One-Year Follow-up in the Coronary Angioplasty Versus Excisional Atherectomy Trial (CAVEAT I)
Background Directional atherectomy is a frequently used percutaneous revascularization strategy, but its long-term outcomes have not previously been compared with those of balloon angioplasty in a prospective trial.
Methods and Results The 1012 patients enrolled in the Coronary Angioplasty Versus Excisional Atherectomy Trial (CAVEAT I) were followed for at least 1 year after randomization. Analyses of predetermined end points were performed, including a detailed analysis of the 14 patients who died. At 1 year, 11 patients had died in the atherectomy group compared with 3 in the angioplasty group (2.2% versus 0.6%, P=.035), with an excess of out-of-hospital deaths (2.2% versus 0.2%, P=.01) and late cardiac deaths (1.6% versus 0%, P=.01). Univariate predictors of death included age, abrupt closure, periprocedural enzyme elevation, and peripheral vascular complications. There was no evidence that the excess of deaths after atherectomy was linked to perforation, ectasia, or deep resection. Cumulative rates of myocardial infarction were higher in those who had been randomized to atherectomy than in those randomized to angioplasty (8.9% versus 4.4%, P=.005) with a trend toward excess Q-wave and non–Q-wave infarctions. By multivariate analysis, atherectomy was the only variable predictive of the combined end point of death or myocardial infarction. No clinical or angiographic characteristics added to this index. Rates of repeat percutaneous intervention at the target site (24.4% after atherectomy versus 25.9% after angioplasty), coronary artery bypass surgery (9.3% versus 9.1%), hospitalization (50% versus 47.1%), and stroke (1% in both groups) were not significantly different.
Conclusions Long-term follow-up of the 1012 patients randomized to atherectomy or angioplasty has revealed a statistically significant excess of deaths after directional atherectomy that was not evident at 6 months. This difference could be due to the chance occurrence of a low mortality rate in those randomized to angioplasty. The excess of myocardial infarctions after atherectomy remains statistically significant at 1 year. Further investigation is warranted to improve the safety of atherectomy.
The Coronary Angioplasty Versus Excisional Atherectomy Trial (CAVEAT I) was a prospective multicenter trial in which patients with native coronary artery stenoses were randomly assigned to undergo directional atherectomy or balloon angioplasty.1 Both angiographic and clinical end points were analyzed. Removing coronary plaque by atherectomy led to a larger acute gain in lumen diameter and a small reduction in angiographic restenosis at 6-month follow-up, particularly for lesions in the proximal left anterior descending artery. However, this did not translate into an advantage in clinical outcomes. Atherectomy was associated with a higher rate of in-hospital myocardial infarction and increased hospitalization costs. At 6 months, the probability of the combined end point of death and myocardial infarction was higher in the atherectomy group (10.4% versus 4.6%, P<.001), but there was no difference in the composite clinical end point of death, infarction, coronary artery bypass surgery, and the need for subsequent percutaneous coronary intervention.1
The short-term results of atherectomy and angioplasty have been compared in two other randomized trials; treatment of lesions in the proximal left anterior descending coronary artery and saphenous vein grafts were assessed in the Canadian Coronary Atherectomy Trial (CCAT)2 and CAVEAT II,3 respectively. However, there are no prospective comparative studies of long-term outcomes after atherectomy or after randomization to atherectomy or angioplasty. In this study, we have extended the follow-up in the CAVEAT I project to 12 months. We have also performed a detailed analysis of the baseline characteristics and clinical courses of the 14 patients in the CAVEAT I Study who died during the first year after randomization.
Details of eligibility criteria, and methods of randomization, revascularization, and follow-up have been presented previously.1 Participating investigators were selected on the basis of experience with both balloon angioplasty and directional atherectomy. Patients with symptoms of ischemic heart disease who were deemed suitable for either procedure were asked to give informed consent. Angiographic criteria included de novo lesions causing at least 60% diameter stenosis that were less than 12 mm in length by visual estimate and that were suitable for either a ≥6F cutter or a ≥3.0-mm balloon. In the presence of multivessel disease, the target lesion was specified. Patients with a history of myocardial infarction within 5 days or previous percutaneous intervention of the target vessel were excluded.
