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Ann Thorac Surg 2007;83:241-251
© 2007 The Society of Thoracic Surgeons
-1 Antitrypsin Deficiency
a Division of Medicine, Section of Respiratory Therapy, The Cleveland Clinic Foundation, Cleveland, Ohio
b Department of Pulmonary, Allergy, and Critical Care Medicine, The Cleveland Clinic Foundation, Cleveland, Ohio
d Department of Quantitative Health Sciences, The Cleveland Clinic Foundation, Cleveland, Ohio
c University of California, San Diego School of Medicine, San Diego, California
Accepted for publication July 28, 2006.
* Address correspondence to Dr Stoller, Department of Pulmonary, Allergy and Critical Care Medicine–A90, The Cleveland Clinic Foundation, 9500 Euclid Ave, Cleveland, OH 44195 (Email: stollej{at}ccf.org).
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Abstract |
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 Top Abstract IntroductionMaterial and MethodsResultsCommentMembers of the NETT...Clinical CentersOther ParticipantsOther AcknowledgmentsFootnotesAcknowledgmentsReferences |
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-1 antitrypsin (AAT) deficiency is unclear. METHODS: To assess the role of LVRS in individuals with severe deficiency of AAT, outcomes within the National Emphysema Treatment Trial were analyzed.
RESULTS: Of 1218 randomized subjects, 16 (1.3%) had severe AAT deficiency (serum level < 80 mg/dL) and a consistent phenotype (when available). Characteristics of these 16 patients include 87.5% male; median serum AAT level, 55.5 mg/dL; age, 66 years; forced expiratory volume in 1 second (FEV1), 27% predicted; and 50% had upper-lobe-predominant emphysema. All 10 subjects randomized to LVRS underwent the procedure. Although the small number of subjects hampered statistical analysis, 2-year mortality was higher with surgery (20% versus 0%) than with medical treatment. Comparison of outcomes between the 10 AAT-deficient and the 554 AAT-replete subjects undergoing LVRS showed a greater increase in exercise capacity at 6 months in replete subjects and a trend toward lower and shorter duration FEV1 rise in deficient individuals.
CONCLUSIONS: This study extends to 49 cases the published experience of LVRS in severe AAT deficiency. Although the small number of subjects precludes firm conclusions, trends of lower magnitude and duration of FEV1 rise after surgery in AAT-deficient versus AAT-replete subjects and higher mortality in deficient individuals randomized to surgery versus medical treatment suggest caution in recommending LVRS in AAT deficiency.
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Introduction |
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TopAbstractIntroductionMaterial and MethodsResultsCommentMembers of the NETT...Clinical CentersOther ParticipantsOther AcknowledgmentsFootnotesAcknowledgmentsReferences |
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-1 antitrypsin (AAT) deficiency. Indeed, some randomized trials of LVRS have explicitly excluded individuals with AAT deficiency [3]. On the other hand, some have speculated that individuals with panlobular emphysema, minimal smoking histories, and less small airways disease, such as may be seen with AAT deficiency, may be likely to benefit from LVRS [4]. To date, findings in the three small observational series describing 6 [4], 12 [5], and 21 patients [6] suggest that LVRS can confer similar [5, 6] or more modest [4] initial improvements in forced expiratory volume in 1 second (FEV1) and that these benefits are more short-lived in AAT-deficient individuals than in AAT-replete patients with chronic obstructive pulmonary disease (COPD) [5, 6]. Overall, this sparse available experience invites further examination of the role of LVRS in patients with emphysema related to AAT deficiency.
In the NETT, 1218 patients were randomized to LVRS or medical therapy. We sought to address three questions:
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Material and Methods |
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TopAbstractIntroductionMaterial and MethodsResultsCommentMembers of the NETT...Clinical CentersOther ParticipantsOther AcknowledgmentsFootnotesAcknowledgmentsReferences |
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The primary outcomes were survival and change in exercise capacity measured by maximal, incremental, symptom-limited exercise on a cycle ergometer, both within 24 months. Secondary outcomes included pulmonary function, symptoms, and quality of life performed as previously described (Table 1) [1, 2].
