Cause of in-hospital death in 12,232 consecutive patients undergoing percutaneous transluminal coronary angioplasty

Cause of in-hospital death in 12,232 consecutive patients undergoing percutaneous transluminal coronary angioplasty

Cause of in-hospital death in 12,232 consecutive patients undergoing percutaneous transluminal coronary angioplasty David J. Malenka, MD,a,c Daniel O’...

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Cause of in-hospital death in 12,232 consecutive patients undergoing percutaneous transluminal coronary angioplasty David J. Malenka, MD,a,c Daniel O’Rourke, MD, MS,d Mark A. Miller, MS,b Michael J. Hearne, MD,e Samuel Shubrooks, MD,f Mirle A. Kellett Jr, MD,g John F. Robb, MD,a John R. O’Meara, MD,g Peter VerLee, MD,h William A. Bradley, MD,e David Wennberg, MD, MPH,i Thomas Ryan Jr, MD,g Paul T. Vaitkus, MD,j Bruce Hettleman, MD,a Matthew W. Watkins, MD,j Paul D. McGrath, MD,i and Gerald T. O’Connor, PhD, DSc,b,c for the Northern New England Cardiovascular Disease Study Group Lebanon, Hanover, and Manchester, NH; White River Junction and Burlington, Vt; Boston, Mass; and Portland and Bangor, Maine

Background Some deaths after percutaneous coronary angioplasty (PTCA) occur in high-risk situations (eg, shock), whereas others are unexpected and related to procedural complications. To better describe the epidemiologic causes of death after PTCA, we undertook a systematic review of all in-hospital PTCA deaths in Northern New England from 1990 to 1993.

Methods The medical records of 121 patients who died during their acute hospitalization for PTCA were reviewed with a standardized data extraction tool to determine a mode of death (eg, low output failure, arrhythmia, respiratory failure) and a circumstance of death (eg, death attributable to a procedural complication, preexisting acute cardiac disease). Any death not classified as a procedural complication was reviewed by a committee and the circumstance of death assigned by a majority rule.

Results Low-output failure was the most common mode of death occurring in 80 (66.1%) of 121 patients. Other modes of death included ventricular arrhythmias (10.7%), stroke (4.1%), preexisting renal failure (4.1%), bleeding (2.5%), ventricular rupture (2.5%), respiratory failure (2.5%), pulmonary embolism (1.7%), and infection (1.7%). The circumstance of death was a procedural complication in 65 patients (53.7%) and a preexisting acute cardiac condition in 41 patients (33.9%). Women were more likely to die of a procedural complication than were men.

Conclusion Procedural complications account for half of all post-PTCA deaths and are a particular problem for women. Other deaths are more directly related to patient acuity or noncardiac, comorbid conditions. Understanding why women face an increased risk of procedural complications may lead to improved outcomes for all patients. (Am Heart J 1999;137:632-8.)

See related Editorial on page 582. There is scant literature about how people actually die after percutaneous coronary angioplasty (PTCA).The few studies available have been small series or focused on the issue of unsupported or primary angioplasty.1-4 Although some deaths occur in high-risk situations (eg, PTCA for shock), others are unexpected events and From the Sections of Cardiologya and Clinical Research,b Dartmouth-Hitchcock Medical Center, Lebanon; the cCenter for the Evaluative Clinical Sciences, Dartmouth Medical School, Hanover; dWhite River Junction VA Hospital, White River Junction; eCatholic Medical Center, Manchester; fDepartment of Cardiology, Beth Israel-Deaconess Hospital, Boston; gDivision of Cardiology, Maine Medical Center, Portland; hEastern Maine Medical Center, Bangor; iDivision of Health Services Research, Maine Medical Center, Portland; and the jSection of Cardiology, Fletcher-Allen Health Care, Burlington. Received April 10, 1998; accepted July 1, 1998. Reprint requests: David J. Malenka, MD, Section of Cardiology, Dartmouth-Hitchcock Medical Center, One Medical Center Dr, Lebanon, NH 03756. E-mail: [email protected] Copyright © 1999 by Mosby, Inc. 0002-8703/99/$8.00 + 0 4/1/94259

