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Asian Cardiovasc Thorac Ann 2003;11:48-51
© 2003 Asia Publishing EXchange Ltd


ORIGINAL CONTRIBUTIONS

Cardiac Morphology in Lung Volume Reduction Surgery for Endstage Emphysema

Wickii T Vigneswaran, MD, Eva V Chomka, MD, Vladmir Jelnin, MD, M Janeen Hernan, MSN, Francis J Podbielski, MD

Division of Cardiothoracic Surgery, The University of Illinois at Chicago Medical Center, Chicago, Illinois, USA

For reprint information contact: Wickii T Vigneswaran, MD Tel: 1 708 327 2488 Fax: 1 708 327 2382 email: wvignes{at}lumc.edu Loyola University Medical Center, 2160 South First Avenue, Maywood, IL 60153 USA.


    ABSTRACT
 TOP
 ABSTRACT
 INTRODUCTION
 PATIENTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Lung volume reduction surgery for endstage emphysema produces significant improvements in various pulmonary parameters, but its effects on cardiac morphology and function have not been clearly defined. Ten patients scheduled for lung volume reduction surgery underwent pulmonary function testing, right-heart catheterization, and electron beam computed tomography of the heart. These studies were repeated 12–16 weeks after the procedure. Quantitative assessments of right and left ventricular function and left ventricular muscle mass were obtained. Postoperatively, all patients showed significant improvements in forced expiratory volume at one minute compared to the preoperative value (1.57 ± 0.24 L versus 1.10 ± 0.21 L), predicted residual lung volume (115% ± 15% versus 205% ± 15%), and 6-minute walk test (318 ± 17 m versus 267 ± 24 m). There were no significant differences between postoperative and preoperative right ventricular end-diastolic volumes (167.3 ± 21.2 mL versus 169.2 ± 17.3 mL) or left ventricular end-diastolic volumes (112.5 ± 10.2 mL versus 119.2 ± 9.7 mL).


    INTRODUCTION
 TOP
 ABSTRACT
 INTRODUCTION
 PATIENTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Lung volume reduction surgery (LVRS) has been shown to provide symptomatic and objective improvements in selected patients with endstage emphysema. The mechanism is thought to involve multiple facets of the respiratory system, including enhanced airflow, oxygenation, elastic recoil, and overall chest wall dynamics. The effects on cardiac function and structure are currently undocumented but LVRS is postulated to improve pulmonary blood flow by right ventricular (RV) unloading and enhanced left ventricular (LV) filling. M-mode and two-dimensional echocardiography have been used to evaluate RV and LV structure and function. However, emphysema of the lung may pose technical difficulties in assessing cardiac function. Electron beam computed tomography (EBCT) is a noninvasive imaging modality that provides an accurate, reproducible, and quantitative assessment of both RV and LV volume, mass, and dynamics. Image acquisition by EBCT is not hindered by emphysematous lung tissue surrounding the heart and does not require inherent assumptions of ventricular geometry.1,2 Thus, EBCT is suitable for serial follow-up of cardiac anatomy and function in emphysematous patients after LVRS. This prospective study was designed to assess RV and LV structure and function before and after LVRS by EBCT using a standardized protocol in patients with endstage emphysema.


    PATIENTS AND METHODS
 TOP
 ABSTRACT
 INTRODUCTION
 PATIENTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Ten patients undergoing LVRS at the University of Illinois at Chicago Medical Center were studied. There were 7 men and 3 women, with a mean age of 68.5 ± 5.5 years (range, 63–78 years). Informed consent was obtained prior to performing diagnostic and surgical procedures. All patients were significantly incapacitated by respiratory insufficiency and required home oxygen at rest. Computed tomography of the chest and lung perfusion scans were used as guides to operative strategy. When evidence of emphysema and target areas were identified, patients were screened by dobutamine echocardiography to evaluate LV function. Five patients underwent coronary angiography following abnormal stress test results or because of previous cardiac disease. Pulmonary hemodynamic measurements were obtained by right heart catheterization in all cases to assess the severity of pulmonary hypertension. Patients underwent preoperative cardiac imaging by ultrafast computed tomographic scanning after they had completed a pulmonary rehabilitation program, and postoperative imaging between 12 and 16 weeks after LVRS.