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The radiographic distribution of emphysema was classified as either heterogeneous or homogeneous, as determined by high-resolution computed tomographic (CT) scans read by radiologists using a visual scoring system. Patterns of emphysema were (1) predominantly affecting the upper lobes, (2) predominantly affecting the lower lobes, (3) diffuse, or (4) predominantly affecting the superior segments of the lower lobes. The latter three groups were combined to form a "predominantly non-upper-lobe disease" category.
As in the primary NETT analysis [2], baseline measurements were those obtained at the visit closest to randomization after completion of required pulmonary rehabilitation and before randomization to medical treatment or LVRS.
Bilateral stapled LVRS was performed by median sternotomy or by bilateral video-assisted thoracoscopy. The surgical goal was to resect 20% to 30% of each lung, targeting the most diseased portions.
Statistical analysis was conducted using the SAS software (SAS Institute, Cary, NC). Analysis of groups at baseline and follow-up was performed using 
2 for categoric features and Wilcoxon rank sum tests for continuous measures. Survival analyses through October 31, 2004 were performed using Kaplan-Meier mortality estimates with the log-rank test. Values of p < 0.05 were considered statistically significant. Comparisons of changes between AAT-deficient versus AAT-replete subjects were adjusted for multiple comparisons at 6, 12, and 24 months using a Bonferroni correction, resulting in a significance criterion of p < 0.016.
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Results |
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TopAbstractIntroductionMaterial and MethodsResultsCommentMembers of the NETT...Clinical CentersOther ParticipantsOther AcknowledgmentsFootnotesAcknowledgmentsReferences |
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Levels of AAT were available for 711 (27.8%) of the 2557 screened subjects who did not satisfy inclusion criteria for NETT. Severe AAT deficiency was present in 13 (1.8%) of the 711, leaving 16 individuals (1.3%) with severe AAT deficiency among the 1218 randomized in NETT. Their phenotypes were PI*SZ in 7, PI*ZZ in 4, PI*Null Null in 1, and other/unknown in 4, whose serum levels were in the severe deficiency range of 38 to 71 mg/dL. One subject, with a serum level 38 mg/dL (phenotype reported unknown), was randomized to medical treatment and did not return for any clinic visits.
Comparison of the 16 eligible individuals with the 13 ineligible AAT-deficient individuals showed no significant baseline differences. [Table 1 presents the baseline characteristics of the 16 AAT-deficient NETT subjects, stratified by allocation to LVRS (n = 10) or medical treatment (n = 6). The mean ± SD age was 64.5 ± 7 years, 12.5% were women, and the baseline mean postbronchodilator FEV1 was 28.2% ± 6.4% predicted. Ten of the AAT-deficient subjects were randomized to LVRS, and all underwent the procedure.
Two of the 16 subjects died within 24 months for an overall 6-month survival rate of 87% (95% confidence interval [CI], 69% to 100%). The survival rate at 12 and 24 months was 87% (95% CI, 69% to 100%); no deaths occurred from 6 to 24 months. None of the 12 AAT-deficient subjects assessed at 6 months showed increased exercise capacity by more than 10 watts, though such improvement was seen in 25% at 12 months and in 20% at 24 months. Improvement in the St. George’s Respiratory Questionnaire (SGRQ) score by more than 8 (twice the minimal clinically important difference) was observed in 23% at 6 months, in 12.5% at 12 months, and in 10% at 24 months.
