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(Chest. 2005;127:40-46.)
© 2005 American College of Chest Physicians

Persistence of Lung Function Abnormalities Despite Sustained Success of Percutaneous Mitral Valvotomy*

The Need for an Early Indication

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

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

Correspondence to: Joan A. Gómez-Hospital, PhD, Cardiac Catheterization Laboratory, Hospital of Bellvitge, C/ Feixa Llarga s/n, Hospitalet del Llobregat, 08907 Barcelona, Spain; e-mail: 26587jgh{at}comb.es


   Abstract
TOP
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 References
 
Aims: We assessed early and long-term pulmonary function changes after percutaneous balloon mitral valvotomy (PBMV).

Methods and results: Mitral area, lung function, and exercise capacity were evaluated before, immediately after, and 3 months, 6 months, and 12 months after successful PBMV in 24 patients. PBMV resulted in a significant and sustained increase in mitral area, from 1.0 ± 0.1 to 1.9 ± 0.1 cm2 (p = 0.001) [mean ± SD], with a progressive increase in exercise tolerance at 6-month follow-up (from 22.6 ± 1.4 to 28.2 ± 1.2 mL/kg, p = 0.0001). An immediate drop in the diffusing capacity of the lung for carbon monoxide (DLCO) was observed (from 26.7 ± 1.5 to 22.3 ± 1.1 mL/min/mm Hg, p = 0.0002) after PBMV, followed by a gradual regression to baseline values at 3 months; at 1 year, the DLCO remained elevated (27.3 ± 6.3 mL/min/mm Hg). The flow in the small airways was reduced at baseline, and there was no significant change during follow-up.

Conclusions: PBMV produces an initial decrease in DLCO, suggesting a reduction of pulmonary congestion. During follow-up, the regression to the initial lung diffusion values despite a sustained hemodynamic improvement suggests that some irreversible interstitial changes were present. In patients with mitral stenosis, an impairment of lung function parameters suggests that PBMV must be performed early, even if patients have few symptoms.

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


   Introduction
TOP
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 References
 
Dyspnea is the most relevant symptom in patients with mitral stenosis and the most important functional limitation.12 The reduction in mitral valve area causes a transvalvular gradient that requires an increase in left atrial pressure to maintain cardiac output; consequently, venous pulmonary congestion develops passively and an alteration in the lung interstitium occurs.3 This alteration, detectable by lung function tests, is the physiopathologic basis of the dyspnea.45

Mitral valve surgery is one of the options for the treatment of mitral stenosis. Some investigators67 have studied the changes in lung function following mitral valve replacement and have observed a correlation between lung function changes and the degree of hemodynamic improvement. However, cardiac surgery requires a thoracotomy, which causes considerable thoracic structural and functional changes that suggest that these pulmonary function tests would need to be interpreted with caution.

Percutaneous balloon mitral valvotomy (PBMV) is a viable alternative to surgery for many patients with mitral stenosis.89 The procedure results in an increase in mitral valve area and an acute decrease in mitral valve gradient and left atrial pressure. These changes are detected immediately following the procedure1011 and would appear to persist for a considerable period of time.1213 The percutaneous technique avoids changes in the thoracic structures and, as such, represents an ideal model to study the changes in lung function following the correction of mitral stenosis. Immediate changes in lung function parameters have been observed,14151617 some of which have been controversial, but no long-term evaluation of these parameters has been published. We conducted the present study to evaluate the initial and the long-term changes in lung function parameters together with exercise capacity following successful PBMV.


   Materials and Methods
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 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 References
 
Study Population
Patients with moderate-to-severe mitral valve stenosis eligible for PBMV were recruited. An echocardiographic score > 11, a left atrial thrombus persisting after 6 months of anticoagulant therapy, and severe coronary artery disease with bypass graft indication were considered as exclusion criteria. A successful result of PBMV was defined as a final mitral valve area > 1.5 cm2 or an increase > 25% relative to the baseline value, without a final mitral regurgitation of > 2/4. Only patients with successful PBMV were entered into the subsequent study so as to focus on maximal hemodynamic improvement. All patients provided written informed consent, and the study procedures were approved by the hospital ethical committee.

Study Protocol
Before Valvotomy:
A transthoracic, two-dimensional, Doppler echocardiographic study was performed in all patients. Two-dimensional area and Doppler ultrasound-derived half-time pressure confirmed the diagnosis. Mitral valve morphology was evaluated, and the echocardiographic score was calculated. The degree of mitral regurgitation was assessed by Doppler ultrasound. Patients with a favorable morphology were selected, and a transesophageal echocardiography was performed to exclude the presence of left atrial thrombus. If an image suggesting thrombus was observed, an oral anticoagulant regimen was implemented and the transesophageal echocardiographic study was repeated at 6 months. If the thrombus did not resolve, the patient was transferred out of the PBMV study.