Bilateral LVRS was performed in all patients; 2 underwent a median sternotomy, and a single-stage video-assisted thoracoscopic approach was used in the other 8, as described previously.3 Patients were admitted on the day of surgery. In the operating room, a radiopaque epidural catheter was placed at the 4th/5th thoracic vertebral interspace. On induction of anesthesia, the patient was intubated with a left-sided double-lumen endotracheal tube, the correct position of which was verified by fiberoptic bronchoscopy. Usually, a horseshoe-shaped portion of lung was removed from the upper lobes. All patients were extubated in the operating room. The median postoperative hospital stay was 11 days (mean, 12 ± 6 days).

Ventricular anatomy and function were quantitatively assessed on a serial basis using an ultrafast computed tomographic scanner (Imatron C-100; GE Imatron, South San Francisco, CA, USA).2,4 The circulation time was estimated during normal respiration after administering a bolus intravenous injection of 1 mL indocyanine green. A densitometer was placed on the earlobe to estimate the circulation time and facilitate accurate timing of the contrast injection and scanning sequences. During imaging, a power injector delivered an infusion of non-ionic contrast medium through an intravenous catheter at 3 mL•sec-1 for 20 sec. Commencing image acquisition at the circulation time ensured excellent and simultaneous opacification of both LV and RV cavities at all levels scanned. Imaging, initiated at the electrocardiographic R wave, consisted of 13 consecutive frames throughout the cardiac cycle at 6 contiguous parallel tomographic levels. After 2–3 min, the scanning table was moved 6 cm (with the patient lying still) and the scanning sequence and contrast injection were repeated. The total amount of iodinated contrast medium used per patient for each scan in the series was approximately 1.2 mL•kg -1. All scan data were stored on an optical storage disk for viewing and analysis on a microcomputer workstation. When the raw image data were analyzed, numerical results were recorded directly into a relational database.

Data were analyzed at each ventricular tomographic level in an identical fashion for all patients at each EBCT study. First, the end-diastolic (image temporally related to the R wave on the electrocardiogram) and the end-systolic (smallest LV chamber volume during the cardiac cycle) scans were identified at each tomographic level. For each heart, images were analyzed from the LV apex through the basal tomographic sections, including the RV outflow tract. This constituted information from 10–12 separate tomographic slices per study, depending on the overall long-axis dimensions of the ventricles. Tomographic chamber volumes were the product of tomographic area (end-diastolic or end-systolic) and slice thickness. Tomographic LV muscle mass was the product of muscle area, slice thickness, and an assumed specific gravity of myocardium (1.05 g•mL-1). Global (or total) ventricular chamber volumes and LV muscle mass were determined by adding the tomographic chamber (end-diastolic and end-systolic) volumes and tomographic muscle (end-diastolic) masses of all slices (modified Simpson’s rule) from apex to base, respectively.

All data are presented as mean values ± standard deviation. Comparisons between the two scans were performed using a paired two-tailed t test. Differences were considered significant if the null hypothesis could be rejected at p < 0.05.


    RESULTS
 TOP
 ABSTRACT
 INTRODUCTION
 PATIENTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
The mean pulmonary artery pressure for the group ranged from 15 to 38 mm Hg (mean, 29 mm Hg). Significant changes were observed for forced expiratory volume at one second (FEV1), total lung capacity, residual volume, and 6-minute walk distance at 8 to 12 weeks postoperatively (Table 1Go). The FEV1 increased by a mean of 43% (range, 0%–137%) from the preoperative value, while total lung capacity and residual volume decreased. There were no significant changes in the partial pressures of arterial oxygen or carbon dioxide, or the carbon monoxide diffusion capacity. There were no significant changes in any of the cardiac parameters measured after LVRS (Table 2Go).


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Table 1. Pulmonary Function and 6 Minute Walk Tests in 10 Patients
 

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Table 2. Ventricular Chamber Volumes and Muscle Mass in 10 Patients
 

    DISCUSSION
 TOP
 ABSTRACT
 INTRODUCTION
 PATIENTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Many investigators have demonstrated that resection of large unilateral or bilateral emphysematous bullae significantly improves respiratory parameters and overall functional status. A resurgence of LVRS, first described by Brantigan and Mueller,5 has resulted from experience of lung transplantation for endstage emphysema and the observation of chest wall remodeling.6–8 The effects on pulmonary hemodynamics and cardiac function appear more complex. Autopsy studies of patients with endstage emphysema showed changes in both RV and LV morphology.9 A negative correlation exists between FEV1 and carbon monoxide diffusion capacity and the pulmonary arterial pressure and pulmonary vascular resistance in patients with moderate to severe emphysema.10 In our study, we did not observe any significant difference in LV or RV morphology and function after LVRS, despite the change in FEV1. These findings were unexpected, however, it must be stressed that our follow-up period was only 12 to 16 weeks.