Although the small number of AAT-deficient subjects precluded meaningful statistical comparison, Table 2 describes outcomes of the 16 AAT-deficient individuals by treatment group. Two subjects in the LVRS group died within 6 months, for an overall LVRS mortality rate of 20% (95% CI, 0.0% to 44.0%), and a rate of 0.010 deaths per person-year compared with 0 deaths per person-year in medically treated subjects and 0.004 deaths per person-year for the whole AAT-deficient cohort. More subjects allocated to LVRS than to medical therapy had increased exercise capacity by more than 10 watts at 24 months (2/6, [33.3%] versus 0/4 [0%]). Also, at 24 months, LVRS recipients showed a mean 4.4-unit fall (improvement) in the SGRQ score versus a mean 8.2-unit rise in medically treated subjects (Wilcoxon rank sum, p = 0.11). Improvement in the SGRQ (by >8 points) was observed more frequently in LVRS-treated subjects at all time points.
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Comment |
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TopAbstractIntroductionMaterial and MethodsResultsCommentMembers of the NETT...Clinical CentersOther ParticipantsOther AcknowledgmentsFootnotesAcknowledgmentsReferences |
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The findings of this analysis extend to 49 the number of reported patients with severe AAT deficiency undergoing LVRS [4–6]. To date, published experience with LVRS in patients with AAT deficiency has, to our knowledge, been limited to 39 patients in three series [4–6]. A comparison of these series shows differences in surgical interventions and outcomes, as well as differences in the characteristics of the patients studied. Cassina and colleagues [5], for example, evaluated 12 consecutive PI*ZZ AAT-deficient patients undergoing LVRS [5] and observed similar though shorter-lived improvement after LVRS than that experienced by 18 AAT-replete individuals undergoing standard upper lobe LVRS.
Gelb and colleagues [4] described no change in the FEV1 at 27 months in 6 PI*ZZ AAT-deficient individuals who underwent targeted resection of the lower lobes (including segmentectomy and lobectomy), but noted small improvements in other pulmonary function measures such as total lung capacity, residual volume, diffusing capacity of the lung for carbon dioxide, and static lung recoil pressure.
Most recently, Tutic and colleagues [6] reported outcomes in 21 patients with severe AAT deficiency (18 PI*ZZ, 2 PI*SZ, and 1 PI*Z Null), 10 of whom underwent lower lobe resection, and the remainder, upper lobe LVRS. As in the series by Cassina and colleagues [5], significant improvements in lung function, exercise capacity, and dyspnea (ie, FEV1, lung volumes, arterial blood gases, 6-minute walk distance, and Medical Research Council dyspnea score) were evident but were of shorter duration than in the AAT-replete patients with whom their results were compared.
Comparison of results of LVRS among the three available studies [4–6] with these results from NETT is hampered by potentially important differences in the characteristics of the patients and in the surgical techniques used in the respective studies. For example, the mean age of the 12 AAT-deficient subjects in the report by Cassina and colleagues [5] was 49 ± 10 years. These individuals underwent bilateral muscle-sparing anteroaxillary thoracotomy to resect areas of the lung that trapped air, "typically ... of ... basal distribution." In the series by Gelb and colleagues [4], the 6 patients were older (mean age, 61 ± 9 years) and underwent bilateral lower lobe LVRS by a thoracoscopic approach. The median age of patients in the series by Tutic and colleagues [6] was 56 years (range, 38 to 74 years) and a variety of surgical approaches were undertaken; for example, 3 AAT-deficient patients underwent unilateral LVRS alone and 2 patients with "complete lower lobe destruction" underwent anatomic lobectomy. Of the total 21 AAT-deficient patients undergoing LVRS, 10 underwent lower lobe resection, 4 had upper lobe resection, and 7 had resection of portions of both the upper and lower lobes. In the NETT study, AAT-deficient subjects undergoing LVRS were older than subjects in the preceding series (median age, 66 years).
