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J Thorac Cardiovasc Surg 1994;108:1002-1009
© 1994 Mosby, Inc.

SURGERY FOR CONGENITAL HEART DISEASE

Pulmonary function thirteen to twenty-six years after repair of tetralogy of Fallot

Stockholm, Sweden

From the Departments of Thoracic Surgery ^a and Clinical Physiology, ^b Thoracic Clinics, Karolinska Hospital, and the Department of Radiology, ^c St. Görans Children's Hospital, Stockholm, Sweden.

Received for publication Jan. 6, 1994. Accepted for publication July 28, 1994. Address for reprints: Torbjörn Ivert, MD, Thoracic Surgical Clinic, Karolinska Hospital, 171 76 Stockholm, Sweden.

Abstract

Lung function was evaluated in 68 patients 13 to 26 (median 19) years after repair of tetralogy of Fallot. Age at repair was 7 years (9 months to 42 years) and 51% had a palliative shunt. An outflow patch was inserted in 56%. Median vital capacity was 84% of predicted, forced expiratory volume in 1 second 83%, maximal voluntary ventilation at 40 breaths/min 70%, and diffusing capacity for carbon monoxide 77% of predicted. Scintigraphy demonstrated abnormal pulmonary perfusion in 86%. Average right lung perfusion was 57% (predicted 52%). Regional hypoperfusion could in some patients be explained by previous palliative shunt, pulmonary artery obstruction, or presence of aortopulmonary collaterals. Median symptom-limited work capacity was 82% (95% confidence limits 78% to 90%) of predicted. Twenty-eight physically active patients had high values for symptom-limited work capacity, vital capacity, forced expiratory volume in 1 second, and maximal voluntary ventilation at 40 breaths/min compared with those of inactive patients. Lung function variables were related to physical exercise and previous palliative shunt. Moderate or severe pulmonary valve incompetence had negative but not significant influence on lung function. There was no significant influence of acyanosis before repair, use of transannular patch, duration of follow-up, or smoking. We found moderately reduced work capacity and lung function late after repair of tetralogy of Fallot that did not cause symptoms. Lung function variables were high in young active male patients and low in patients with previous palliative shunt. A better lung function in active patients indicates that physical activity should be encouraged after repair of tetralogy of Fallot. (J THORAC CARDIOVASC SURG 1994;108:1002-9)

The cardiovascular malformations associated with tetralogy of Fallot cause pulmonary hypoperfusion, hypoxia, and polycythemia. Lung function abnormalities including ventilation/perfusion imbalance have been reported both before and after intracardiac repair. ^1-10 A reduced ventilatory capacity can be attributed to factors such as hypoplasia of a lung, reflect a low level of physical activity, and be secondary to altered chest wall mechanics after operation (shunt palliation, definitive repair, and sometimes reoperation) that caused trauma to ribs and pleural adhesions. A disturbed inspiratory flow rate can occur in connection with upper airway obstruction as a sequel to tracheotomy. Abnormal perfusion includes unbalanced distribution of blood perfusion between the lungs, depending on dimensional changes of lungs and enlargement or displacement of the heart. ⁴ Regional hypoperfusion within a lung can be a result of the presence of native branch stenosis, pulmonary artery obstruction after dismantling of a shunt, increased pulmonary vascular resistance caused by a hyperperfusion shunt, or associated arborization anomalies with large aortopulmonary collaterals. ^1,4,11

The aim of the present study was to evaluate lung function as described by static and dynamic spirometry, diffusion capacity for carbon monoxide (D_LCO), and perfusion scintigraphy in patients followed up more than 13 years after repair of tetralogy of Fallot and to analyze relations to patient variables such as palliative shunt, age, smoking, degree of physical activity, and work capacity.