occur despite apparently successful procedures. Likewise, the cause of some deaths is instantly recognizable (ie, in-lab abrupt closure), whereas for others, particularly those in patients who die away from the laboratory, the proximate cause of death is less clear.These deaths are from a variety of problems, including out-of-lab abrupt closure, ventricular arrhythmias, stroke, and bleeding.To better describe how and why people die after PTCA, we undertook a systematic review of all inhospital deaths after PTCA in Northern New England from 1990 to 1993.We assessed what proportion of deaths were from a complication of the procedure and what was the mode, or proximate cause, of death (eg, low output failure, bleeding).This information will be useful in focusing future efforts to reduce mortality rate.

Methods Between October 1, 1989, and December 31, 1993, data were contributed on 12,919 consecutive hospitalizations for interventional procedures by members of the Northern New England Cardiovascular Disease Study Group, a voluntary consor-

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Figure 1

Circumstance of 121 consecutive in-hospital deaths after PTCA in northern New England.

tium of clinicians, administrators, and scientists associated with the 5 institutions in Maine, New Hampshire, and Vermont that are the sole regional providers of coronary artery bypass grafting (CABG) and percutaneous coronary interventions and 1 institution in Massachusetts with similar services. Since 1987, this group has met at least 3 times a year and pursued studies on the quality and outcomes of care for CABG and valve surgery5-7 and coronary interventions.8-10 Information was collected on demographics, medical history, primary indication for the intervention, priority, therapy, cardiac anatomy and function, the procedure, and in-hospital outcomes.8 The data collection was validated with hospital discharge abstracts and chart review. The medical records of patients who died during the study period were reviewed by one interventional cardiologist at each institution.A standardized data extraction tool was used to determine the chronologic sequence of events leading to the patient’s demise and to determine a “circumstance” of death and a primary “mode” of death.

Circumstances of death The circumstance of death was classified as one of 5 occurrences. A complication of the procedure. A complication was defined as worsened congestive heart failure, a new myocardial infarction, emergency CABG, new arrhythmias, vascular complications, worsened renal failure, infection, or a new cerebral event at the time of, or after, the PTCA leading to or associated with death. Preexisting acute cardiac disease. New myocardial infarction (MI), cardiogenic shock, or a refractory arrhythmia was an indication for the procedure, with subsequent death caused by

Table I. Mode of death after PTCA Mechanism Low-output failure Ventricular arrhythmia Renal failure Cerebrovascular accident Bleeding Respiratory failure Ventricular rupture* Pulmonary embolism Infection Other

Frequency (%) (n = 121)

Rate per 1000 PTCAs

80 (66.1) 13 (10.7) 5 (4.1) 5 (4.1) 3 (2.5) 3 (2.5) 3 (2.5) 2 (1.7) 2 (1.7) 3 (2.5)

6.54 1.06 0.41 0.41 0.25 0.25 0.25 0.16 0.16 0.25

*Documented on autopsy.

the underlying pathologic conditions when the PTCA did not result in complications or clearly worsen the clinical course. Progression of chronic cardiac disease. Progression was defined as ongoing clinical deterioration from an underlying, preexisting, chronic, progressive cardiac disease and when the PTCA did not result in complications or in any way contribute to deterioration of the preexisting condition. Death resulted from the natural progression of underlying disease. Acute or chronic noncardiac conditions. PTCA did not result in complications or in any way contribute to deterioration of the preexisting condition, and death resulted from the natural progression of the underlying disease. Unable to determine. For any death not classified as a procedural complication, the extracted information and chart were reviewed by a committee composed of interventionists