As in the earlier reports, NETT LVRS recipients underwent resection of the most diseased portions of the lung; however, in contrast to the usual basilar distribution of emphysema in individuals with severe AAT deficiency [13], 70% of AAT-deficient LVRS recipients in NETT had upper-lobe-predominant emphysema. This may reflect a selection bias in NETT towards patients with predominantly upper lobe disease but highlights the point that patients with AAT deficiency should be evaluated for LVRS based on the same characteristics as other patients and not excluded because of AAT deficiency alone.
Overall, the results of the current study are mixed, with some favoring medical therapy and others LVRS. In the context that these mixed results do not permit a firm conclusion about the efficacy of LVRS compared with medical therapy, caution in recommending LVRS for AAT-deficient individuals must be based on the higher mortality trends observed. We also suggest caution in applying these findings to the general population of AAT-deficient patients because of the somewhat atypical characteristics of AAT-deficient NETT participants receiving LVRS.
First, the prevalence of severe AAT deficiency among COPD populations has been shown to be 1.9% to 2.8% [10, 11], whereas only 1.3% of NETT participants (16/1218) had severe AAT deficiency, suggesting that AAT-deficient individuals are under-represented in the NETT cohort. Furthermore, features of the AAT-deficient NETT participants differ from those in other AAT-deficient groups in potentially important ways. For example, in contrast to the roughly even gender distribution of subjects in the National Heart, Lung, and Blood Institute AAT Registry [11], 80% of AAT-deficient NETT participants were male. Also, although the typical panlobular emphysema of AAT deficiency more commonly involves the lung bases [12–15] in NETT, 70% of AAT-deficient subjects undergoing LVRS had upper-lobe-predominant emphysema. A recent detailed CT analysis of PI*ZZ subjects by Parr and colleagues [13], for example, indicated that 64% demonstrated basal predominance of emphysema and that only 36% had upper-lobe-predominant emphysema.
Several important limitations of the current study warrant mention. First, as in the three earlier reports [4–6], the number of AAT-deficient subjects undergoing LVRS was small. Second, AAT-deficient subjects undergoing LVRS in NETT more frequently resembled those with "usual" AAT-replete emphysema in having predominantly upper lobe disease. Third, because none of the 10 patients undergoing LVRS in this series fall into the group with the most favorable response to LVRS in the NETT trial (ie, upper-lobe-predominant disease with low exercise capacity after rehabilitation [1]), we cannot discount the possibility that the less favorable outcomes relate to these baseline prognostic features rather than to their having AAT deficiency. Finally, because the AAT-deficient subjects in the NETT trial were generally older than AATD subjects undergoing LVRS in other series [4–6] and other AAT-deficient individuals for whom LVRS is considered in clinical practice, caution is needed in applying our results to other settings.
In conclusion, comparison of LVRS versus medical treatment in AAT-deficient subjects in NETT suggested a trend toward higher mortality in LVRS recipients. Also, our findings suggest that overall, the benefits of LVRS are more modest in AAT-deficient subjects than in AAT-replete individuals and are in accord with some others in recommending caution about LVRS for individuals with severe deficiency of AAT.
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Appendix |
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Members of the NETT Research Group |
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TopAbstractIntroductionMaterial and MethodsResultsCommentMembers of the NETT...Clinical CentersOther ParticipantsOther AcknowledgmentsFootnotesAcknowledgmentsReferences |
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Clinical Centers |
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TopAbstractIntroductionMaterial and MethodsResultsCommentMembers of the NETT...Clinical CentersOther ParticipantsOther AcknowledgmentsFootnotesAcknowledgmentsReferences |
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Brigham and Women’s Hospital, Boston, Massachusetts: John Reilly, MD (Principal Investigator); David Sugarbaker, MD (Co-principal Investigator); Carol Fanning, RRT (Principal Clinic Coordinator); Simon Body, MD; Sabine Duffy, MD; Vladmir Formanek, MD; Anne Fuhlbrigge, MD; Philip Hartigan, MD; Sarah Hooper, EP; Andetta Hunsaker, MD; Francine Jacobson, MD; Marilyn Moy, MD; Susan Peterson, RRT; Roger Russell, MD; Diane Saunders; Scott Swanson, MD (Co-principal Investigator, 1996–2001).