PATIENTS AND METHODS

Patients
Tetralogy of Fallot was repaired in 165 patients at this clinic between January 1966 and 1976. Twenty-four patients (15%) died within 30 days of the operation and a further 16 had died by December 1991. Fifteen (11%) of 141 hospital survivors lived abroad and were lost to follow-up. Pulmonary function was assessed in 68 (62%) of 110 survivors a median of 230 months (range 160 to 310) after operation.

Patients data at repair and at follow-up are listed in Table I. Eight patients (12%) did not have any history of cyanosis. Thirty-five (58%) of the 60 patients with cyanosis had a systemic– to–pulmonary artery palliative shunt inserted at a median age of 3 years (range 1 to 29). Thirty-one patients had a Blalock-Taussig anastomosis (right in 11 and left in 20), three a Potts anastomosis, and one a Waterston anastomosis. Median age at repair was 7 years (range 9 months to 42 years) in 33 patients without a palliative shunt compared with 9 years (range 4 to 40 years) in patients with a palliative shunt (p = 0.04).

Surgical technique
All patients were operated on via a median sternotomy with the aid of cardiopulmonary bypass and hypothermia at 28° to 32° C. A vertical ventriculotomy was used in all patients to close the ventricular septal defect with a patch of Dacron or Teflon material. The outflow tract was widened by resection of parietal extension of the infundibular septum and obstructing trabeculae. The pulmonary valve was dilated with a Hegar probe in 3 patients (4%), commissurotomy was done in 19 (28%), the pulmonary anulus was transected and the malformed valve often excised in 17 (25%), and in 29 patients annular size and valve function were considered adequate.

The outflow tract was widened to achieve a lumen at least as large as the largest diameter of the main pulmonary artery, as measured with Hegar probes. The right ventricle was closed without patch in 30 patients (44%). An outflow tract patch restricted to the right ventricle was inserted in 21 patients (31%) and a transannular patch was used in 17 (25%).

Postrepair pressures were measured in the operating room after cardiopulmonary bypass was discontinued. If the postrepair right ventricular/left ventricular pressure ratio exceeded 0.8, further widening of the right ventricular outflow tract was considered.

Follow-up
The follow-up was conducted between April 1, 1988, and December 31, 1991. The study was approved by the committee of ethics at this hospital and the patients' informed consent was obtained. The investigations were undertaken in every patient who consented to the study regardless of cardiac or pulmonary symptoms. All 68 patients included in this study were evaluated in the hospital 13 to 26 years after repair. After the operation, eight patients (16%) had a tracheotomy and were treated with a respirator for 7 to 35 days. Six of the patients underwent a repeat cardiac operation because of right ventricular outflow tract obstruction (n = 4) or intracardiac shunt (n = 2) 5 to 216 months after intracardiac repair.

Physical development
The height and weight of the patients in relation to age were compared with those of healthy children. ¹²

Physical activity
Patients with a sedentary lifestyle were classified as inactive, those with physically demanding employment but without physical exercise as intermediately active, and patients who had regular physical exercise such as running, cycling, or swimming at least twice a week were classified as active.

Exercise capacity
Symptom-limited work capacity (W_SL) was assessed in the sitting position on a bicycle ergometer (Siemens-Elema AB, Stockholm, Sweden) until limiting symptoms such as dyspnea, general fatigue, or leg fatigue caused the patient to stop. Limiting symptoms were rated from 0 to 10 according to the scale of Borg and associates. ¹³ Normal values for W_SL werecalculated from sex, age, and body weight. ¹⁴ Percent W_SL of each patient was the ratio of performed/predicted W_SL x 100.