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Table II. Patient characteristics stratified by circumstances of death Circumstance of death Patient characteristics Age (mean) Female (%) Diabetes (%) Peripheral vascular disease (%) COPD (%) Preprocedure renal failure (%) Prior CABG (%) Prior PTCA (%) Number of diseased vessels (mean) Ejection fraction (mean)* LVEDP (mean mm Hg)* Indication (%) Stable angina Unstable angina Post-MI angina Primary treatment of MI Cardiogenic shock Other Priority (%) Nonurgent Urgent Emergent

Procedural complication (n = 65)

Other (n = 56)

P value

71.6 64.6 40.0 23.1 20.0 3.1 9.2 7.7 2.0 51.6 20.0

69.7 33.9 33.9 17.9 14.3 8.9 25.0 7.1 2.1 35.6 24.6

.33 <.01 .48 .55 .48 .23 .02 .98 .41 <.01 .03

6.2 46.1 33.9 4.6 6.2 3.1

0.0 17.9 28.6 19.6 33.9 0.0

<.01

12.5 57.4 30.4

3.1 32.3 64.6

<.01

COPD, Chronic obstructive pulmonary artery disease; LVEDP, left ventricular end-diastolic pressure. *Means are from a subset of all deaths for which values were available.

from each institution and the circumstance of death was assigned by a majority rule. We used a liberal definition of a procedural complication. Unless we could prove otherwise, a death was considered a complication of the procedure. For example, an unexplained postprocedure sudden death was classified as a procedural complication, even though the presumed arrhythmia might have been a consequence of preexisting scar or ischemia in a remote distribution, or the cause of death might have been a cardiac rupture rather than an arrhythmia. However, unless it could be proven otherwise, we assumed that the cause of death was a procedure-related complication.

Mode of death The mode of death was classified as low-output failure, ventricular arrhythmia, primary respiratory failure, bleeding, infection, neurological event, or “other.”The chronologic sequence of events leading up to the death was abstracted from the chart and used to determine which of these possibilities was the proximate mode of death. To assess the reliability of coding, one noninterventional cardiologist from the region was blinded to the original classifications of mode and circumstance of death and asked to recode 50 charts.The recoded deaths were randomly chosen and uniformly distributed by site. Interrater reliability was assessed with the kappa statistic,11 in which 0.0 indicates all observed agreement could be chance, 0.40 to 0.75 represents fair to good agreement beyond chance, and 1.0 indicates perfect agreement. Mode of death was coded the same for 70% of the cases κ = 0.47), and circumstance of death was coded the same

in 79% of cases (κ = 0.63). However, virtually all the disagreements in coding circumstance of death involved the noninterventionist deciding the death was not from a procedural complication when the interventionist had thought otherwise.This demonstrates that if there were bias on the part of the original reviewers, it was toward, rather than away from, attributing circumstance of death to a procedural complication. Standard statistical methods were used for calculation of the chi-square test, z score, odds ratios (OR), and their 95% confidence intervals (95% CI).All P values were 2-tailed. Logistic regression (SAS, SAS Institute Inc.) was used to identify which patient, disease, or treatment characteristics in the entire data set of 12,232 procedures were associated with death from a procedural complication. Independent variables associated with outcomes at or below P = .10 in univariate analysis were candidates for inclusion in the multivariate model. Continuous variables (ejection fraction, left ventricular end-diastolic pressure, etc) were examined to determine the categorization that best related them to the dependent variables.Age, which is not linearly related to death, was examined by decade starting at age 60. Reference categories were those with the lowest rate of adverse outcomes. Of the 12,919 hospitalizations, directional atherectomy was performed on 687 patients who were excluded from the analysis, leaving 12,232 patients undergoing PTCA in the study group. None of these patients received a stent.