To evaluate lung function alterations, a series of pulmonary function tests was performed in every patient included in the study. The test included spirometry, and the following parameters were determined: FVC, FEV1, the FEV1/FVC quotient expressed as a percentage, maximal expiratory flow at 50% of FVC (MEF50), and maximal expiratory flow at 25% of FVC (MEF25). Functional residual capacity (FRC) was assessed using helium dilution in 7-min, closed-circuit rebreathing. Expiratory reserve volume (ERV) was determined following a slow vital capacity maneuver. The following static lung volumes were calculated: residual volume (RV), as FRC – ERV; and total lung capacity (TLC), as slow vital capacity + RV. The RV/TLC ratio as a percentage was calculated. Diffusing capacity of the lung for carbon monoxide (DLCO) was determined by the single-breath technique according to Cotes.18 An apnea of 10 s was used. Alveolar volume (VA) was measured, and the quotient DLCO/VA or Krough index (KCO) was calculated. In all instances, European Respiratory Society standardized procedures were followed.19 The equipment used was a pulmonary testing system (Plus Pulmonary Testing System; W. E. Collins; Braintree, MA). Predicted values were those published by the European Respiratory Society.18

A treadmill stress test with the Bruce protocol was used to assess baseline exercise tolerance. Before, during, and after the test, arterial BP and heart rate were recorded and the reason for discontinuation of the test was noted. Peak oxygen uptake (O2) and metabolic units were calculated.

Immediately before the procedure, a hemodynamic study was performed. Right-heart pressures (right atrium, right ventricle, pulmonary artery, and pulmonary capillary wedge) were recorded. To evaluate mitral valve gradient, simultaneous left atrial (transseptal approach) and left ventricular pressures were recorded. Cardiac output was determined by the thermodilution method, and mitral valve area was calculated by the Gorlin formula. Left ventricular angiography was performed to evaluate left ventricular ejection fraction and the degree of mitral regurgitation. Coronary angiography was performed to identify patients with coronary artery disease.

PBMV:
PBMV was performed with a single balloon using the Inoue technique.20 The balloon was positioned across the mitral valve, and sequential inflations were performed. The same hemodynamic measurements 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 the superior and inferior cava veins, pulmonary artery, and aorta were obtained to calculate the residual left-to-right atrial shunt.

After Valvotomy:
Transthoracic, Doppler echocardiographic studies were performed 48 h and 96 h after the procedure to evaluate the final mitral valve area and to assess the degree of residual mitral regurgitation. The presence of a significant left-to-right shunt was ruled out with two-dimensional and Doppler echocardiographic studies. A pulmonary function test was performed at 2 to 6 days and 1 month after valvotomy to assess early lung function changes. The transthoracic echocardiogram, treadmill stress test, and lung function tests were repeated at 3 months, 6 months, and 12 months after valvotomy.

Statistical Analysis:
A statistical software package (SPSS, 10.0; SPSS; Chicago, IL) was used for the statistical study. Continuous variables are expressed as mean ± SD, and discrete variables are expressed as absolute values and percentages. Immediate changes after PBMV were analyzed with a paired t test for continuous variables, and discrete variables were analyzed with the {chi}2 test. Linear regression (r coefficient of Pearson) was used to assess correlation between continuous variables. Analysis of variance for repeated measures was used to evaluate changes of continuous variables during follow-up; p < 0.05 was considered statistically significant.


   Results
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 References
 
Baseline Assessment
Thirty consecutive patients with moderate-to- severe mitral stenosis and an appropriate echocardiographic score underwent PBMV over the recruitment period. A successful result was obtained in 24 patients, and these constitute the present study group.

The baseline clinical and echocardiographic characteristics are summarized in Table 1 . Patients had a moderate-to-severe mitral stenosis, as measured by echocardiography, with a mean mitral valve area of 1.01 ± 0.1 cm2. The mean left atrial dimension was 51 ± 8 mm, and the mean echocardiographic score was 6.1 ± 2.1. The hemodynamic study confirmed the severity of mitral valve stenosis. The mean pre-PBMV mitral valve area was 1.1 ± 0.3 cm2. Twenty-two patients (91%) had pulmonary hypertension, which was mild in 14 patients (58%) and moderate in 8 patients (33%). No patients had severe pulmonary hypertension. Left ventricular function was normal (58 ± 9%), and only two patients had an ejection fraction < 60%. One patient had a significant stenosis of the right coronary artery, and coronary angioplasty was performed immediately after PBMV.


