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(Chest. 2004;125:2188-2195.)
© 2004 American College of Chest Physicians

Effect of Lung Volume Reduction Surgery on Diaphragmatic Neuromechanical Coupling At 2 Years*

Franco Laghi, MD, FCCP; Amal Jubran, MD, FCCP; Arzu Topeli, MD; Patrick J. Fahey, MD, FCCP; Edward R. Garrity, Jr, MD, FCCP; Donald J. de Pinto, MD and Martin J. Tobin, MD, FCCP; for the Loyola/Hines Lung Volume Reduction Surgery Research Group{dagger}

* From the Division of Pulmonary and Critical Care Medicine, Edward Hines Jr. Veterans Administration Hospital, and Loyola University of Chicago Stritch School of Medicine, Hines, IL. {dagger} A list of participants is given in the Appendix.

Correspondence to: Franco Laghi, MD, FCCP, Division of Pulmonary and Critical Care Medicine, Edward Hines, Jr. VA Hospital, 111N, Fifth Ave and Roosevelt Rd, Hines, IL 60141; e-mail: flaghi{at}lumc.edu


   Abstract
TOP
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 Appendix
 References
 
Study objectives: We previously reported that patients with emphysema show an increase in diaphragmatic neuromechanical coupling at 3 months after lung volume reduction surgery. Diaphragmatic neuromechanical coupling was quantified as the quotient of tidal volume (normalized to total lung capacity) to tidal change in transdiaphragmatic pressure (normalized to maximal transdiaphragmatic pressure). As such, neuromechanical coupling estimates the fraction of diaphragmatic capacity used to generate tidal breathing. The present investigation was conducted to determine whether benefit is maintained at 2 years.

Subjects: Fifteen patients with severe COPD, 8 of whom completed the 2-year study.

Methods: Lung volumes, exercise capacity (6-min walking distance), diaphragmatic function (maximal transdiaphragmatic pressure and twitch transdiaphragmatic pressure elicited by phrenic nerve stimulation), and diaphragmatic neuromechanical coupling were recorded before surgery, and at 3 months and 2 years after surgery.

Results: Two years after surgery, lung volumes deteriorated to preoperative values, but patients showed persistent improvements in 6-min walking distance (p < 0.05). Three months after surgery, maximal transdiaphragmatic pressure (p < 0.05), twitch transdiaphragmatic pressure (p < 0.01), and diaphragmatic neuromechanical coupling (p < 0.01) had increased over preoperative values. The improvements in neuromechanical coupling resulted from improvements in diaphragmatic strength and, to a lesser extent, from a decrease in transdiaphragmatic pressure required to maintain tidal breathing. The change in respiratory muscle function at 2 years varied among patients: diaphragmatic contractility was > 10% of preoperative value in half of the patients who concluded our study, and neuromechanical coupling was > 10% of preoperative value in three fourths of the patients who concluded our study. Patients who maintained their gains in neuromechanical coupling also maintained their gains in 6-min walking distance.

Conclusion: Patients undergoing lung volume reduction surgery can maintain early gains in neuromechanical coupling and exercise capacity 2 years later.

Key Words: chronic obstructive • exercise • pulmonary disease • respiratory muscles • thoracic surgery


   Introduction
TOP
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 Appendix
 References
 
Lung volume reduction surgery has recently gained widespread attention for palliative treatment of severe emphysema.123 Possible mechanisms for early symptomatic improvement after surgery include decrease in mechanical load,4 improved right ventricular function,5 and improvement in respiratory muscle contractility.6789

We previously reported on changes in respiratory muscle function in patients at 3 months after surgery.6 We found that enhanced neuromechanical coupling of the diaphragm was an important mechanism in explaining the symptomatic improvement after surgery. We quantified neuromechanical coupling of the diaphragm as the quotient of tidal volume (VT), normalized to total lung capacity (TLC), to tidal change in transdiaphragmatic pressure (Pdi), normalized to maximal Pdi (Pdimax). The increase in neuromechanical coupling of the diaphragm resulted from a combination of improved diaphragmatic function and improved pulmonary mechanics. The contribution of the diaphragm to tidal breathing also increased after surgery, as a result of an increase in diaphragmatic function, measured as an increase in Pdi elicited by twitch stimulation of the phrenic nerves (twitch Pdi).6 Other investigators have confirmed that twitch Pdi is increased at 3 months78 to 12 months8 after surgery.