Results In-hospital death occurred in 122 cases, for a mortality rate of 1.0%.The medical records of 121 of these patients

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Table III. Procedural characteristics stratified by circumstances of death Circumstance of Death Procedural characteristic No. vessels attempted (mean)* ≥2 Lesions attempted (%) Vessel attempted (%)† Graft Proximal LAD artery Mid-LAD artery Proximal circumflex artery Proximal right artery Other Pre-procedure stenosis (%)† 100% 90%-99% <90% ACC/AHA lesion type (%)† Type A Type B Type C

Other (n = 56)

P value

1.4 27.7

1.3 26.8

.59 .91

1.5 27.7 23.1 20.0 23.1 4.6

12.5 41.1 8.9 7.1 17.9 12.5

<.01

20.0 60.0 20.0

32.1 55.4 12.5

.24

27.7 43.1 19.0

28.6 30.4 41.1

.28

Procedural complication (n = 65)

LAD, Left anterior descending artery; ACC/AHA, American College of Cardiology/American Heart Association. *Includes both grafts and native vessels. †Stenosis of first vessel attempted.

were available for review.The mode of death for 80 patients (66.1%) was low-output failure (Table I).Ventricular arrhythmias accounted for another 13 deaths (10.7%).Additionally, 5 patients died of preexisting renal failure, 5 of a cerebrovascular accident, 3 of bleeding, 3 of respiratory failure, 3 of ventricular rupture, 2 of pulmonary embolism, 2 of infection, and 3 of other causes. Of the 3 deaths caused by bleeding complications, 1 was from an undetected liver laceration sustained during a syncopal episode in the setting of an MI, 1 to a retroperitoneal bleed, and 1 to bleeding that occurred after an emergent CABG for a failed PTCA. Of the deaths that fell into the “other” category, 2 were from ischemic bowel, 1 from severe interstitial lung disease, and 2 could not be determined.The distribution of mode of death was similar at all 5 hospitals. The circumstance of death was determined to be a complication of the procedure in 53.7% of deaths (n = 65) (Figure 1). Death from preexisting acute cardiac disease was the circumstance in 33.9% of deaths (n = 41). Far fewer deaths occurred in the setting of chronic cardiac disease (3.3%) or noncardiac conditions (7.4%). For 2 deaths the circumstance could not be determined. Regardless of the circumstance of death, low-output failure occurred with comparable frequency (64.4% of deaths from a procedural complication versus 67.9% of deaths in other circumstances, P = .7086). Most deaths (n = 101) occurred after the patient had left the catheterization laboratory, and the majority of these deaths were from low-output failure (n = 61). Deaths

that occurred in the catheterization laboratory were almost exclusively from low-output failure (n = 19) except for 1 death from arrhythmia. To determine how patients who died of a procedural complication differed from those who died in other circumstances, we examined patient (Table II) and procedural characteristics (Table III).There was a higher percentage of women among patients who died of procedural complications (64.6%) compared with patients who died in other circumstances (33.9%). Patients dying of complications of the procedure had better left ventricular function and were more likely to have unstable angina and a mid-left anterior descending or proximal circumflex coronary artery PTCA.They were also more likely to have an acute closure in the laboratory (25.6% vs 5.4%, P < .01) and to undergo emergency CABG (18.5% vs 5.4%, P = .03).They were much less likely to be in shock or have an acute MI (10.8%, or 7 of 65 patients dying of a procedural complication vs 53.5%, or 30 of 56 patients dying in other circumstances). These patients were also less likely to have undergone a previous CABG and, perhaps as a corollary, to have a PTCA in a graft.There was also a strong trend toward them being less likely to have an intervention on a total occlusion or a type C lesion.This finding may be a consequence of a greater chronicity of disease in patients dying of other causes, as evidenced by their high rate of prior revascularizations and their being much more often in shock or having an acute MI. Both groups of patients had comparable numbers of vessels and lesions attempted.