It has been postulated that the increased pulmonary artery pressure is related to hyperinflation of the lung with increased alveolar and pleural pressures. Resection of the worst areas of the emphysematous lung during LVRS would be expected to alter alveolar and pleural pressures. This hypothesis was supported by the findings of Oswald-Mammosser and colleagues11 of a respiratory pressure swing following LVRS. This was not substantiated by Scharf and colleagues12 who failed to demonstrate a significant inspiratory swing in esophageal pressure monitoring after LVRS. However, it is important to note that single lung transplantation for endstage emphysema results in significant changes in cardiac morphology and function.13–15 It has been well documented that single lung transplantation augments atrial filling and thus right heart preload. These factors coupled with overall decreases in pulmonary pressures have been shown to reduce myocardial strain with a concomitant decrease in wall thickness and tension. Long-term follow-up of these patients with EBCT showed marked ventricular remodeling after 1 to 3 years.16 We predict that changes will occur in our patients over a longer time frame, and further follow-up is mandated.

It has been postulated that the increase in pulmonary pressures after surgery should result in added RV strain and progressive myocardial hypertrophy. The results of our study have demonstrated, at least in early follow-up, at rest, that there is no significant increase in end-diastolic RV volume post-LVRS. Removal of diseased lung tissue decreases intrathoracic dead space and hence decreases intrathoracic pressure, both of which should improve ventricular filling during diastole. Nevertheless, it is possible that removal of lung tissue might actually reduce the vascular bed and counteract the effects of the reduction in intrathoracic pressure.

Previous assessments of cardiac morphology and function have been via echocardiography and heart catheterization. An EBCT examination provides quantitative assessment of ventricular function and morphology. This technique offers several advantages over other noninvasive modalities: it provides accurate information on right heart dimensions (often more difficult to visualize with echocardiography), and it is not affected by the extensive air interface of pulmonary hyperinflation commonly seen in emphysema patients and often made worse by a kyphotic, barrel-chested body habitus. It is also less invasive than heart catheterization and requires less intravenous contrast medium. We believe the digitized image acquisition in EBCT at various incremental planes through the heart permits more reproducible calculations of cardiac chamber size and muscle mass than the various real-time echocardiographic techniques.

Limitations of this study include the small number of patients and rigid inclusion criteria in terms of performance testing. These patients were a highly select group undergoing cardiac and pulmonary testing prior to LVRS, whereas lung transplant patients tend to have more severe emphysema and poorer cardiac function. The small differences noted in end-diastolic ventricular volume and ventricular muscle mass might have reached significance with a larger study group. Exercise produces abnormalities in pulmonary hemodynamics in mild to moderate emphysema even prior to the appearance of abnormal resting pulmonary artery pressures.17,18 It is possible that we might have been able to detect differences in pulmonary hemodynamics and cardiac function following LVRS if the tests has been performed during exercise. The contradictory results in many reports on pulmonary hemodynamics following LVRS may be related to differences in selection criteria and the small numbers of patients in these studies.11,19


    Footnotes
 
Presented at the 8th European Conference on General Thoracic Surgery, European Society of Thoracic Surgeons, November 1–3, 2000, London, UK.