Heart volume
Chest roentgenography was done in all patients. The radiologic heart volume in the standing position was calculated according to the method of Jonsell. ¹⁵

Static and dynamic spirometry
Static and dynamic spirometry were assessed with the helium equilibration technique and a spirometer (Gould 2400, Gould Electronics, Bilthoven, The Netherlands). ¹⁶ Vital capacity, residual volume, total lung capacity, maximal voluntary ventilation at 40 breaths/min (MVV₄₀), forced inspiratory volume in 1 second, and forced expiratory volume in 1 second (FEV_1.0) were calculated. A technician encouraged the patient to perform maximally during the examination. In all patients spirometric flow-volume curves were analyzed. Predicted normal values in healthy patients were calculated from age, sex, and body size. ^17,18

Diffusing capacity
D_LCO was determined according to the method of Ogilvie and associates. ¹⁹ Smoking was discontinued at least 18 hours before the assessment. The ratio K_CO was calculated as D_LCO x V_A ^-1(V_A, alveolar volume).

Perfusion scintigraphy
Perfusion scintiscans were obtained in 63 patients (93%) by radionuclide imaging after intravenous injection of 80 mBq (2 mCi) technetium-labeled human albumin macroaggregates (diameter of 20 to 40 µm). The scintiscan was considered abnormal in case of unbalanced perfusion or regional hypoperfusion. In healthy subjects right lung perfusion is 52%, SD* 3%. ²⁰

Total amount of hemoglobin
The predicted normal value of the total amount of hemoglobin for men is 10.5 gm, SD 1.2, and for women 8.2 gm, SD 0.6 x weight. ²¹

Echocardiography
Regurgitation was registered with the Doppler technique (Vingmed CFM 750, Horten AS, Norway, with a 3.25/2.5 MHz probe or Acuson XP10, Mountain View, Calif., with a 2.5/2.0 probe) and classified as none, trivial, slight, moderate, or severe from the color and continuous-wave signals.

Angiography
Thirty-nine preoperative angiograms that could be recovered were scrutinized to identify pulmonary artery anomalies and presence of aortopulmonary collaterals.

Statistical methods
Continuous group variables were presented as median and range, mean, and SD or 95% confidence limits (95% CL). Student's t test or the Mann-Whitney U test was used to compare two samples. Analysis of variance or in case of skew distributions the Kruskal-Wallis nonparametric test was applied to compare three distributions. Qualitative data were analyzed with Fisher's exact test. Stepwise regression analysis was applied to relate lung function to patient variables. The effects of MVV₄₀, total hemoglobin, heart volume, and D_LCO to determine W_SL were analyzed. Lung function with MVV₄₀, vital capacity, and D_LCO, respectively, as dependant variables were related to prognostic variables at time of repair (sex, acyanosis, palliative shunt, transannular patch), length of follow-up, age at follow-up, and explanatory variables at follow-up (smoking, regular physical exercise, and moderate or severe pulmonary valve incompetence). Natural distribution plots and Cook's D test were applied to detect curved relationships and evaluate the effect of outlying values. The null hypothesis was rejected if p was less than 0.05. Calculations were done according to the methods of Armitage and Berry ²² and Draper and Smith. ²³

RESULTS

All patients had physical development within 2 SD of predicted at follow-up. There were wide ranges of age and body size (Table I). None of the patients had a history of lung disease, reported airway symptoms, or were limited in their daily life because of dyspnea at exertion. There was no paralysis of the diaphragm on chest roentgenography.

Static and dynamic spirometry
Median values of lung volumes, inspiratory and expiratory airway flow rates, and MVV₄₀ ranged from 70% to 94% of predicted (Table II). Forced inspiratory volume in 1 second was 59% of predicted in one patient with a previous tracheotomy, indicating upper airway obstruction. One patient could not cooperate at the spirometry and performed only 32% of predicted MVV₄₀.

Table II

Smoking habits
Nineteen patients (28%) were smokers. MVV₄₀ tended to be low in smokers 65 (95% CL 59 to 71)% compared with that in nonsmokers 71 (95% CL 65 to 77)% but these values did not differ significantly (p = 0.25). The values for D_LCO 74 (95% CL 67 to 71)% versus 78 (95% CL 74 to 82)% (p = 0.22) also did not differ between smokers and nonsmokers.