The long-term changes in lung function, exercise capacity, respiratory symptoms, and quality of life after lung volume reduction surgery have been the focus of several investigations.1810111213 The magnitude of initial improvement and rate of decline are variable.2 Improvement in FEV1 peaks at 3 to 6 months after surgery, and subsequently declines by 100 to 150 mL/yr.81112 Data on quality of life are conflicting.121011 The results of the large National Emphysema Treatment Trial (NETT)2 do not provide precise identification of which individual patient (as opposed to a group of patients) will improve after surgery. The NETT2 was not designed to determine whether or not early improvement in respiratory muscle function persists for up to 2 years after surgery. The aim of this investigation was thus to determine the long-term effects of surgery on respiratory muscle function and neuromechanical coupling.


   Materials and Methods
TOP
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 Appendix
 References
 
Patients
Thirteen men and two women (mean age, 63 ± 2 years [± SE]) with severe and fixed airflow limitation and radiographic evidence of emphysema were studied. The study was approved by the local human studies subcommittee, and informed consent was obtained from each patient. Approximately 25% of each lung was resected via a median sternotomy. All patients were enrolled in a structured, supervised exercise rehabilitation program for a minimum of 6 weeks before and 12 weeks after surgery. No patient with a cardiac pacemaker was enrolled. Some baseline and 3-month follow-up results of these studies have been previously reported.6

Experimental Setup
Flow and Pressure Measurements:
Esophageal pressure (Pes) and gastric pressure (Pga) were separately measured with two thin-walled, latex balloon-tipped catheters (Erich Jaeger; Wurzberg, Germany) coupled to pressure transducers (MP-45; Validyne; Northridge, CA). A balloon containing 1.0 mL of air was positioned in the mid-esophagus; a gastric balloon containing 2.0 mL of air was advanced 70 cm from the nares. Proper positioning of the esophageal balloon was ensured with the occlusion technique. Pdi was obtained by electronic subtraction of Pes from Pga. Airway pressure was measured at the mouthpiece using a tap connected to a third transducer. Transpulmonary pressure was obtained by subtracting Pes from airway pressure.

Inspiratory flow was measured with a heated Fleisch pneumotachograph (Model 3700; Hans Rudolph; Kansas City, MO) connected to a differential pressure transducer. Volumes were obtained by electronic integration of the flow signal.

Compound Diaphragmatic Action Potentials:
Compound diaphragmatic motor action potentials were recorded bilaterally with surface electromyographic electrodes placed at the seventh and eighth intercostal space and the anterior axillary line. All electromyographic signals were amplified, band pass filtered (band width, 10 Hz to 1 kHz; Gould; Valley View, OH), and displayed on a storage oscilloscope (Gould; Ilford, UK). To optimize the skin-to-electrode conduction of the diaphragmatic electromyographic signal, the skin was carefully prepared with an abrasive paste, alcohol, and an antiperspirant solution.14

Bilateral phrenic nerve stimulation was performed using a magnetic stimulator (Magstim 200; Magstim Co. Ltd; Dyfed, Wales, UK) with a 90-mm coil (P/N 9784–00). This device stimulates neuromuscular structures by inducing electrical currents in the tissue secondary to a time-varying magnetic field of brief duration (< 1 ms total pulse duration); at maximal output, the magnetic field is 2.0 T. To achieve stimulation of the phrenic nerves, the patient’s neck was flexed and the coil was placed over the cervical spine. While the patient relaxed at functional residual capacity (FRC), the site of optimal stimulation was determined by moving the coil between C5 and C7. This position was marked with a felt pen, and all subsequent stimulations were performed at this point. Patients were studied without abdominal binding, waist belts removed and trousers unbuttoned.