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  		Table 1. Baseline Clinical, Echocardiographic, and Lung Function Parameters of the 24 Patients Included in the Study*

 
The baseline pulmonary function test results are presented in Table 1. Patients showed a reduced baseline value of flow in the small airways, detected as a decrease of the predicted values of MEF25 (55.1 ± 25.9%) and MEF50 (69.6 ± 31.1%). An increase in diffusing capacity was indicated by an elevation of DLCO (117.9 ± 29.7%) and KCO (122.8 ± 29.7%). Fourteen of these patients had a normal spirometric flow pattern, 8 patients had a mild-to-moderate obstructive pattern, and only 1 patient had a restrictive pattern. A correlation between DLCO, as a percentage of the predicted value, and mean pulmonary artery pressure was detected (r = – 0.49; p < 0.03).

Exercise capacity was low before valvotomy, with a peak O2 of 22.6 ± 6.6 mL/kg. A significant correlation between baseline peak O2 and mean pulmonary artery pressure was observed (r = – 0.46, p = 0.032).

Changes After Valvotomy
Immediate Changes:
Immediately after PBMV, an increase in mitral valve area from 1.1 ± 0.3 to 1.9 ± 0.5 cm2 (p < 0.001) was detected (Table 2 ). We also detected a significant increase in cardiac output (from 4.3 ± 1.1 to 4.8 ± 0.9 L/min, p = 0.001), together with a reduction in mitral valve gradient and left atrial pressure (from 12.3 ± 3.2 to 5.6 ± 3.1 mm Hg, p < 0.001; and from 17.1 ± 3.7 to 12.5 ± 4.9 mm Hg, p < 0.001; respectively). No change in mean pulmonary artery pressure was detected (from 23.8 ± 6.4 to 22.5 ± 5.4 mm Hg, p = not significant [NS]). In pulmonary function tests performed 2 to 6 days after PBMV, we detected a decrease in DLCO (from 26.7 ± 7 to 22.3 ± 5.3 mL/min/mm Hg, p < 0.001) and KCO values (from 6.2 ± 1.4 to 5.2 ± 1.1 mL/min/mm Hg/L), without changes in spirometric flows and static lung volumes (Table 3 ). The pathologic values of flow in the small airways persisted immediately after mitral valvotomy despite successful PBMV. No correlations between hemodynamic changes and pulmonary changes were detected, but the change in DLCO values correlated with baseline DLCO values (r = 0.65, p < 0.001): patients with the higher baseline DLCO values had the greater immediate percentage decrease (– 18 ± 9%) in comparison with those having a normal or decreased baseline DLCO (– 4 ± 18%, p < 0.05).


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  		Table 2. Hemodynamic Parameters Before and Immediately After PBMV in the 24 Patients Included in the Study*

 

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  		Table 3. Lung Function Parameters Before and After PBMV in the 24 Patients Included in the Study*

 
Follow-up Changes:
Functional class improved in all patients, and no restenosis was observed after 1 year of follow-up. A sustained increase in mitral valve area was shown in the regular echocardiographic checks during follow-up (Fig 1 ), and the final mitral valve area was 1.92 ± 0.1 cm2. Despite this sustained hemodynamic improvement, values for DLCO and KCO began to increase at 1 month of follow-up (Fig 2 ) and remained persistently elevated, approaching baseline value. Twelve-month post-PBMV values for flow in the small airways remained altered, such that MEF25 and MEF50 were decreased (Table 3).



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  		Figure 1. Mitral valve area changes before PBMV and during the follow-up period.

 


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  		Figure 2. Diffusing capacity changes expressed as DLCO before PBMV and during the follow-up period.

 
A progressive increase in exercise capacity was detected after PBMV. The minutes of exercise achieved and peak O2 increased progressively up to 6 months of follow-up (Fig 3 ), but did not reach a normal value for age. No changes in BP or heart rate were detected.



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  		Figure 3. Exercise capacity changes expressed as peak O2 before PBMV and during the follow-up period.

 

   Discussion
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
References
 
This is the first study that analyses the long-term evolution of lung function parameters after successful PBMV. We wish to emphasize the "nonparallel" evolution of hemodynamic, functional capacity, and lung function parameters over time. Our patients showed an acute increase in mitral valve area and a decrease in left atrial pressure.1011 We found no detectable changes in mitral valve area achieved immediately after PBMV at 1 year of follow-up, similar to the findings by other authors.1213

Exercise capacity progressively increased up to 6 months of follow-up, and this was sustained at 1 year. Similar results have been reported,1621 and no correlation with hemodynamic improvement was detected.222324 A normal exercise capacity was not reached because of two factors: (1) the persistence of a mild mitral stenosis, and (2) the presence of lung function changes at the level of the interstitium, which we have detected.

