmonary Diseases (Drs. Romero and Cañete), Hospital de Bellvitge, University of Barcelona, Barcelona, Spain.

Correspondence to: Angel Cequier, MD, Cardiac Catheterization Laboratory, Hospital de Bellvitge, C. Feixa Llarga s/n, Hospitalet del Llobregat, 08907 Barcelona, Spain; e-mail: acequier{at}csub.scs.es


   Abstract
TOP
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 References
 
Study objectives: This study was performed to assess the changes in pulmonary function after a successful percutaneous balloon mitral valvotomy (PBMV) in 23 consecutive patients with symptomatic mitral stenosis.

Methods and results: Lung function preprocedure and postprocedure were evaluated by spirometric flow, static pulmonary volumes, and diffusion capacity of the lung for carbon monoxide (DLCO). At baseline, a reduction in small airways flow (maximal expiratory flow at 50% of vital capacity, 70 ± 29% of predicted value; maximal expiratory flow at 25% of vital capacity, 55 ± 26% of predicted value) and an increase in DLCO (118 ± 29%) and Krough Index (KCO; 123 ± 29% of predicted value) were observed. PBMV caused an improvement in hemodynamic parameters with an increase in mitral valve area (from 1.0 ± 0.3 to 1.9 ± 0.5 cm2; p < 0.001) and a decrease in left atrial pressure (from 17 ± 3 to 12 ± 5 mm Hg; p < 0.001). These changes were associated with a significant increase in FVC (from 2.8 ± 0.84 to 2.9 ± 0.80 L; p < 0.05) and in FEV1 (from 2.2 ± 0.72 to 2.3 ± 0.68 L; p < 0.05). A decrease in DLCO was observed after PBMV (from 26.7 ± 7 to 22.5 ± 5.4 mL/min/mm Hg; p < 0.001; and KCO, from 6.2 ± 1.4 to 5.2 ± 1.2 mL/min/mm Hg/L; p < 0.001). No significant changes in small airways flow were detected, suggesting only a partial improvement in pulmonary congestion.

Conclusion: We conclude that the initial impairment of lung function in patients with symptomatic mitral stenosis is only partially ameliorated by PBMV.

Key Words: mitral stenosis • percutaneous balloon mitral valvotomy • pulmonary function


   Introduction
TOP
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 References
 
Mitral valve stenosis is a chronic disease that produces an increase in left atrial pressure and, consequently, venous pulmonary hypertension.1 2 These chronic changes in pulmonary circulation cause alterations in pulmonary vessels and in the composition of lung tissue. Accumulation of water, proteins, and proteoglycans in the interstitium has been described in this condition.3 These interstitial changes are the basis of the clinical manifestations of mitral stenosis and can be detected by pulmonary function tests.4 5 6

Until recently, mitral valve surgery was the only method for the treatment of severe mitral valve stenosis. Some authors have described a late improvement in lung function parameters after surgical mitral commissurotomy that was correlated, initially, with improvement in pulmonary pressures.7 8 9 However, cardiac surgery requires a thoracotomy that causes considerable structural and functional lung changes10 11 and, as such, the pulmonary function changes described after surgical commissurotomy need to be interpreted with caution.

Percutaneous balloon mitral valvotomy (PBMV) is a reasonable alternative to surgery for many patients with mitral valve stenosis. A successfully performed PBMV produces an increase in mitral valve area with reductions in mitral valve gradient and left atrial pressure. We only selected patients with successful results in order to obtain maximal improvement in hemodynamic data. These changes are detected immediately after the procedure12 13 and persist at long-term follow-up.14 15 16 17 With respect to pulmonary function changes after left atrial pressure reduction, PBMV is a nearly ideal method of treatment because neither anatomical nor structural pulmonary changes have procedure-related causes.

This study was performed in a series of patients with mitral valve stenosis to determine the immediate changes in pulmonary function associated with an acute reduction in left atrial pressure following a successful PBMV.


   Materials and Methods
TOP
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 References
 
Thirty consecutive patients with moderate-to-severe mitral valve stenosis who were eligible for PBMV were introduced into the study. Exclusion criteria were: patients with an echocardiographic score18 > 11; left atrial thrombus that had persisted despite 6 months of anticoagulant therapy; severe coronary artery disease with coronary bypass graft indications. Only patients with successful outcomes after PBMV (defined as a final mitral valve area > 1.5 cm2 or an increase > 25% relative to baseline values) were finally included. A residual mitral regurgitation > 2/4 after PBMV was considered an exclusion criteria. All patients gave fully informed written consent before entering the study, and the procedures were in accordance with the ethical guidelines of our institution.