Protocol
Data were recorded in each patient 2 to 3 weeks before, and 3 months and approximately 2 years after surgery. Patients were studied in the sitting position with the back supported at a 90° angle. After placement of all transducers, Pdimax was measured as the best of five to nine Mueller maneuvers. Oscilloscope recordings of Pdi provided visual feedback, and at least 1 min of rest was provided between each maneuver. Following 15 min of rest, flow, Pes, Pga, and signals were recorded during at least 1 min of resting breathing. During this period, patients were instructed to remain silent, breathe quietly, and not to cough or sigh, so as to avoid the induction of twitch potentiation (a transient increase in the amplitude of the twitch Pdi when nerve stimulation is preceded by a forceful muscle contraction).1516 Then, twitch Pdi was measured using 8 to 13 magnetic stimulations while the nose and mouth were closed. Lung volumes and 6-min walking distance were also recorded.

Physiologic Measurements
Twitch Pdi:
Twitch Pdi was measured as the difference between the maximum Pdi displacement secondary to phrenic nerve stimulation and the value immediately before stimulation. Individual twitches were accepted for analysis if they displayed the following: (1) consistent end-expiratory lung volume before each stimulation, as reflected by constancy of Pes; (2) absence of esophageal peristalsis at the time of the twitch stimulation; (3) a < 20% variability in amplitude of the compound diaphragmatic action potentials (either hemidiaphragm); (4) absence of ECG artifact in the compound diaphragmatic action potentials; and (5) relaxation of the diaphragm (as signaled by diaphragmatic electromyographic activity exceeding baseline) [criteria are modified161718]. The within-occasion coefficient of variation of twitch Pdi before and after surgery ranged from 2.0 to 9.6%. The within-occasion coefficient of variation of Pdimax in 20 experiments performed before and after surgery ranged from 1 to 10%. The coefficient of variation was > 10% at baseline and 2 years after surgery in one patient who had difficulty in performing the maximal voluntary maneuver.

Pdimax and Diaphragmatic Neuromechanical Coupling:
Pdimax was measured during Mueller maneuvers against an occluded airway at FRC.15 Diaphragmatic neuromechanical coupling was quantified using a modification of the approach of Laghi and coworkers6: the quotient of VT (normalized by TLC) to mean Pdi during inhalation (normalized by Pdimax). As such, neuromechanical coupling estimates the fraction of diaphragmatic capacity used to generate tidal breathing. We employ the term neuromechanical coupling in accordance with current usage in the literature,619 although a direct measurement of neuronal activity, such as motor neuron firing frequency, is not included in the calculation. The average value of diaphragmatic neuromechanical coupling, ie, (VT/TLC)/(mean Pdi/Pdimax) ratio during 1 min of recording was calculated.

Pulmonary Mechanics and Intrinsic Positive End-Expiratory Pressure:
Intrinsic positive end-expiratory pressure was measured during spontaneous breathing as the negative deflection in Pes between the onset of inspiratory effort (end-expiratory Pes) and the onset of inspiratory flow. Relaxation of the abdominal muscles at the onset of inspiration can contribute to the fall in Pes at the onset of inspiratory effort.20 Accordingly, any increase in Pga over the course of the preceding exhalation was subtracted from the Pes signal.2122 Dynamic lung compliance was calculated as the ratio of change in volume (VT) over the change in transpulmonary pressure between instants of zero flow within the same breath, and the average value during 1 min of recording was calculated.

Pressure-Time Product for the Respiratory Muscles:
The pressure output of the respiratory muscles, quantified as the esophageal pressure-time product (PTPes), ie, the time integral of the difference between measured Pes and the estimated chest wall relaxation pressure. PTPes per minute (PTPes/min) was calculated as the product of PTPes per breath and respiratory frequency.