Cedars-Sinai Medical Center, Los Angeles, California: Rob McKenna, MD (Principal Investigator); Zab Mohsenifar, MD (Co-principal Investigator); Carol Geaga, RN (Principal Clinic Coordinator); Manmohan Biring, MD; Susan Clark, RN, MN; Jennifer Cutler, MD; Robert Frantz, MD; Peter Julien, MD; Michael Lewis, MD; Jennifer Minkoff-Rau, MSW; Valentina Yegyan, BS, CPFT; Milton Joyner, BA (1996–2002).
Cleveland Clinic Foundation, Cleveland, Ohio: Malcolm DeCamp, MD (Principal Investigator); James Stoller, MD (Co-principal Investigator); Yvonne Meli, RN,C (Principal Clinic Coordinator); John Apostolakis, MD; Darryl Atwell, MD; Jeffrey Chapman, MD; Pierre DeVilliers, MD; Raed Dweik, MD; Erik Kraenzler, MD; Rosemary Lann, LISW; Nancy Kurokawa, RRT, CPFT; Scott Marlow, RRT; Kevin McCarthy, RCPT; Pricilla McCreight, RRT, CPFT; Atul Mehta, MD; Moulay Meziane, MD; Omar Minai, MD; Mindi Steiger, RRT; Kenneth White, RPFT; Janet Maurer, MD (Principal Investigator, 1996–2001); Terri Durr, RN (2000–2001); Charles Hearn, DO (1998–2001); Susan Lubell, PA-C (1999–2000); Peter O’Donovan, MD (1998–2003); Robert Schilz, DO (1998–2002).
Columbia University, New York, in consortium with Long Island Jewish Medical Center, New Hyde Park, New York: Mark Ginsburg, MD (Principal Investigator); Byron Thomashow, MD (Co-principal Investigator); Patricia Jellen, MSN, RN (Principal Clinic Coordinator); John Austin, MD; Matthew Bartels, MD; Yahya Berkmen, MD; Patricia Berkoski, MS, RRT (Site coordinator, LIJ); Frances Brogan, MSN, RN; Amy Chong, BS, CRT; Glenda DeMercado, BSN; Angela DiMango, MD; Sandy Do, MS, PT; Bessie Kachulis, MD; Arfa Khan, MD; Berend Mets, MD; Mitchell O’Shea, BS, RT, CPFT; Gregory Pearson, MD; Leonard Rossoff, MD; Steven Scharf, MD, PhD (Co-principal Investigator, 1998–2002); Maria Shiau, MD; Paul Simonelli, MD; Kim Stavrolakes, MS, PT; Donna Tsang, BS; Denise Vilotijevic, MS, PT; Chun Yip, MD; Mike Mantinaos, MD (1998–2001); Kerri McKeon, BS, RRT, RN (1998–1999); Jacqueline Pfeffer, MPH, PT (1997–2002).
Duke University Medical Center, Durham, North Carolina: Neil MacIntyre, MD (Principal Investigator); R. Duane Davis, MD (Co-principal Investigator); John Howe, RN (Principal Clinic Coordinator); R. Edward Coleman, MD; Rebecca Crouch, RPT; Dora Greene; Katherine Grichnik, MD; David Harpole, Jr., MD; Abby Krichman, RRT; Brian Lawlor, RRT; Holman McAdams, MD; John Plankeel, MD; Susan Rinaldo-Gallo, MED; Sheila Shearer, RRT; Jeanne Smith, ACSW; Mark Stafford-Smith, MD; Victor Tapson, MD; Mark Steele, MD (1998–1999); Jennifer Norten, MD (1998–1999).