Random assignment to either atherectomy or angioplasty was made through a telephone service to Duke University, using a blocked randomization sequence developed on a site-by-site basis. The initial procedure was considered successful if a residual stenosis of ≤50% was obtained. Crossover to the other treatment method was strongly discouraged. Aspirin and a calcium antagonist were given at least once before the procedure; the calcium-channel antagonist was continued for at least 1 month and the aspirin indefinitely. All cineangiograms were forwarded to the Angiography Core Laboratory at the Cleveland Clinic Foundation for independent, blinded assessment. Images that showed the treatment device were spliced out before analysis. Tissue specimens retrieved from the atherectomy catheter were forwarded to St Elizabeth’s Hospital in Boston for Core Pathology Laboratory assessment.
Data were prospectively recorded, and patients were followed by the research coordinators and investigators at each site. Long-term follow-up was facilitated by collecting information about next of kin and neighbors at randomization. Quality of data was ensured by audit and double data entry at the Coordinating Center. Predetermined end points were verified using clinical records and death certificates. Myocardial infarction was diagnosed clinically at the participating site and verified by an adjudication committee blinded to treatment assignment, on the basis of the development of new Q waves or an increase in creatinine kinase myocardial band isoenzymes to more than three times the upper limit of normal for the site. In all cases of death, detailed documentation was reviewed by the authors to ascertain the exact circumstances of death.
Clinical models were also developed for the three composite outcomes: death or infarction; death, infarction, or bypass surgery; and death, infarction, or repeat intervention. The clinical factors considered for each end point were age, sex, weight, height, hypertension, hyperlipidemia, diabetes, history of smoking, current smoking, previous cerebrovascular disease, previous peripheral vascular disease, angina class, angina at rest or with associated ECG changes, previous myocardial infarction, previous balloon angioplasty, prior bypass surgery, and comorbid disease. The lesion morphology factors considered were contour, eccentricity, ostial, presence of thrombus, local calcification, proximal calcification, angulation, proximal tortuosity, bifurcation, lesion length, and lesion type.4 Vessel morphology factors included the number of diseased vessels, proximal left anterior descending location, and the number of lesions (1 versus more than 1). The angiographic factors considered were preprocedural and postprocedural diameters, expressed as percent diameter stenosis and as minimum lumen diameter (millimeters).
Cox proportional hazard modeling techniques were used to determine the joint effect of these factors for each of the three outcomes. The results of both backwards and stepwise procedures for variable selection were evaluated. These evaluations led to the decisions of which important factors to retain for the joint prediction of each outcome. Univariable significance of treatment with outcome was determined using a log-rank test in each case.
Baseline Characteristics and Clinical Outcomes
Baseline clinical and angiographic characteristics in those patients who died in the first 12 months are compared with those in the entire cohort in Table 1⇓. Procedural and in-hospital outcomes are compared in Table 2⇓. All events occurring during the initial hospitalization were classified as “in-hospital.”
Eleven patients died in the first 12 months after atherectomy compared with 3 after angioplasty (2.2% versus 0.6%, respectively; P=.035; Fig 1⇓), with more out-of-hospital deaths (2.2% versus 0.2%, P=.01) or late cardiac deaths (1.6% versus 0%, P=.01). Baseline clinical and angiographic characteristics and a summary of the clinical course of each of the 14 patients who died are presented in Table 3⇓⇓.
All except 1 of the patients died from cardiovascular causes, either as a consequence of the procedure or of a late cardiac event. Of the 11 deaths after atherectomy, 5 died suddenly, 3 died of cardiogenic shock, 1 of pulmonary emboli (related to a femoral hematoma), 1 of an intracerebral hemorrhage after repeat angioplasty, and 1 after vascular surgery for recurrent leg ischemia. Of the 3 patients who died after angioplasty, 2 died in-hospital of complications related to abrupt closure during or on the day of angioplasty; the late death was due to disseminated cancer.