Ratio of Swings in Pga to Swings in Pes:
The relative contribution of the rib cage and expiratory muscles to tidal breathing was estimated by calculating the ratio of swings in Pga ({Delta}Pga) to swings in Pes ({Delta}Pes).23 {Delta}Pes was measured from the beginning of effort to its nadir. {Delta}Pga was measured from the beginning of effort (also identified from the Pes tracing) to its maximum excursion.24

Pulmonary Function Tests and Exercise Performance (6-min Walking Distance):
Lung volumes were measured by plethysmography and timed spirometry. Arterial blood was sampled from the radial artery while patients were breathing room air at rest. Blood gas values were measured using an automatic blood gas analyzer (Model 1620; Instrumentation Laboratory; Lexington, MA). Six-minute walking distance was performed according to the standard procedure.25

Data Analysis
Data were recorded at 2,000 Hz and digitized using a 12-bit analog-to-digital converter connected to a computer. Measurements of twitch Pdi, Pdimax, and pulmonary mechanics obtained before and 3 months and 2 years after surgery were compared by one-way analysis of variance with repeated measures and Newman-Keuls test of multiple comparisons between individual means when appropriate. Results are reported as mean and SE.


   Results
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 Appendix
 References
 
Of the 15 patients enrolled in the study, 2 patients died 2 weeks after surgery. Of the remaining 13 patients, 10 agreed to be reassessed at 3 months after surgery, but 2 patients were unable to participate because of a prolonged exacerbation of COPD. Of the 10 patients who agreed to reassessment at 3 months after surgery, 8 agreed to reassessment at 2 years after surgery. Of the remaining two patients, one refused reassessment and the other had died. One patient who refused reassessment at 3 months died within 2 years after surgery. Data presentation is confined to the eight patients who were reassessed at 2 years.

Compared with the eight patients who agreed to reassessment at 2 years, the four patients who died combined with the three patients who refused additional testing after surgery had lower twitch Pdi before surgery (11.1 ± 1.7 cm H2O vs 19.5 ± 2.7 cm H2O; p = 0.03). Pdimax, 6-min walking distances, blood gas values, and lung volumes (except for percentage of predicted FRC) were equivalent in the two groups.

Pulmonary Function and Exercise Performance
At 3 months after surgery, lung function and the distance covered during 6 min of walking improved (Table 1 , Fig 1 ). The improvements in 6-min walking distance, but not in lung function, were sustained at 2 years after surgery (Table 1).


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  		Table 1. Pulmonary Function of the Patients Before and After Surgery*

 


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  		Figure 1. Six-minute walk distance improved from 865 ± 127 feet (± SE) before surgery to 1,246 ± 99 feet at 3 months after surgery (p < 0.05). Two years after surgery, 6-min walk distance, 1,121 ± 77 feet, was still higher than the value before surgery (p < 0.05). Dotted lines connect the values of neuromechanical coupling before and at 2 years after surgery in the two patients who could not be assessed at 3 months after surgery because of a prolonged COPD exacerbation.

 
Diaphragmatic Contractility
Compared with the value before surgery, Pdimax was higher at 3 months after surgery: 106.6 ± 9.6 cm H2O vs 81.0 ± 7.3 cm H2O (p < 0.05) [Fig 2 ]. The value of Pdimax at 2 years after surgery, 99.3 ± 7.4 cm H2O, was not significantly different from the value before surgery. Compared with the value before surgery, twitch Pdi was higher at 3 months after surgery: 28.3 ± 3.6 cm H2O vs 19.5 ± 2.7 cm H2O (p < 0.01) [Fig 2]. The 3-month increases in twitch Pdi and Pdimax for five of the patients were included in our earlier report.6 The value of twitch Pdi at 2 years after surgery, 23.3 ± 2.2 cm H2O, had decreased from the value recorded 3 months after surgery (p < 0.05), and was not significantly different from the value before surgery.



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  		Figure 2. Left: Voluntary Pdimax increased from 81.0 ± 7.3 cm H2O before surgery to 106.6 ± 9.6 cm H2O at 3 months after surgery (p < 0.05). Two years after surgery, Pdimax (99.3 ± 7.4 cm H2O) was not different from the values before surgery. Right: Twitch Pdi response to phrenic nerve stimulation increased from 19.5 ± 2.7 cm H2O before surgery to 28.3 ± 3.6 cm H2O at 3 months after surgery (p < 0.01). Two years after surgery, twitch Pdi, 23.3 ± 2.2 cm H2O, was not different from the values before surgery. Dotted lines connect the pressure values before and at 2 years after surgery in the two patients who could not be assessed at 3 months after surgery because of a prolonged COPD exacerbation. One patient refused phrenic nerve stimulation at 2 years after surgery.