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Table IV. Risk factors for dying of a procedural complication Variable Age (y) ≤59 60-69 70-79 ≥80 Sex Male Female No. diseased coronary vessels 1 2 3 Taking intravenous nitroglycerine before the procedure Received an intraaortic balloon pump before the procedure Priority Elective/urgent Emergent Proximal LAD PTCA

OR

95% CI

P value

Beta coefficient*

1.00 1.14 2.71 4.15

— 0.50-2.58 1.32-5.58 1.69-10.15

— .75 <.01 <.01

— 0.1324 0.9984 1.4220

1.00 3.41

— 1.93-6.04

— <.01

— 1.2278

1.00 2.55 4.84 2.48

— 1.35-4.82 2.47-9.47 1.41-4.37

— <.01 <.01 <.01

5.95

1.49-23.81

.01

— 0.9373 1.5773 0.9090 0.7073 1.7839

1.00 3.97 1.83

— 2.08-7.58 1.01-3.31

— <.01 .05

— 1.3795 0.6041

*Intercept –7.7298.

In our dataset of 12,232 patients, significant predictors of death from a complication (n = 65,Table IV) were age, sex, the number of diseased native coronary arteries, emergent priority, the preoperative use of intravenous nitroglycerine or an intraaortic balloon pump, and attempting the procedure in the proximal left anterior descending coronary artery.The use of intravenous nitroglycerine is likely a marker for a particularly unstable lesion(s), whereas the other risk factors may reflect situations in which there is a large amount of myocardium at risk.

Discussion We found that one half of the deaths that occur in the setting of a PTCA can be attributed to a complication of the procedure.The other half are a consequence of the fact that some patients are critically ill going into the procedure, either from acute or chronic heart disease or from another serious illness.This finding means that for the average patient considering PTCA, the risk of death from a procedural complication is lower than the 1.0% mortality rate usually reported.12,13 In fact, it may be even less than is suggested by our data because we used a liberal definition of a procedural complication. In these data, women are at a much higher risk for a complication of the procedure than are men. In fact, 68.9% of all deaths in women (42 deaths in 61 women) resulted from a procedural complication compared with 38.2% in men (23 deaths in 60 men). In our multivariate model (Table IV), the OR of women dying from a complication of the procedure compared with men is

3.26 (95% CI 1.84 to 5.75).As with coronary bypass surgery, women may be at an increased risk for death from a procedural complication because of their relatively smaller vessel size.14 Several other studies have reported on death after PTCA. Kahn et al1 reported 30 deaths from the 1988 to 1991 experience with 5000 PTCAs at a single institution. Patients within 30 days of an MI or with previous bypass surgery were excluded.There were 30 deaths (0.6%). Abrupt vessel closure was thought to be the mechanism of death for 67% of these patients, and 93% of deaths were reported as procedure related.These results differ from ours because we included patients with prior bypass surgery, post-MI angina, and shock. Ellis et al2 reported 32 deaths (0.4%) from a tertiary care database of 8032 patients having undergone PTCA, excluding primary angioplasty. Eighty-one percent of these patients had acute vessel closure resulting in cardiac death, whereas the remaining deaths were not attributed to cardiac complications. Left ventricular failure was the mode of death in 57% of patients.They, too, identified female sex as a risk factor for a procedure-related death.Their lower overall mortality rate and higher death rate from procedural complications may reflect differences in patient selection. The major limitation of our study is that we relied on a retrospective assessment of the medical record and a 1-page registry form to determine the mode and circumstance of death. Even with autopsy data (available for 3.3% of our deaths), establishing mode of death is difficult. Our approach was to abstract from the chart the chronologic sequence of major events that