With only 14 deaths, there was insufficient power to perform multiple comparisons. However, important differences appear from the descriptive statistics comparing the 14 patients who died with the 998 survivors. The median age of those who died was 65 years (25th to 75th percentile, 62, 70 years) compared with 59 (51, 67) years for survivors at 1 year. The treatment groups were well balanced at baseline for age with a median age of 59 years in both groups. Abrupt closure was documented in 3 (21%) of those who died compared with 60 (6%) of the survivors at 1 year. Periprocedural enzyme elevations occurred in 5 (36%) of those who died compared with 129 (13%) of survivors.
Peripheral vascular complications occurred in 7 (50%) of the 14 who died compared with 67 (6.6%) of the entire cohort. Five had undergone atherectomy and 2 had undergone angioplasty. In addition to the 3 patients who had abrupt closure, a further 2 patients had important vascular complications that contributed to their death (Table 3⇓). One woman (DCA 2 in Table 3⇓) was discharged with a large femoral hematoma after atherectomy and subsequently readmitted with pulmonary emboli and died. The second (DCA 4) was found to have a pseudoaneurysm of the femoral artery after discharge from hospital and was treated conservatively until she developed recurrence of angina. She was then admitted for elective repair of the femoral aneurysm before coronary angiography. She did not receive blood products because of her religious convictions, and her postoperative hemoglobin stabilized at 8 g/dL. On the second postoperative day, she developed atrial fibrillation, received multiple antiarrhythmic agents, and subsequently died after an asystolic arrest. She did not have a follow-up angiogram or autopsy.
Other clinical, procedural, or in-hospital outcomes did not appear different, including median ejection fraction [50%, 25th, 75th quartiles of 50, 60, respectively, in those who died compared with 60% (50, 65) in survivors], the presence of multivessel disease, or comorbid conditions.
Follow-up angiography had been performed in 6 of the 14 patients who died including five studies within 4 weeks of death. The completeness of angiographic follow-up was dependent on the length of time between randomization and death. None of the 5 patients who died in the first 2 months had angiographic follow-up, compared with 4 of the 6 who died between 2 and 6 months and 2 of the 3 patients who died between 6 and 12 months. Restenosis, defined as greater than 50% diameter stenosis as assessed by the Core Lab, was demonstrated in 1 patient who was studied after myocardial infarction (DCA 8, Table 3⇓). Diameter stenosis ranged from 7% to 50% in the other 5 patients (Table 3⇓).
Myocardial infarction rates were low during the year after discharge from hospital after either procedure. Between 6 and 12 months’ follow-up, there were two myocardial infarctions in each group. However, due to the significant excess of periprocedural infarction, the cumulative rate of myocardial infarction at 1-year follow-up was higher after atherectomy compared with angioplasty (8.9% versus 4.4%, P=.005, Table 4⇓). There was an excess of both non–Q-wave infarctions (P=.041) and Q-wave infarctions (P=.053, Table 4⇓). This analysis does not include those patients with enzyme elevations detected only by central adjudication. Restenosis (with stenoses of 66%, 80%, and 89%) had been demonstrated in 3 of the 4 patients who suffered myocardial infarctions after 6 months.
Approximately one quarter of both treatment groups underwent repeat percutaneous intervention at the target site. A further 6% of both groups underwent percutaneous intervention at another site in the coronary tree, and 9 percent underwent coronary bypass surgery during the first year (Table 4⇑). There were no significant differences in the rates of percutaneous or surgical intervention in the two groups. Similarly, almost half of each group were hospitalized during the first year (Table 4⇑).
Multivariate Analysis of Combined Clinical End Points
The use of atherectomy was associated with a higher risk of the combined end point of death or infarction (P<.001, Fig 2⇓). No clinical or angiographic characteristics added to this finding. Atherectomy (P=.022) and unstable angina at revascularization (P=.0062) were the only variables associated with the combined end point of death, myocardial infarction, and coronary bypass surgery. There were no significant differences in the combined end points of death, myocardial infarction, coronary bypass surgery, and target lesion percutaneous intervention (Fig 3⇓) or in the combined end point of death, myocardial infarction, coronary bypass surgery, and any percutaneous intervention (Fig 4⇓).