 
Respiratory Muscle Recruitment and Diaphragmatic Neuromechanical Coupling
Compared with the value before surgery, the {Delta}Pga/{Delta}Pes ratio was more negative (ie, indicating a greater diaphragmatic contribution to tidal breathing) at 3 months after surgery: – 1.2 ± 0.3 vs – 0.6 ± 0.1 (p < 0.01). The value of the {Delta}Pga/{Delta}Pes ratio at 2 years after surgery, – 0.8 ± 0.1, was not different from the value before surgery.

Compared with the value before surgery, diaphragmatic neuromechanical coupling—(VT/TLC)/(mean Pdi/Pdimax)—was higher at 3 months after surgery: 1.42 ± 0.15 vs 0.76 ± 0.15 (p < 0.01) [Fig 3 ]. The value of diaphragmatic neuromechanical coupling at 2 years after surgery, 0.86 ± 0.05, was not different from the value before surgery. The gain in Pdimax after surgery (Fig 2) was the main factor responsible for the changes in neuromechanical coupling. A decrease in mean Pdi also participated in the improvement of neuromechanical coupling: mean Pdi during tidal breathing was 9.9 ± 1.1 cm H2O before surgery, 7.1 ± 1.1 cm H2O at 3 months after surgery, and 8.5 ± 0.8 cm H2O at 2 years after surgery (p = 0.067). In contrast to Pdi and Pdimax, VT/TLC did not change over the 2 years of observation: mean VT/TLC during tidal breathing was 0.080 ± 0.008 before surgery, 0.099 ± 0.015 at 3 months after surgery, and 0.076 ± 0.010 at 2 years after surgery (p = 0.25).



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  		Figure 3. Diaphragmatic neuromechanical coupling, quantified as the quotient of Vt (normalized to TLC) to tidal change in Pdi (normalized to Pdimax), improved from 0.76 ± 0.15 before surgery to 1.42 ± 0.15 at 3 months after surgery (p < 0.01). Two years after surgery, diaphragmatic neuromechanical coupling, 0.86 ± 0.05, was not different from the values before surgery. Dotted lines connect the values of neuromechanical coupling before and at 2 years after surgery in the two patients who could not be assessed at 3 months after surgery because of a prolonged COPD exacerbation.

 
Respiratory Mechanics and Pressure Output of the Respiratory Muscles
Compared with the value before surgery, intrinsic positive end-expiratory pressure was lower at 3 months after surgery: 1.7 ± 0.6 cm H2O vs 3.8 ± 0.7 cm H2O (p < 0.01). The value of intrinsic positive end-expiratory pressure at 2 years after surgery, 3.1 ± 0.8 cm H2O, was not different from the value before surgery. Inspiratory resistance of the lung was 7.4 ± 0.9 cm H2O/L/s before surgery, 5.6 ± 0.4 cm H2O/L/s at 3 months after surgery, and 7.0 ± 0.6 cm H2O/L/s at 2 years after surgery (p = 0.24). Dynamic compliance of the lung was 448 ± 84 mL/cm H2O before surgery, 446 ± 61 mL/cm H2O at 3 months after surgery, and 519 ± 80 mL/cm H2O at 2 years after surgery (p = 0.53).

Compared with the value before surgery, PTPes/min was lower at 3 months after surgery: 104 ± 8 cm H2O/s/min vs 185 ± 20 cm H2O/s/min (p < 0.01). The value of PTPes/min at 2 years after surgery, 150 ± 18 cm H2O/s/min, was not different from the value before surgery.


   Discussion
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
Appendix
 References
 
At 3 months after lung volume reduction surgery, patients displayed increases in diaphragmatic neuromechanical coupling, lung function, and exercise performance. At 2 years after surgery, patients no longer showed overall increases in diaphragmatic neuromechanical coupling and lung function, and only exercise performance was improved over the values before surgery. The 2-year response to surgery, however, was not uniform.