Study Protocol
Before PBMV: Transthoracic two-dimensional and Doppler echocardiographic studies were performed in all patients. Diagnosis was confirmed by two-dimensional area19 and Doppler ultrasound-derived pressure half-time.20 Mitral valve morphology was evaluated by calculating the echocardiographic score, as defined by Wilkins et al.18 The degree of mitral regurgitation was assessed by Doppler study.21 Patients with a favorable morphology were selected, and a transesophageal echocardiography was performed to exclude the presence of left atrial thrombus.22 If the image suggested a thrombus, an oral anticoagulant regimen was initiated and the transesophageal echocardiographic study was repeated 6 months later. If no resolution of thrombus had occurred, PBMV was not performed.

To evaluate lung function disturbances, a battery of pulmonary function tests was applied to every patient initially included. Spirometry was performed according to the European Respiratory Society recommendations.23 The following parameters were determined: FVC; FVC1; the quotient FEV1/FVC; and maximal expiratory flows at 50% and 25% of vital capacity (MEF50 and MEF25, respectively). Functional residual capacity (FRC) was measured by helium dilution over 7 min of rebreathing in closed circuit. Expiratory reserve volume (ERV) was determined after a slow vital capacity maneuver. The following static lung volumes were calculated: residual volume (RV) as FRC - ERV; total lung capacity (TLC) as slow vital capacity + RV. The ratio RV/TLC was calculated and expressed as a percentage. Diffusion of carbon monoxide (DLCO) was determined by the single-breath technique, as described by Cotes.24 An apnea of 10 s was used. Alveolar volume (VA) was measured and the quotient DLCO/VA or Krough Index (KCO) was calculated. The equipment used was a Collins Plus Pulmonary Testing System (Warren E. Collins Inc; Braintree, MA).

A study of hemodynamic variables was performed before the procedure. Right heart pressures (right atrial, right ventricular, pulmonary artery, and pulmonary capillary wedge) were obtained. To evaluate the mitral valve gradient, simultaneous left atrial (transseptal approach) and left ventricular pressures were registered. Cardiac output was determined by the thermodilution method. Mitral valve area was calculated by the Gorlin formula.25 A left ventriculography was performed to assess the left ventricular ejection fraction and the degree of mitral regurgitation. A coronary angiography was performed to select outpatients with coronary artery disease needing surgical intervention.

PBMV: PBMV was performed with a single balloon using the Inoue technique.26 The balloon was positioned across the mitral valve and, in order to avoid a significant mitral regurgitation after valvotomy, sequential inflations were performed.27 As for the preprocedure workup, the same hemodynamic measures were obtained immediately after the procedure. Mitral valve area was calculated and a left ventricular angiography was performed to determine the degree of residual mitral regurgitation. Blood samples from superior and inferior vena cava, pulmonary artery, and aorta were obtained to calculate the residual left-to-right atrial shunt.

After PBMV: A transthoracic Doppler-echocardiographic study was repeated 48 to 96 h after the procedure to evaluate the final mitral valve area and to assess the degree of residual mitral regurgitation. The presence or absence of a left-to-right shunt was assessed with two-dimensional and Doppler studies. The same battery of pulmonary function tests was repeated to assess the immediate changes in lung function parameters.

One month after the procedure, a clinical checkup and pulmonary function tests were performed again.

Statistical Analysis
Continuous variables were expressed as mean ± SD, and discrete variables were expressed both as absolute values and as percentages. Comparison between values before and after PBMV were analyzed using the appropriate Student’s t test (continuous variables) and {chi}2 test (categorical variables). Correlations between continuous variables were evaluated with Pearson’s coefficient. All analyses were conducted using the SPSS statistical package (SPSS; Chicago, IL) and a probability value of < 0.05 was considered statistically significant.


   Results
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 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 References
 