W_SL
Median W_SL was 140 watts (95% CL 130 to 160 watts) corresponding to 82% (95% CL 78% to 90%) of predicted. Dyspnea limited 45 patients (66%) at a median Borg score of 6/10 (range 6 to 9). General or leg fatigue limited the remaining 23 patients at a median Borg score of 7/10 (range 6 to 9).

Physical activity
At follow-up 28 patients (41%) were active, 9 (13%) intermediately active, and 31 (46%) inactive. W_SL, vital capacity, FEV_1.0, MVV₄₀, and V_A were significantly higher in active patients (Table III) than in patients in the other groups.

Table IV

Unbalanced perfusion between the lungs or regional hypoperfusion or both, was observed in patients with and without previous palliative shunt (Table V). In patients with available angiograms, 13 (93%) of 14 pulmonary artery obstructions and 7 (88%) of 8 aortopulmonary collaterals corresponded to regional hypoperfusion. Dismantling of a Waterston anastomosis caused pulmonary artery narrowing that restricted right lung perfusion (Fig. 1). In contrast right lung perfusion was 85% in one patient with left pulmonary artery atresia and left aortopulmonary collaterals. All patients with previous left Blalock-Taussig anastomosis had regional left lung hypoperfusion as did 81% of those without palliative shunt (p = 0.07).

View larger version (160K): [in this window] [in a new window]   Fig. 1. Right lung hypoperfusion of 23% (predicted 52%) in 25-year-old woman 20 years after repair of tetralogy of Fallot and dismantling ofWaterston shunt. Dx, Right; Sin, left.

Table VI

View larger version (28K): [in this window] [in a new window]   Fig. 2. MVV40 in relation to WSL (r = 0.73, p <0.001) in 68 patients 13 to 26 years after repair of tetralogy of Fallot. Acyanosis and palliative shunt at repair and regression line with 95% CL are indicated.

Table VII

Table VIII

Table IX

Tables VII through IX)

View larger version (22K): [in this window] [in a new window]   Fig. 3. MVV40 in relation to sex and age 13 to 26 years after repair of tetralogy of Fallot in 68 patients. Difference between sexes; p<0.001.

View larger version (21K): [in this window] [in a new window]   Fig. 4. DLCO in relation to sex and age 13 to 26 years after repair of tetralogy of Fallot in 68 patients. Difference between sexes: p<0.001.

During the 1960s we still encountered adults with tetralogy of Fallot who had survived without correct diagnosis and repair, which explains the large age span among our patients. In general intracardiac repair was if possible delayed until the patient was of preschool age, and a palliative shunt was constructed at an early age to alleviate hypoxia. The old age at repair implied years of pulmonary hypoperfusion that may have caused irreversible damage. Thus our findings of persisting moderate lung dysfunction cannot be extrapolated to patients who currently have early intracardiac repair. The eight patients without cyanosis at repair had only slightly reduced lung function at follow-up.

Lung volumes, airway flows, and flow-volume curves were used to evaluate restrictive and obstructive lung disease. Spirometric values are higher in men, increase with body size, and decline with age. ^16,24 The physiologic decline of lung function with age was corroborated by us in long-term survivors after repair of tetralogy of Fallot who had a reduced function compared with predicted.

Diffusing capacity reflects the transfer capacity for oxygen. A reduced diffusing capacity after repair of tetralogy of Fallot has been observed previously. ^8,9,25 Physiologic dead space and alveolar-arterial oxygen tension difference during exercise are increased in patients examined several years after repair of tetralogy of Fallot, which suggests impaired gas exchange possibly secondary to pulmonary vascular disease. ²⁵ In our patientsD_LCO, V_A, and also the ratio K_CO were reduced, which indicates that the impaired diffusing capacity was not only related to small alveolar volume but also to qualitative changes of the lung. In contrast Takkunen and associates ⁸ reported reduced diffusing capacity but a normal pulmonary diffusing capacity/alveolar volume ratio after repair of tetralogy of Fallot in adults.