Mayo Foundation, Rochester, Minnesota: James Utz, MD (Principal Investigator); Claude Deschamps, MD (Co-principal Investigator); Kathy Mieras, CCRP (Principal Clinic Coordinator); Martin Abel, MD; Mark Allen, MD; Deb Andrist, RN; Gregory Aughenbaugh, MD; Sharon Bendel, RN; Eric Edell, MD; Marlene Edgar; Bonnie Edwards; Beth Elliot, MD; James Garrett, RRT; Delmar Gillespie, MD; Judd Gurney, MD; Boleyn Hammel; Karen Hanson, RRT; Lori Hanson, RRT; Gordon Harms, MD; June Hart; Thomas Hartman, MD; Robert Hyatt, MD; Eric Jensen, MD; Nicole Jenson, RRT; Sanjay Kalra, MD; Philip Karsell, MD; Jennifer Lamb; David Midthun, MD; Carl Mottram, RRT; Stephen Swensen, MD; Anne-Marie Sykes, MD; Karen Taylor; Norman Torres, MD; Rolf Hubmayr, MD (1998–2000); Daniel Miller, MD (1999–2002); Sara Bartling, RN (1998–2000); Kris Bradt (1998–2002).
National Jewish Medical and Research Center, Denver, Colorado: Barry Make, MD (Principal Investigator); Marvin Pomerantz, MD (Co-principal Investigator); Mary Gilmartin, RN, RRT (Principal Clinic Coordinator); Joyce Canterbury; Martin Carlos; Phyllis Dibbern, PT; Enrique Fernandez, MD; Lisa Geyman, MSPT; Connie Hudson; David Lynch, MD; John Newell, MD; Robert Quaife, MD; Jennifer Propst, RN; Cynthia Raymond, MS; Jane Whalen-Price, PT; Kathy Winner, OTR; Martin Zamora, MD; Reuben Cherniack, MD (Principal Investigator, 1997–2000).
Ohio State University, Columbus, Ohio: Philip Diaz, MD (Principal Investigator); Patrick Ross, MD (Co-principal Investigator); Tina Bees (Principal Clinic Coordinator); Jan Drake; Charles Emery, PhD; Mark Gerhardt, MD, PhD; Mark King, MD; David Rittinger; Mahasti Rittinger.
Saint Louis University, Saint Louis, Missouri: Keith Naunheim, MD (Principal Investigator); Robert Gerber, MD (Co-principal Investigator); Joan Osterloh, RN, MSN (Principal Clinic Coordinator); Susan Borosh; Willard Chamberlain, DO; Sally Frese; Alan Hibbit; Mary Ellen Kleinhenz, MD; Gregg Ruppel; Cary Stolar, MD; Janice Willey; Francisco Alvarez, MD (Co-principal Investigator, 1999–2002); Cesar Keller, MD (Co-principal Investigator, 1996–2000).
Temple University, Philadelphia, Pennsylvania: Gerard Criner, MD (Principal Investigator); Satoshi Furukawa, MD (Co-principal Investigator); Anne Marie Kuzma, RN, MSN (Principal Clinic Coordinator); Roger Barnette, MD; Neil Brister, MD; Kevin Carney, RN, CCTC; Wissam Chatila, MD; Francis Cordova, MD; Gilbert D’Alonzo, DO; Michael Keresztury, MD; Karen Kirsch; Chul Kwak, MD; Kathy Lautensack, RN, BSN; Madelina Lorenzon, CPFT; Ubaldo Martin, MD; Peter Rising, MS; Scott Schartel, MD; John Travaline, MD; Gwendolyn Vance, RN, CCTC; Phillip Boiselle, MD (1997–2000); Gerald O’Brien, MD (1997–2000).