During the first 12 months of the CAVEAT I study, more deaths and myocardial infarctions occurred among those randomized to directional atherectomy than in those assigned to balloon angioplasty. The excess of infarction was predominately related to periprocedural events and was already manifest at the time of hospital discharge. There was no further divergence between the two groups over the subsequent year, with the difference in rate of clinically evident myocardial infarction increasing from 4% at hospital discharge to 4.4% at 6 months and 4.5% at 1 year. In contrast, the excess of deaths in the group randomized to atherectomy was not evident at hospital discharge or statistically significant at 6-month follow-up. At 1 year, the excess of deaths after atherectomy was statistically significant with respect to total deaths, out-of-hospital deaths, or late cardiac deaths.
Predictors of Death
Logistic regression analysis of predictors of death alone was not attempted in this data set because of the small numbers of deaths at 12 months. However, univariate analysis suggests important associations between abrupt closure, periprocedural enzyme elevations, peripheral vascular complications, and subsequent death. Three of the patients who had experienced abrupt closure had important cardiac and vascular complications ultimately proving to be fatal. Even in the era of coronary stenting, and with experienced surgical backup, abrupt closure remains a serious complication of percutaneous revascularization. Peripheral vascular complications directly contributed to the death of other patients, including the patient who died after readmission with pulmonary emboli (DCA 2, see Table 3⇓) and the patient who died after elective repair of a femoral pseudo- aneurysm (DCA 4). One-year mortality was 7.5% in those who had procedural vascular complications compared with 1.1% in those who did not.5 Only one (7%) of the patients who died had a diagnosis of peripheral vascular disease at baseline compared with 6% in the entire cohort. Thus, the association between peripheral vascular complications and subsequent death is not explained by known preexisting vascular disease.
Comorbidity probably contributed to the late deaths of 2 patients after atherectomy. The patient on peritoneal dialysis due to end-stage renal failure (DCA 11) had two subsequent angiograms demonstrating progression of multiple coronary lesions and a myocardial infarction in a non–target artery distribution. He died after a further myocardial infarction. Comorbid disease may also have contributed to the death of DCA 9. This man had chronic atrial fibrillation and hypertension with congestive cardiac failure and diabetes. Follow-up angiography at 6 months demonstrated restenosis of the non–target lesion in the circumflex coronary artery and a severe stenosis distal to the target lesion in the right coronary artery. Both lesions were dilated successfully. However, he suffered an intracerebral hemorrhage 2 days later and died. Possible mechanisms for his intracerebral bleeding event could include cerebral embolism from mural thrombus as well as catheter-induced embolus. No autopsy was performed.
The 75-year-old woman who died of tamponade after perforation of the right ventricle is of interest. She was enrolled in the trial after her first presentation with class III angina without ST-segment changes. After her atherectomy procedure, she developed recurrent right coronary artery spasm, presenting with chest pain, hypotension, heart block, and inferior ST-elevation on her 12-lead ECG. Spasm in the right coronary artery was documented at follow-up angiography, at which time there was a 50% stenosis at the atherectomy site, and the decision was made to electively implant a permanent pacemaker. Implantation of the pacemaker was complicated by a further episode of chest pain and bradycardia then asystole. Unfortunately, her right ventricle was perforated by a temporary pacing wire during cardiopulmonary resuscitation, and she died.
Multivariate Analysis of Combined End Points
In this trial, atherectomy was the only variable significantly associated with the combined clinical end point of myocardial infarction and death at 1 year; none of the baseline clinical characteristics, procedural, or angiographic variables tested add to this finding. The relatively small number of events gives little power to examine additional factors. However, lesion morphology and quantitative angiographic findings also had remarkably little association with the combined clinical end point of death, infarction, bypass surgery, or angioplasty at 1 year, consistent with analyses at 30 days and 6 months of follow-up.