    REFERENCES
 TOP
 ABSTRACT
 INTRODUCTION
 PATIENTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 

  1. Vigneswaran WT, McDougall JC, Olson LJ, Breen JF, McGregor CGA, Rumberger JA. Right ventricular assessment in patients presenting for lung transplantation. Transplantation 1993;55:1051–5.[Medline]

  2. Rees MR, Feiring AJ, Rumberger JA, MacMillan RM, Clark DL. Heart evaluation by cine CT: use of two new oblique views. Radiology 1986;159:804–6.[Abstract/Free Full Text]

  3. Vigneswaran WT, Podbielski FJ. Single-stage bilateral video-assisted thoracoscopic lung volume reduction surgery. Ann Thorac Surg 1997;63:1807–9.[Abstract/Free Full Text]

  4. Behrenbeck T, Reed JE, Rumberger JA. A knowledge-based software package for image analysis and data extraction of complex cardiac images. Eur Heart J 1991;12(Suppl):92.[Free Full Text]

  5. Brantigan OC, Mueller E. Surgical treatment of pulmonary emphysema. Am Surgeon 1957;23:789–804.[Medline]

  6. Cooper JD, Trulock EP, Triantafillou AN, Patterson GA, Pohl MS, Deloney PA, et al. Bilateral pneumonectomy (volume reduction) for chronic obstructive pulmonary disease. J Thorac Cardiovasc Surg 1995;109:106–16.[Abstract/Free Full Text]

  7. McKenna RJ Jr, Brenner M, Gelb AF, Mullin M, Singh N, Peters H, et al. A randomized prospective trial of stapled lung reduction versus laser bullectomy for diffuse emphysema. J Thorac Cardiovasc Surg 1996;111:317–22.[Abstract/Free Full Text]

  8. Vigneswaran WT, Podbielski FJ, Halldorsson A, Kong L, Schwab T, Janulaitis CM, et al. Single-stage, bilateral, video-assisted thoracoscopic lung volume reduction surgery for end-stage emphysema. World J Surg 1998;22:799–802.[Medline]

  9. Kohama A, Tanouchi J, Hori M, Kitabatake A, Kamada T. Pathologic involvement of the left ventricle in chronic cor pulmonale. Chest 1990;98:794–800.[Abstract/Free Full Text]

  10. Oswald-Mammosser M, Apprill M, Bachez P, Ehrhart M, Weitzenblum E. Pulmonary hemodynamics in chronic obstructive pulmonary disease of the emphysematous type. Respiration 1991;58:304–10.[Medline]

  11. Oswald-Mammosser M, Kessler R, Massard G, Wihlm JM, Weitzenblum E, Lonsdorfer J. Effect of lung volume reduction surgery on gas exchange and hemodynamics at rest and exercise. Am J Respir Crit Care Med 1998;158:1020–5.[Abstract/Free Full Text]

  12. Scharf SM, Rossoff L, McKeon K, Graver LM, Graham C, Steinberg HN. Changes in pulmonary mechanics following lung volume reduction surgery. Lung 1998;176:191–204.[Medline]

  13. Vigneswaran WT, Rumberger JA, Breen JF, Peters SG, McGregor CGA, McDougall JC. Pulmonary hemodynamics and right ventricular function following single lung transplantation for end-stage emphysema. Chest 1993;104(Suppl):6S.

  14. Bjortuft O, Simonsen S, Geiran OR, Fjeld JG, Skovlund E, Boe J. Pulmonary haemodynamics after single lung transplantation for end-stage pulmonary parenchymal disease. Eur Resp J 1996;9:2007–11.[Abstract]

  15. Keller CA, Naunheim KS, Osterloh J, Krucylak PE, Baudendistel L, McBride L, et al. Hemodynamics and gas exchange after single lung transplantation and unilateral thoracoscopic lung reduction. J Heart Lung Transplant 1997;16:199–208.[Medline]

  16. Rensing BJ, McDougall JC, Breen JF, Vigneswaran WT, McGregor CG, Rumberger JA. Right and left ventricular remodeling after orthotopic single lung transplantation for end-stage emphysema. J Heart Lung Transplant 1997;16:926–33.[Medline]

  17. Wright JL, Lawson L, Pare PD, Hooper RO, Peretz DI, Nelems JM, et al. The structure and function of the pulmonary vasculature in mild chronic obstructive pulmonary disease. The effect of oxygen and exercise. Am Rev Resp Dis 1983;128:702–7.[Medline]

  18. Schulman LL, Lennon PF, Wood JA, Enson Y. Pulmonary vascular resistance in emphysema. Chest 1994;105; 798–805.[Abstract/Free Full Text]

  19. Weg IL, Rossoff L, McKeon K, Graver LM, Scharf SM. Development of pulmonary hypertension following lung volume reduction surgery. Am J Respir Crit Care Med 1999;159:552–6.[Abstract/Free Full Text]





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