University of California, San Diego, San Diego, California: Andrew Ries, MD, MPH (Principal Investigator); Robert Kaplan, PhD (Co-principal Investigator); Catherine Ramirez, BS, RCP (Principal Clinic Coordinator); David Frankville, MD; Paul Friedman, MD; James Harrell, MD; Jeffery Johnson; David Kapelanski, MD; David Kupferberg, MD, MPH; Catherine Larsen, MPH; Trina Limberg, RRT; Michael Magliocca, RN, CNP; Frank J. Papatheofanis, MD, PhD; Dawn Sassi-Dambron, RN; Melissa Weeks.
University of Maryland at Baltimore, Baltimore, in consortium with Johns Hopkins Hospital, Baltimore, Maryland: Mark Krasna, MD (Principal Investigator); Henry Fessler, MD (Co-principal Investigator); Iris Moskowitz (Principal Clinic Coordinator); Timothy Gilbert, MD; Jonathan Orens, MD; Steven Scharf, MD, PhD; David Shade; Stanley Siegelman, MD; Kenneth Silver, MD; Clarence Weir; Charles White, MD.
University of Michigan, Ann Arbor, Michigan: Fernando Martinez, MD (Principal Investigator); Mark Iannettoni, MD (Co-principal Investigator); Catherine Meldrum, BSN, RN, CCRN (Principal Clinic Coordinator); William Bria, MD; Kelly Campbell; Paul Christensen, MD; Kevin Flaherty, MD; Steven Gay, MD; Paramjit Gill, RN; Paul Kazanjian, MD; Ella Kazerooni, MD; Vivian Knieper; Tammy Ojo, MD; Lewis Poole; Leslie Quint, MD; Paul Rysso; Thomas Sisson, MD; Mercedes True; Brian Woodcock, MD; Lori Zaremba, RN.
University of Pennsylvania, Philadelphia, Pennsylvania: Larry Kaiser, MD (Principal Investigator); John Hansen-Flaschen, MD (Co-principal Investigator); Mary Louise Dempsey, BSN, RN (Principal Clinic Coordinator); Abass Alavi, MD; Theresa Alcorn, Selim Arcasoy, MD; Judith Aronchick, MD; Stanley Aukberg, MD; Bryan Benedict, RRT; Susan Craemer, BS, RRT, CPFT; Ron Daniele, MD; Jeffrey Edelman, MD; Warren Gefter, MD; Laura Kotler-Klein, MSS; Robert Kotloff, MD; David Lipson, MD; Wallace Miller, Jr., MD; Richard O’Connell, RPFT; Staci Opelman, MSW; Harold Palevsky, MD; William Russell, RPFT; Heather Sheaffer, MSW; Rodney Simcox, BSRT, RRT; Susanne Snedeker, RRT, CPFT; Jennifer Stone-Wynne, MSW; Gregory Tino, MD; Peter Wahl; James Walter, RPFT; Patricia Ward; David Zisman, MD; James Mendez, MSN, CRNP (1997–2001); Angela Wurster, MSN, CRNP (1997–1999).
University of Pittsburgh, Pittsburgh, Pennsylvania: Frank Sciurba, MD (Principal Investigator); James Luketich, MD (Co-principal Investigator); Colleen Witt, MS (Principal Clinic Coordinator); Gerald Ayres; Michael Donahoe, MD; Carl Fuhrman, MD; Robert Hoffman, MD; Joan Lacomis, MD; Joan Sexton; William Slivka; Diane Strollo, MD; Erin Sullivan, MD; Tomeka Simon; Catherine Wrona, RN, BSN; Gerene Bauldoff, RN, MSN (1997–2000); Manuel Brown, MD (1997–2002); Elisabeth George, RN, MSN (Principal Clinic Coordinator 1997–2001); Robert Keenan, MD (Co-principal Investigator 1997–2000); Theodore Kopp, MS (1997–1999); Laurie Silfies (1997–2001).