W_SL offers a good estimation of aerobic capacity and the reason for interrupting the test can be rated by the psychophysical scaling of Borg. ^13,26 Total hemoglobin reflects variations in sex, body size, and physical activity irrespective of age. ²¹ Our results indicate that physical activity should be encouraged after repair. Wessel and co-workers ²⁷ reported improved exercise performance in athletes and after primary repair of tetralogy of Fallot. Wessel and colleagues ¹⁰ also stated that lung volumes remain stable with time without a positive effect on function of increased physical activity in excess of volumes predicted from somatic growth.

W_SL, vital capacity, MVV₄₀, and D_LCO were less than 80% of predicted 2 decades after repair in 44%, 38%, 71%, and 44% of patients, respectively. There are numerous reports of reduced exercise capacity after repair of tetralogy of Fallot in children and adults. ^{3,7,9,25,27-31} Likewise restrictive and obstructive lung changes have been documented after repair of tetralogy of Fallot. ^{2,3,7-10,25,30} We found no tendency of a normalization of work capacity and lung function during an observation period of 2 decades.

Several authors have documented a relation between reduced exercise capacity, impaired lung function, and pulmonary valve regurgitation after repair of tetralogy of Fallot. ^{3,7,8,10,30,31} It has been suggested that an increased right ventricular stroke volume associated with pulmonary valve incompetence contributes to a decreased lung compliance. ³⁰ There is a strong correlation between abnormal lung volumes and poor surgical results, particularly pulmonary valve incompetence and increased heart size. ¹⁰ In our patients there was a tendency of adverse effects on lung function of moderate and severe pulmonary valve regurgitation.

Patients without a palliative shunt had better lung function at follow-up than those with shunt but the shunt per se may not have been the entire cause of the reduced lung function. Those who required a palliative shunt at a young age in our series represented a group of patients with more severe disease who underwent two-stage repair. Takkunen and associates ⁸ observed small lung volumes in adults after repair of tetralogy of Fallot but no significant difference between those with and without shunt. A reduced lung function in patients with shunts can be caused by hypoplasia of a lung, impaired ventilatory mechanics, severe cyanosis and lung hypoperfusion, increased blood viscosity, thrombosis and subsequent occlusion of small vessels, or an effect of long-standing hyperperfusion that caused intimal and medial thickening with pulmonary hypertension. ^6,32 Crawford and co-workers ³ observed only minimal pulmonary vascular damage associated with large aortopulmonary shunts and higher pulmonary artery pressure related to reduced vital capacity. Potts and Waterston shunts can cause pulmonary vascular disease as a result of excessive blood flow and furthermore have a tendency to distort the pulmonary artery and result in preferential flow to one lung, as happened in at least one of our patients. ^11,33 Such mechanisms may also have contributed to a high incidence of perfusion abnormalities on the ipsilateral side in our patients with previous Blalock-Taussig shunts.

A high incidence of pulmonary perfusion abnormalities, resulting in ventilation/perfusion mismatch, has been observed before and after repair and in patients with previous shunts with tetralogy of Fallot. ^1,4,8,34 Patients who underwent repair at a young age may exhibit gas exchange abnormalities compatible with maldistribution of lung perfusion. ⁵ After repair blood is directed toward the developed lung and patients with unbalanced pulmonary blood flow distribution have a higher right ventricular pressure. ³⁴ In our patients abnormal pulmonary perfusion observed at scintigraphy tended to be associated with reduced lung function.

We found normal physical development late after repair of tetralogy of Fallot and moderately reduced work capacity and lung function that did not cause symptoms. Lung function variables were high in young active male patients and low in patients with previous palliative shunt. The better lung function in active patients indicated that physical activity should be encouraged after repair of tetralogy of Fallot.

We acknowledge statistical advice and calculations performed by Ulf Brodin, MSc, in Medical Statistics, Karolinska Institute, Stockholm, Sweden.

Footnotes

*Standard deviation.

References

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