What is original in this article is the evolution of lung function parameters. Our patients had a drop in diffusion capacity immediately after PBMV, similar to that found by other authors.1516 Diffusing capacity may reflect the difficulty for gas exchange in the alveolar-capillary space and, according to the equation of Roughton and Forster,25 depends on two components: intravascular and extravascular. The extravascular component is the conductance of the alveolar capillary membrane, which is related to structural changes at the level of the alveolar- capillary barrier. Electron microscopy studies of the alveolar-capillary space in chronic pulmonary congestion indicated a proliferation of type II granular pneumocytes and an irregular thickening of capillary basement membrane, both of which were related to the increase in pulmonary wedge pressure and the duration of heart failure.262728 The intravascular component is related to the volume of blood in the alveolar capillaries (capillary volume) and to the rate of the reaction of carbon monoxide with oxyhemoglobin. This reaction rate is proportional to the amount of hemoglobin present, and it varies inversely with the PO2. No changes were detected in membrane diffusion factor,29 so the immediate decrease in DLCO found in our patients can be related to the improvement in pulmonary congestion because of the decrease in capillary volume. This finding was also observed by nuclear test by Hirose et al.30 Accordingly, we observed that those patients having an increased baseline DLCO have a greater immediate percentage decrease than those having a normal or decreased baseline DLCO. These results agree with the hypothesis of Ray et al,14 that a postintervention decrease of DLCO would not be observed if interstitial involvement was great enough to prevent or compensate for the decrease in alveolar-capillary volume. We detected no changes in flow in the small airways, which also suggests that the problems in the interstitium do not improve despite the successful result of PBMV.

The observation that airflow limitation persisted over the full follow-up period suggests that small airways involvement does not improve after PBMV. Total lung diffusion capacity (DLCO and KCO) showed progressive increases during the first 3 months of follow-up. A similar pattern was observed by Bussieres et al31 in patients undergoing cardiac transplantation. These authors observed an initial drop in DLCO followed by a progressive increase in the first 3 months after intervention, and reaching baseline values at 12 months of follow-up. Although these patients have some differences compared to ours (baseline decreased DLCO value, greater cardiovascular impairment, direct toxicity from pharmacologic agents like cyclosporin, or changes in capillary bed secondary to pulmonary de-enervation), this similarity of DLCO variation appears to reveal a common repair mechanism. It has been shown that remodeling (thickening) of the capillary wall occurs in response to increased wall stress in mitral stenosis through a process of fibroelastogenesis.32 Breen et al33 suggest that mechanical tension extending throughout the structural elements of the lungs is a stimulus for cell proliferation and gene expression of fibroblasts. This regulatory mechanism promotes the formation of a stronger capillary membrane so as to resist the considerable changes in stress during exercise under conditions of chronic left-heart failure and increased capillary pressures. It is possible to hypothesize two mechanisms that may be involved in the recovery of DLCO observed after the initial "decongestive" decrease. One is the repair process of interstitial changes that would recover the thin, delicate structure of the alveolar wall so as to improve membrane diffusion. The second is the plasticity of structural proteins and the connective matrix, which would tend to recover the initial preintervention shape and, hence, to increase capillary volume. Even if the alveolar repair process was responsible for the increase in DLCO following the initial decrease, two aspects remain to be explained. Firstly, the persistence of the small airways involvement that suggests a lack of repair of the interstitial damage. Secondly, the recovery of DLCO levels above normal that suggests a secondary increase in the alveolar capillary volume.

Classically, when cardiac surgery was the only method to treat mitral stenosis, the classification of patients into functional classes according to the symptoms of dyspnea was the "gold standard" in deciding the optimum time to perform mitral correction.12 Nowadays, with the introduction of percutaneous mitral valvotomy, the optimum timing for the procedure is less clear.34 In our series of patients with few symptoms, we observed that they already had some structural changes at the lung interstitium, which were nonreversible despite successful treatment, and implied a functional limitation detected as a lack of normalization of exercise capacity. Hence, pulmonary function tests could be useful in deciding the best time to perform a PBMV in asymptomatic, or poorly symptomatic patients with moderate-to-severe mitral stenosis.


   Footnotes
 
Abbreviations: DLCO = diffusing 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 FVC; MEF50 = maximal expiratory flow at 50% of FVC; NS = not significant; PBMV = percutaneous balloon mitral valvotomy; RV = residual volume; TLC = total lung capacity; VA = alveolar volume; O2 = oxygen uptake

Supported in part by grant RTIC 03/11 by Red Respira of the Instituto de Salud Carlos III.

Received for publication June 15, 2004. Accepted for publication August 19, 2004.


   References
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

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