Diaphragmatic Contractility
The increase of Pdimax noted 3 months after surgery is in line with results of other laboratories.782627 Two years after surgery, the mean Pdimax was not different from that before surgery. Four of the eight patients, however, had Pdimax values 17 to 123% above the values before surgery (Fig 2). Likewise, four patients had twitch Pdi values at 2 years that were 20 to 75% above the values before surgery.

Lung volume reduction surgery results in a decrease in lung volume, and the resulting increase in respiratory muscle length is expected to improve muscle function.9 Lung volumes at 2 years after surgery had returned to values equivalent to those before surgery; nevertheless, four patients maintained the gain in diaphragmatic strength achieved 3 months after surgery. Factors that may contribute to the improvement in diaphragmatic function include improved muscle perfusion through improved right-ventricular function,2829 increased muscle strength through an increase in the number of sarcomeres,830 and an increased muscle mass3132; all of these factors may be consequences of lung volume reduction surgery. It is not known, however, whether some or all of these factors contribute to the continued improvement in diaphragmatic contractility in some patients at 2 years after surgery.

Respiratory Muscle Recruitment and Exercise Capacity
The increased diaphragmatic contribution to tidal breathing at 3 months after surgery recorded in our earlier investigation6 was still evident with the addition of the patients in the present report. Two years after surgery, the mean diaphragmatic contribution to tidal breathing—estimated by the {Delta}Pga/{Delta}Pes ratio—was not different from that before surgery. Five of the eight patients, however, did not show a fall in the diaphragmatic contribution to tidal breathing: the values were 15 to 218% above the values before surgery. In four of these five patients, preservation of greater diaphragmatic contribution to tidal breathing at 2 years after surgery is consistent with their preserved diaphragmatic contractility; values of twitch Pdi were greater at 2 years after surgery than before surgery. Another mechanism explaining the greater diaphragmatic contribution to tidal breathing is the change in pressure output of the respiratory muscles (quantified as PTPes/min) required to maintain adequate alveolar ventilation. Four out of five patients who had the greatest (relative) diaphragmatic contribution to tidal breathing displayed the greatest decrease in PTPes/min at 2 years after surgery. Such decrease in PTPes/min resulted, at least in part, from improved lung mechanics (decrease in intrinsic positive end-expiratory pressure and decrease in resistance). In the fifth patient, the PTPes/min at 2 years after surgery was equivalent to the value before surgery; in this patient, intrinsic positive end-expiratory pressure was still 10% less than the value recorded before surgery.

Diaphragmatic Neuromechanical Coupling
Compared with the value before surgery, neuromechanical coupling of the diaphragm during resting breathing at 3 months after surgery improved from 0.76 ± 0.15 to 1.42 ± 0.15 (p < 0.01). At 2 years after surgery, neuromechanical coupling had returned to preoperative values in one patient, and it was 74% of preoperative value in a second patient (Fig 3). In the remaining six patients, neuromechanical coupling at 2 years after surgery was > 10% greater than the value recorded before surgery (range of improvement from 13 to 260%). Neuromechanical coupling of the diaphragm at 2 years after surgery was correlated with the value recorded before surgery (r = 0.83, p = 0.01) [Fig 4 ]. Separating patients into those with a neuromechanical coupling ratio > or < 0.9 before surgery is insightful. The six patients who had ratios < 0.9 before surgery had postoperative ratios that fell above the line of identity in Figure 4, indicating that their neuromechanical coupling improved. In contrast, the two patients with coupling ratios > 0.9 before surgery either fell on or below the line of identity at 2 years after surgery, indicating deterioration in neuromechanical coupling. Moreover, these two patients were the only patients who decreased the distance walked in 6 min at 2 years after surgery. The combination of variables included in the neuromechanical coupling index before surgery was better than each of the individual component in the index in identifying which patients were not going to subsequently benefit from surgery at 2 years. Of the two patients who did not benefit from surgery, their preoperative mean Pdi values were 3.9 cm H2O and 8.9 cm H2O, and their preoperative mean Pdimax values were 122.8 cm H2O and 85.2 cm H2O. These values are within the range of the overall group. Likewise, the VT/TLC ratios of these two patients before surgery were 0.074 and 0.076. These values are within the range of the overall group. The limited number of observations in our study and the dependence of the index of neuromechanical coupling on Pdimax (a volitional maneuver) does not permit us to confidently conclude that low preoperative coupling predicts greater long-term benefit in exercise capacity after surgery. Nevertheless, persistent gain in neuromechanical coupling probably contributes to the long-term gains in exercise performance (ie, 6-min walking distance) recorded in most of our patients.