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occurred during the hospitalization (from a list of 26 possible events plus free text if necessary) and to use this synopsis to inform the decision about mode of death.Attributing the circumstance of death was also aided by abstracting information on sentinel events. In addition, we developed explicit criteria to define the circumstance of death and observed a strict set of rules about how to apply them. Nonetheless, we recognized our susceptibility to bias in the determination of the circumstance of death.To address this concern, all deaths not labeled a procedural complication were reviewed by a committee, and coding of 50 of the 121 charts was checked by a noninterventionist. These data precede the introduction of stents, which may decrease the incidence of acute closures and mitigate some portion of the increased risk faced by women. Also, our results represent the practice patterns of physicians and hospitals in Northern New England, although our experience8 is comparable to that of others.12,13 In this observational study, we have identified those deaths that are more clearly associated with a complication of the procedure, and that may be avoidable. Death from a procedural complication is uncommon and accounts for one half of the 1% in-hospital mortality rate after PTCA.At least some of these deaths might be preventable if we knew more about how to choose the optimal device, how to size it, the role of intravascular ultrasound, the importance of pharmacologic agents, when to attempt complete revascularization, etc. However, because these events occur so infrequently, individual cardiologists or institutional outcomes will be inadequate to guide the improvement of care.To accomplish this, large, collaborative efforts will be needed. We have identified risk factors for a complication of the procedure and have noted that procedural complications are a particular problem for women. Further work should be done to better understand the mechanisms mediating this increase in risk. Understanding this problem would certainly benefit women, and in all likelihood, would lead to improved outcomes for men.

References 1. Kahn JK, Rutherford BD, McConahay DR, et al. Clinical and angiographic correlates of in-hospital death after percutaneous transluminal angioplasty for conditions other than acute myocardial infarction. Am J Cardiol 1993;7:2:826-7. 2. Ellis SG, Myler RK, King SB III, et al. Causes and correlates of death after unsupported coronary angioplasty: implications for use of angioplasty and advanced support techniques in high-risk settings. Am J Cardiol 1991;68:1447-51. 3. Kahn JK, O’Keefe JH, Rutherford BD, et al. Timing and mechanism of in-hospital and late death after primary coronary angioplasty during acute myocardial infarction. Am J Cardiol 1990;66:1045-8. 4. Brodie BR, Stuckey TD, Hansen CJ, et al. Timing and mechanism of death determined clinically after primary angioplasty for acute myocardial infarction. Am J Cardiol 1997;79:1586-91.

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5. O’Connor GT, Plume SK, Olmstead EM, Coffin LH, Morton JR, Maloney CT, et al. A regional prospective study of in-hospital mortality associated with coronary artery bypass grafting. JAMA 1991;226:803-9. 6. O’Connor GT, Plume SK, Olmstead EM, Coffin LH, Morton JR, Maloney CT, et al for the Northern New England Cardiovascular Disease Study Group. Multivariate prediction of in-hospital mortality associated with coronary artery bypass graft surgery. Circulation 1992;85:2110-8. 7. O’Connor GT, Morton JR, Diehl MJ, Olmstead EM, Coffin LH, Levy DG, et al. Differences between men and women in hospital mortality associated with coronary artery bypass graft surgery. Circulation 1993;88:2104-10. 8. Malenka DJ for the Northern New England Cardiovascular Disease Study Group. Indications, practice and procedural outcomes of percutaneous transluminal angioplasty in northern New England in the early 1990s. Am J Cardiol 1996;78:260-5. 9. Malenka DJ, O’Connor GT, Quinton H, et al. Differences in outcomes between men and women associated with percutaneous transluminal coronary angioplasty. Circulation 1996;94(supp1 11):II-99-II-104. 10. O’Rourke D, Malenka DJ, Robb JF, et al. Directional coronary atherectomy in Northern New England. Am J Cardiol 1997; 79:1465-70. 11. Fleiss JL. Statistical methods for rates and proportions, 2nd ed. New York: Wiley; 1981. p. 212-36. 12. Detre KM, Holmes DR Jr, Holubkov R, et al. Incidence and consequences of periprocedural occlusion: the 1985-1986 National Heart, Lung and Blood Institute Percutaneous Transluminal Coronary Angioplasty Registry. Circulation 1990;82:739-50. 13. Hannan EL, Arani DT, Johnson LW, Kemp HG Jr, Lukacik G. Percutaneous transluminal coronary angioplasty in New York state: risk factors and outcomes. JAMA 1992:268:3092-7. 14. O’Connor NJ, Morton JR, Birkmeyer JD, Olmstead EM, O’Connor GT, for the Northern New England Cardiovascular Disease Study Group. Effect of coronary artery diameter in patients undergoing coronary bypass surgery. Circulation 1996;93:652-5.