Baseline Values
Of the 30 patients with moderate to severe mitral stenosis and an appropriate echocardiographic score who underwent PBMV, 23 patients had a successful outcome and constitute the present study group. The baseline clinical and echocardiographic characteristics are summarized in Table 1 . Patients had a moderate to severe mitral stenosis with a mean mitral valve area of 1.0 ± 0.1 cm2. The mean left atrial dimension was 52 ± 8 mm, and the mean echocardiographic score was 6.3 ± 1.7. Only one patient was an active smoker and two patients were past smokers so, in effect, the majority of patients (87%) were nonsmokers. The results of baseline pulmonary function tests are summarized in Table 2 . Patients showed a reduced baseline value of peripheral airways flow, detected as a decrease of percent of predicted values of MEF50 (70 ± 29%) and MEF25 (55 ± 25%). Fourteen patients had a normal spirometric flow, 8 had a mild to moderate obstructive pattern, and only 1 patient had a restrictive pattern. The hemodynamic study confirmed the severity of mitral valve stenosis. The mean pre-PBMV mitral valve area was 1.0 ± 0.3 cm2 (Table 3 ). Pulmonary hypertension was detected in 22 patients, mild in 14 (58%) and moderate in 8 (33%). No patient had severe pulmonary hypertension. Overall, left ventricular function was normal (58.9 ± 9.4%; range, 31 to 72%), and only two patients had an ejection fraction < 60%. A significant coronary stenosis in the right coronary artery was detected in one patient, and coronary angioplasty was performed immediately after PBMV. A moderate, but statistically significant negative correlation was found between baseline mean pulmonary artery pressure and the DLCO expressed as a percentage of predicted value (r = -0.49; p < 0.03; Fig 1 ).


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  		Table 1.. Baseline Clinical and Echocardiographic Characteristics of the 23 Patients Included in the Study*

 

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  		Table 2.. Baseline Lung Function Parameters of the 23 Patients Included in the Study*

 

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  		Table 3.. Hemodynamic Parameters of the 23 Patients Before and After PBMV*

 


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  		Figure 1.. Inverse correlation between baseline mean pulmonary artery pressure and predicted value of DLCO.

 
Hemodynamic Changes After PBMV
Relative to baseline values, PBMV produced a significant increase in mitral valve area (from 1.0 ± 0.3 cm2 to 1.9 ± 0.5 cm2; p < 0.001) with reductions in left atrial pressure and mitral valve gradient (Table 3) . An increase in cardiac output was also detected. The Doppler echocardiographic study performed 2 to 6 days (mean 4 days) after PBMV confirmed the increase obtained in the mitral valve area (1.0 ± 0.1 cm2 before PBMV vs 1.8 ± 0.4 cm2 after PBMV; p < 0.001). No changes were observed in right atrial, right ventricular, or pulmonary artery pressures. Increases in mitral regurgitation were detected in six patients. Residual left-to-right shunt was present in six patients (pulmonary/systemic flow ratio < 1.3 in all cases). No change in blood hemoglobin concentration was detected (14.1 ± 1.1 before PBMV vs 13.9 ± 1.4 mg/dL after PBMV; p = not significant).

Pulmonary Function Changes After PBMV
Pulmonary function tests were performed both before and 2 to 6 days after PBMV. Table 4 summarizes the changes observed in lung function. Significant increases in FVC and FEV1 were observed. However, no significant changes in maximal flows or static lung volumes were detected. Significant decreases in DLCO and KCO were also observed, without significant changes in VA. No significant correlations were observed between the changes in the hemodynamic parameters and pulmonary function changes. However, the change in lung diffusing capacity was correlated with the initial value of DLCO (r = 0.65; p = 0.001; Fig 2 ).


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  		Table 4.. Lung Function Parameters of the 23 Patients Before, Immediately After, and 1 Month After PBMV*

 


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  		Figure 2.. Correlation between baseline DLCO value and change in DLCO after PBMV.

 
To investigate the pathophysiologic significance of the decrease in DLCO after PBMV, we grouped the subjects with respect to the initial value of DLCO as a percentage of the predicted value. Before the procedure, subjects with increased DLCO (> 110% of predicted value, group A) had a significantly lower mean pulmonary pressure than subjects with normal or decreased DLCO (< 110% of predicted value, group B): 21 ± 5 vs 29 ± 8 mm Hg, respectively (p = 0.02). After PBMV, subjects in group A showed a significant reduction in DLCO (-18 ± 9% of previous value), whereas those in group B did not (-4 ± 18% of previous value).

The results at the 1-month checkup did not differ statistically from those obtained immediately after the procedure.

Clinical Changes After PBMV
One month after the procedure, we documented a dramatic improvement in clinical status of all of the patients. Twenty patients (87%) were in functional class I, and 3 patients (13%) were in functional class II.