There is thus a dichotomy between angiographic and clinical outcomes after atherectomy or angioplasty. As evidence of this, the acute angiographic result obtained in the patients who subsequently died was not inferior to that obtained in the CAVEAT group as a whole (Tables 2⇑ and 3⇑), nor was there an increased number of dissections or vascular trauma as assessed by angiography or by postmortem histology. Furthermore, several patients died despite a “satisfactory” appearance of the target lesion at follow-up angiography within 4 weeks of death (see Table 3⇑). Restenosis was not the cause of death of the majority of late deaths. The cause of death was related to progression of disease in other coronary arteries, to peripheral vascular complications, to other cardiac events, or to a noncardiac cause, for example, metastatic lung carcinoma. No follow-up angiograms were obtained in the 5 patients who died within 2 months of randomization: 1 patient (DCA 1) had thrombus demonstrated at the site of atherectomy at autopsy. Most of these patients died from procedural complications.
Comparison With Other Trials
Six-month follow-up is available from two other randomized prospective studies comparing atherectomy and angioplasty in the treatment of de novo lesions in the proximal left anterior descending coronary artery, CCAT,2 or in saphenous vein bypass grafts, the CAVEAT II.3 In both trials, atherectomy was associated with a higher procedural success rate and greater acute gains in lumen diameter compared with angioplasty. However, in CCAT, there was no excess of acute complications, including Q-wave or non–Q-wave myocardial infarction, after atherectomy and only two further myocardial infarctions (both in patients assigned to angioplasty) during the first 6 months of follow-up.2 The lower incidence in acute complications after atherectomy in CCAT compared with CAVEAT I may be related to differences in baseline characteristics, with trends to a higher proportion of younger men, a lower incidence of unstable angina or multivessel disease, to the exclusion of patients with ostial lesions or lesions that included large side branches, to the technical differences in atherectomy of the proximal left anterior descending artery compared with more distal sites or with other arteries, to the less frequent use of 7F cutters, or to the use of total CK rather than CKMB subfractions to define myocardial infarction in CCAT. The reason(s) for the lower incidence of events during follow-up is not certain but may be related to the differences in baseline characteristics. The results of 1-year follow-up have not been presented.
In CAVEAT II, 305 patients with saphenous vein bypass graft lesions were enrolled. The patients randomized in CAVEAT II were an average of 6 years older, with a lower mean ejection fraction, and were more likely to have had a previous myocardial infarction or have unstable angina or multivessel disease than the patients in CAVEAT I.3 The incidence of acute non–Q-wave infarction and abrupt closure was much higher in CAVEAT II than in CAVEAT I, presumably related to the higher risk of distal embolization during treatment of diseased vein grafts compared with native coronary vessels as well as the above differences in baseline characteristics. As in CAVEAT I and in contrast to CCAT, the risk of acute complications was greater after atherectomy than after angioplasty in CAVEAT II. However, there were no significant differences in the rates of death or myocardial infarction after 6 months of follow-up. Long-term follow-up of CCAT and CAVEAT II is in progress. Pending these results, there is no evidence that atherectomy offers any advantage over balloon angioplasty in the treatment of de novo lesions in coronary arteries.
One-year mortality was only 0.6% in the balloon angioplasty group in CAVEAT I. This rate is lower than reported rates from most recent registry and randomized trial data sets. Previous angioplasty registry reports suggest mortality rates of 1% to 2.1% in patients with single-vessel disease6 7 8 and 1.8% to 4.6% in patients with multivessel disease6 7 8 : one third of the patients in CAVEAT I had multivessel disease. An earlier analysis of the NHLBI Balloon Registry reported a 1-year mortality rate of 3% in patients undergoing angioplasty for unstable angina due to single-vessel disease9 : two thirds of the patients in CAVEAT I had unstable angina at enrollment. Data are now available from several trials in which patients have been randomized to balloon angioplasty or coronary bypass surgery. One-year mortality rates in those randomized to angioplasty have ranged from 1.2% in the GABI study10 to 2% in the RITA study, in which half the patients had single-vessel disease.11 One-year mortality in the placebo arms of recent restenosis studies was between 1.0% and 3.4%.12 13 14 In contrast, mortality after atherectomy in CAVEAT I was consistent with that in atherectomy registry data sets (2% after 1 year15 and 3% after 6 months16 ). Thus, the statistical difference in late mortality between the treatment arms in CAVEAT I may be a chance finding due to the relative paucity of deaths after angioplasty rather than an excess of deaths after atherectomy. However, it is unlikely that a randomized trial would show a difference in the most important clinical outcome by chance alone as a function of the randomized treatment assignment, when none of the other nonrandomized baseline variables appear important by chance alone.