Appendix Northern New England Cardiovascular Disease Study Group Beth Israel-Deaconess Medical Center: David Brackett, RN, Mary Bogosian, RN, CCP, Christian Campos, MD, Jeannie Fischer, PA, Philip J. Fitzpatrick, MD, Beth Jennings, Robert Johnson, MD,Wendy Kowalker, Patricia Lahey, RN, Stephen J. Lahey, MD, David Leeman, MD, Keith P. Lewis, MD, Stanley Lewis, MD, David Leemah, MD, Maria Lustenberger, RN, Peter R. Maggs, MD, Richard Nesto, MD, Brian O’Connor, CCP, Patty Pawlow, RN, Kathy Peterson, RN, Patricia Rabett, RN, Cheryl Sirois, RN, Samuel Shubrooks, MD,Terri Stokes, RN, MS, Susan Sumner, RN, Paul G.Vivino, MD,Albert Washko, MD, Ronald Weintraub, MD Dartmouth Hitchcock Medical Center: Lindsay D’Anna, PA,Virginia Beggs,ARNP, MS, John D. Birkmeyer, MD, Nancy J.O. Birkmeyer, PhD,William Burke, RCVT, Edward Catherwood, MD, MS, Mike Chamberlain, RN, Lawrence J. Dacey, MD, MS, Gordon Defoe, CCP, Kenneth Dixon-Vestal, RN,Thomas Dodds, MD, Mary Fillinger,

638 Malenka et al

MD, Bruce Friedman, MD, Christine Heins, RN, Bruce Hettleman, MD, Douglas James, MD, John E. Jayne, MD, Karen A. Jean, RN, Pamela Jenkins, MD, Joseph Kasper, ScD, Lori Key, RN,Terry Kneeland, MPH, Judith Kobe, RN, Elizabeth Maislen,ARNP, David J. Malenka, MD, Charles A.S. Martin, MB, BS, Mary Menduni, RN, Nathaniel Niles, MD,William C. Nugent, MD, Gerald T. O’Connor, PhD, DSc, Elaine M. Olmstead, Daniel O’Rourke, MD,Winthrop Piper, MD, Stephen K. Plume, MD, Hebe B. Quinton, MS, John Robb, MD, Cathy S. Ross, John Sanders, MD,William Schults,William F. Sullivan, MS, Jon Wahrenberger, MD, Beth Wolf. Eastern Maine Medical Center: Robert Allen, MD, Jim Blum, MS, Chae C. Choi, MD, Deborah Carey-Johnson, RN, MS,Tina Closson, RN, Robert Clough, MD, Donna Dauphinee, Cynthia M. Downs, RN, MSN, Glen D. Garson, MD, Felix Hemandez Jr, MD, Rebecca Henry, RN, Joseph J. Hessel, MD, Robert M. Hoffman, MD, John H. Jentzer MD, Edward R. Johnson, MD, Peter Marshall, MD, Helen McKinnon, RN, Cathy Mingo, RN, MS, Craig Pedersen, PA,Wendy Perkins, LPN, Robert Rosenthal, MD, Matthew W. Rowe, MD, Katrina Sargent, M. Theodore Silver, MD, Sherry Spraque,Wolfgang J.T. Spyra, MD, Laurie True, RN, Peter Vet Lee, MD, Paul vom Eigen, MD, Craig Warren, CCP Fletcher Allen Health Care: Richard G. Brandenburg, PhD, Pamela Brown, Betsy Burns, RN, Mark Capeless, MD, Kevin Carey, MD, Steve Colmanaro, PA, Steve Crumb, RN, CS, Betty Diette, RN, Roy V. Ditchey, MD, Maureen Dwyer,ARNP, Karen Farrell,ANP, Jan Faucett, RN, Sally Gagnon, RN, Susan Geoffrey, RN, Larry Goetschius, Laurie Grenier,Walter D. Gundel, MD, Richard S. Jackson, MD, David Johnson, MD, Charlie Krumholz, CCP,Ann Laramee, RN, Bruce J. Leavitt, MD, Martin Lewinter, MD, Steve Marcus, PA, Karen McKenny, RN, Mitchell Norotsky, MD, Madeline Norse, RN,William C. Paganelli, MD, PhD, Diane Pappalardo, MHSA, Daniel S. Raabe, MD, Melinda Rabideau, RN, Martha Root, RN, Janice Smith, RN, Christopher M.Terrien Jr, MD, Edward