University of Washington, Seattle, Washingtgon: Joshua Benditt, MD (Principal Investigator), Douglas Wood, MD (Co-principal Investigator); Margaret Snyder, MN (Principal Clinic Coordinator); Kymberley Anable; Nancy Battaglia; Louie Boitano; Andrew Bowdle, MD; Leighton Chan, MD; Cindy Chwalik; Bruce Culver, MD; Thurman Gillespy, MD; David Godwin, MD; Jeanne Hoffman; Andra Ibrahim, MD; Diane Lockhart; Stephen Marglin, MD; Kenneth Martay, MD; Patricia McDowell; Donald Oxorn, MD; Liz Roessler; Michelle Toshima; Susan Golden (1998–2000).
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Other Participants |
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Centers for Medicare and Medicaid Services, Baltimore, Maryland: Steven M Berkowitz, PhD; Tanisha Carino, PhD; Joe Chin, MD; JoAnna Baldwin; Karen McVearry; Anthony Norris; Sarah Shirey; Claudette Sikora Steven Sheingold, PhD (1997–2004).
Coordinating Center, The Johns Hopkins University, Baltimore, Maryland: Steven Piantadosi, MD, PhD (Principal Investigator); James Tonascia, PhD (Co-principal Investigator); Patricia Belt; Amanda Blackford, ScM; Karen Collins; Betty Collison; Ryan Colvin, MPH; John Dodge; Michele Donithan, MHS; Vera Edmonds; Gregory L. Foster, MA; Julie Fuller; Judith Harle; Rosetta Jackson; Shing Lee, ScM; Charlene Levine; Hope Livingston; Jill Meinert; Jennifer Meyers; Deborah Nowakowski; Kapreena Owens; Shangqian Qi, MD; Michael Smith; Brett Simon, MD; Paul Smith; Alice Sternberg, ScM; Mark Van Natta, MHS; Laura Wilson, ScM; Robert Wise, MD.
Cost Effectiveness Subcommittee: Robert M. Kaplan, PhD (Chair); J. Sanford Schwartz, MD (Co-chair); Yen-Pin Chiang, PhD; Marianne C. Fahs, PhD; A. Mark Fendrick, MD; Alan J. Moskowitz, MD; Dev Pathak, PhD; Scott Ramsey, MD, PhD; Steven Sheingold, PhD; A. Laurie Shroyer, PhD; Judith Wagner, PhD; Roger Yusen, MD.
Cost Effectiveness Data Center, Fred Hutchinson Cancer Research Center, Seattle, Washington: Scott Ramsey, MD, PhD (Principal Investigator); Ruth Etzioni, PhD; Sean Sullivan, PhD; Douglas Wood, MD; Thomas Schroeder, MA; Karma Kreizenbeck; Kristin Berry, MS; Nadia Howlader, MS.
CT Scan Image Storage and Analysis Center, University of Iowa, Iowa City, Iowa: Eric Hoffman, PhD (Principal Investigator); Janice Cook-Granroth, BS; Angela Delsing, RT; Junfeng Guo, PhD; Geoffrey McLennan, MD; Brian Mullan, MD; Chris Piker, BS; Joseph Reinhardt, PhD; Blake Robinswood; Jered Sieren, RTR; William Stanford, MD.
Data and Safety Monitoring Board: John A. Waldhausen, MD (Chair); Gordon Bernard, MD; David DeMets, PhD; Mark Ferguson, MD; Eddie Hoover, MD; Robert Levine, MD; Donald Mahler, MD; A. John McSweeny, PhD; Jeanine Wiener-Kronish, MD; O. Dale Williams, PhD; Magdy Younes, MD.
Marketing Center, Temple University, Philadelphia, Pennsylvania: Gerard Criner, MD (Principal Investigator); Charles Soltoff, MBA.
Project Office, National Heart, Lung, and Blood Institute, Bethesda, Maryland: Gail Weinmann, MD (Project Officer); Joanne Deshler (Contracting Officer); Dean Follmann, PhD; James Kiley, PhD; Margaret Wu, PhD (1996–2001).
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