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  		Figure 4. Relationship between the neuromechanical coupling before surgery and the neuromechanical coupling 2 years after lung volume reduction surgery (r = 0.83, p = 0.01; correlation line not shown). The solid line represents the line of identity. The dotted lines signal a neuromechanical coupling ratio of 0.9 before and 2 years after surgery. The six patients who had ratios < 0.9 before surgery had postoperative ratios that fell above the line of identity, indicating that their neuromechanical coupling improved. In contrast, the two patients with coupling ratios > 0.9 before surgery either fell on or below the line of identity after surgery, indicating a deterioration in neuromechanical coupling.

 
The variation from patient to patient in the long-term changes in diaphragmatic function and neuromechanical coupling in response to surgery is in line with reports that the surgery has variable effects on lung volume and exercise capacity.21213 For instance, Gelb and collaborators12 reported that 2 years after surgery lung function was better than baseline values in 46% of their patients. The NETT investigators2 recently reported an improvement in exercise capacity of > 10 W in 16% of patients at 2 years after surgery. Even when analysis was limited to the subgroup displaying the greatest benefit from surgery (upper-lobe predominance and low baseline exercise capacity), the response was heterogeneous, and only approximately 30% of patients showed a > 10-W improvement in exercise capacity at 2 years.2 The heterogeneous response to surgery, even in a subgroup identified as the best responders, underscores the difficulty in predicting the response to surgery for an individual patient.

In summary, this is the first investigation to assess the 2-year response in diaphragmatic contractility and neuromechanical coupling to lung-volume reduction surgery. Two years after surgery, lung volumes had returned to values equivalent to those before surgery; nevertheless, half of our patients maintained the gain in diaphragmatic strength and three fourths maintained the gain in neuromechanical coupling observed at 3 months after surgery. Patients who maintained an improvement in neuromechanical coupling also maintained an improvement in 6-min walking distance. In conclusion, patients undergoing lung volume reduction surgery can maintain the early gains in neuromechanical coupling of the respiratory muscles and exercise capacity 2 years later.


   Appendix
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 Appendix
References
 
Participating investigators are Franco Laghi, MD, FCCP (Hines, IL); Amal Jubran, MD, FCCP (Hines, IL); Arzu Topeli, MD (Ankara, Turkey); Patrick J. Fahey, MD. FCCP (Maywood, IL); Edward R. Garrity, Jr., MD, FCCP (Maywood, IL); Sairam Parthasarathy, MD (Maywood, IL); Paul S. Warshawsky MD (Montreal, Canada); Donald J. de Pinto, MD (Hines, IL); and Martin J. Tobin, MD, FCCP (Maywood, IL).


   Footnotes
 
Abbreviations: FRC = functional residual capacity; NETT = National Emphysema Treatment Trial; Pdi = transdiaphragmatic pressure; Pdimax = maximal transdiaphragmatic pressure; Pes = esophageal pressure; {Delta}Pes = tidal swings in esophageal pressure; Pga = gastric pressure; {Delta}Pga = tidal swings in gastric pressure; PTPes = esophageal pressure-time product; PTPes/min = esophageal pressure-time product per minute; TLC = total lung capacity; twitch Pdi = twitch stimulation of the phrenic nerves; VT = tidal volume

Supported by grants from the Veterans Administration Research Service.

Received for publication September 8, 2003. Accepted for publication January 13, 2004.


   References
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 Appendix
 References
 

  1. . National Emphysema Treatment Trial Research Group. (2001) Patients at high risk of death after lung-volume-reduction surgery. N Engl J Med 345,1075-1083[Abstract/Free Full Text]
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