   Discussion
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
References
 
Rheumatic mitral valve stenosis is a chronic disease resulting in considerable anatomical and functional mitral valve alterations. As a consequence of the stenosis, an increase in left atrial pressure is required to maintain cardiac output. This increase in left atrial pressure causes an increase in pulmonary venous pressures. This condition, chronically maintained, causes water deposition in the lung interstitium and generates an interstitial edema.28 One can detect three phases of impairment in lung structure: (1) The elevation in left atrial pressure passively increases venous pulmonary pressures and induces a recruitment of capillary vessels in order to avoid the apposition of water in extravascular bed. This change increases capillary blood volume,29 increases the diffusing capacity, and can be detected as an increase in DLCO and KCO values in the pulmonary function test. (2) If the increase in pulmonary venous pressures persists, a deposition of water in the lung interstitium occurs and causes an enlargement in the diffusing membrane so that it balances the initial elevation in DLCO and, as such, a normal or pseudonormal value of DLCO and KCO is observed. Also, the apposition of water in lung interstitium decreases the lung distensibility and reduces peripheral airways flows near to RV so that a decrease in MEF (at 50% or 25% of FVC) would be detected. (3) A progressive deposition of proteins, proteoglycans, and collagen fibers occurs in lung interstitium, and interstitial fibrosis occurs. Diffusing capacity decreases by an additional increase in diffusing membrane thickness. Lung compliance also decreases, and a restrictive pattern is found in pulmonary function tests, with a reduction in FVC and an increase in RV.30

Several investigators have studied pulmonary function in patients with mitral stenosis. Cortese31 suggested that there was an inverse relationship between the severity of the mitral stenosis and the observed value of the diffusing capacity. Our results agree with this hypothesis because, in our study, we found a negative correlation between mean pulmonary artery pressure and DLCO, suggesting that the transfer function was dependent on the hemodynamic involvement as described above. We observed some patients with increased lung diffusing capacity who had a greater improvement after PBMV, suggesting a lesser impairment in pulmonary function. These data could explain the discrepancies in the conclusions of different studies; patients with decreased baseline lung diffusing capacity who had more elevated pulmonary pressures had no change after PBMV,6 29 32 whereas patients with a normal or slightly elevated diffusing capacity showed decreases after PBMV.33 34

At baseline, our patients showed a decrease in airways flow near RV. The presence of an increase in extravascular lung water at the level of the interstitium would affect the conductance in the small airways, thereby decreasing maximal expiratory flows at low expiratory volumes close to RV. Absence of changes in small airways involvement indicate that the interstitial problems were not resolved, either because they are still structured or, more likely, because interstitial changes take more time to revert. A restrictive problem was not noticeable in the preprocedure assessment because of its low intensity and the wide variability of the predicted values. However, after PBMV, we observed a significant increase in FVC and FEV1, indicating an immediate decrease in pulmonary congestion, as has been described by others.29 34 Pulmonary congestion, with or without an increase in extravascular lung water, can induce a limitation of vital capacity because of the decrease in lung compliance.

In a study performed by Yoshioka et al33 in patients similar to those in the present investigation, an increase in FVC and a decrease in diffusing capacity were observed—results comparable to ours. However, it is important to note that a decrease in the hemoglobin value after the procedure could have an artifactual effect on diffusing capacity. Also, they observed an improvement in other pulmonary function parameters that was not evident in our study. Pooling the results from the study of Yoshioka et al33 and those from the present study (in patients with mitral stenosis), a successful PBMV induces a decrease of approximately 14% in the parameters of lung diffusing capacity, an increase of 6% in FVC, and an increase of 5% in FEV1. Comparing the changes in small airway flows, we detected an increase of 5% in MEF50 and similar increase (6%) in MEF25. Hence, the only relevant change is the decrease in lung diffusing capacity value, which could explain the improvement in functional status.

In patients with moderate or severe mitral valve stenosis, the timing for PBMV has not yet been well established.35 Classically, the symptoms of the patient dictate the moment of surgery or percutaneous valvotomy. Our data suggests that there are some patients with few symptoms who already have nonreversible early lung structural alterations despite having undergone successful PBMV. This implies that PBMV probably needs to be performed earlier and not be delayed until the patient’s symptoms become clearly manifested. A pulmonary function test could help decide the best time to perform PBMV in asymptomatic patients or patients with few symptoms with moderate to severe mitral stenosis.


   Footnotes
 
Abbreviations: DLCO = diffusion capacity of the lung for carbon monoxide; ERV = expiratory reserve volume; FRC = functional residual capacity; KCO = Krough Index; MEF25 = maximal expiratory flow at 25% of vital capacity; MEF50 = maximal expiratory flow at 50% of vital capacity; PBMV = percutaneous balloon mitral valvuloplasty; RV = residual volume; TLC = total lung capacity; VA = alveolar volume

Received for publication March 25, 1999. Accepted for publication August 10, 1999.


   References
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

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J. A. Gomez-Hospital, A. Cequier, P. V. Romero, C. Canete, C. Ugartemendia, E. Iraculis, and E. Esplugas
Persistence of Lung Function Abnormalities Despite Sustained Success of Percutaneous Mitral Valvotomy: The Need for an Early Indication
Chest, January 1, 2005; 127(1): 40 - 46.
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