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Terrien, MD, Matthew W.Watkins, MD, Jane Wilde, RN, MSN,William Witmer, MD Maine Medical Assessment Foundation: Robert B. Keller, MD, David C. Soule, David Wennberg, MD, MPH Maine Medical Center: Lawrence Adrian, PA,Warren D. Alpem, MD, Eric Anderson, Richard A.Anderson, MD, Linda Banister, RN, Claire Berg, RN, Seth Blank, MD, John Braxton, MD, Carl E. Bredenberg, MD, Michael Brennan, PA, David Burkey, MD, Cantwell Clark, MD, Jane Cleaves, RN,Vincent Conti, CEO, Deborah Courtney, RN, MS, Joshua Cutler, MD, Desmond Donegan, MD, Pat Fallo, RN, Rick Forest, CCP, Robert Groom, CCP, Daniel Hanley, MD, Mary Beth Hourihan MD, Jane Kane, RN, Saul Katz, MD, Mirle A. Kellett Jr, MD, Robert Kramer, MD, Costas T. Lambrew, MD, F. Stephen Lamed, MD, Lee Lucas, Paul D. McGrath, MD, Jeremy R. Morton, MD, Edward R. Nowicki, MD, John R. O’Meara, MD, Sheilia Parker, RN, Patricia Peasley, RN, Cathy Prouty, RN, Reed D. Quinn, MD, Dennis Redfield, Karen Reynolds, MPH,Thomas Ryan Jr, MD, Jean Saunders, MSN, MPH,Alyce Schultz, RN, PhD, Susan Seekins, RN, Paul W. Sweeney, MD, Karen Tolan, RN, Nancy Tooker, RN, Joan F.Tryzelaar, MD, Kathy Viger, RN, Paul T.Vaitkus, MD, Cynthia Westlund, RN,Wanda Whittet, RN Optima Health Care, Catholic Medical Center:Yvon Baribeau, MD,Ann Becker, RN, Craig C. Berry, MD, Kevin Berry, MD,William A. Bradley, MD, David C. Charlesworth, MD, Susan Cuddy, RN, Robert C. Dewey, MD, Frank Fedele, MD, Louis I. Fink, MD, Erik J. Funk, MD,Alan E. Garstka, MD, Karen Grafton, RN, Dan Halstead, CCP, Michael J. Heame, MD, J. Beatty Hunter, MD,Alan D. Kaplan, MD, Dennis Kelly, MD, Mark A. Klinker, MD, Peggy Lambert, RN, Patrick J. Lawrence, MD, Jeffery Lockhart, MD, Christopher T. Maloney, MD, Kathy McNeil, RN, Venkatram Nethala, MD, Edward Palank, MD, John Pieroni, CCP, M. Judith Porelle, RN, Joanne Robichaud, RN, Mary Sanford, RN, James Schnitz, MD, Benjamin M.Westbrook, MD,Thomas P.Wharton, MD, Kirke W.Wheeler, MD, Diane White, RN