Patients have been prospectively randomized to atherectomy or angioplasty in three trials: CAVEAT I,1 CAVEAT II,3 and CCAT.2 Directional atherectomy resulted in greater acute gain in lumen diameter than balloon angioplasty in all three trials. However, the mean residual stenosis after atherectomy still exceeded 25% in all three trials and was achieved at the expense of an increase in acute complications. The possibility that greater acute lumen gain after more aggressive atherectomy will reduce restenosis and reduce cumulative end points without further increase in acute complications is being tested in the Balloon versus Optimal Atherectomy Trial (BOAT). Multivariate regression analysis in CAVEAT I suggests that neither acute nor long-term combined clinical end points are predicted by measurements taken from the images of a successful procedure.
Follow-up in the CAVEAT I study was extended to 1 year to enable longer-term prospective comparison of atherectomy and angioplasty. The findings suggest a lack of association between angiographic outcome and both short- and long-term clinical outcomes after either atherectomy or angioplasty. The excess of myocardial infarction after atherectomy remained statistically significant after 1 year, with further divergence of the curves after discharge from hospital. At 1 year there was also a difference in all-cause mortality (2.2% after atherectomy versus 0.6% after angioplasty, P=.035). There is no evidence that this excess of deaths after atherectomy is linked to differences in baseline variables. The combined end point of death and myocardial infarction was also increased after atherectomy but there were no significant differences in the cumulative rates of target lesion repeat intervention or bypass surgery. Long-term careful surveillance of this and other prospective studies that compare percutaneous interventional techniques is indicated; reliance on 6-month end points alone is not sufficient.
Participating Sites and Investigators
Study Chairman: Eric J. Topol, MD; Cleveland Clinic Foundation, Cleveland: Patrick Whitlow, MD (PI), Stephen G. Ellis, MD, Irving Franco, MD, Sue DeLuca (Coordinator); Loyola Medical Center, Chicago: Fred Leya, MD (PI), Sarah Johnson, MD, Eric Grassman, MD, Bruce Lewis, MD, Laura Wrona (Coordinator); St Vincent’s Hospital, Indianapolis: Cass Pinkerton, MD (PI), Thomas Peters, MD, Belinda Ness (Coordinator); Klinikurn Grosshadem Der Universitat, Munich: Berthold Hofling, MD (PI), Tilman Kolbe (Coordinator); Carolinas Medical Center, Charlotte, NC: Charles Simonton, MD (PI), R.M. Bersin, MD, J. Cedarholm, MD, B. Wilson, MD, Susan Lingelbach (Coordinator); Jewish Hospital, Louisville: Ronald Masden, MD (PI), Vicki Miracle (Coordinator); Midwest Heart Research Foundation, Illinois: Louis S. McKeever, MD (PI), Joseph Marek, MD, Peter Kerwin, MD, Elaine L. Enger (Coordinator); Graduate Cardiology, Philadelphia: Ronald S. Gottlieb, MD (PI), Helen Hunter (Coordinator); Maimonides, Brooklyn: Jacob Shani, MD (PI), Nancy Schulhoff (Coordinator); University of Louvain Medical School, Brussels: William Wijns, MD (PI), Jean Renkin, MD, Thierry Baudhuin, MD (Coordinator); Methodist Hospital, Memphis: Frank Martin, MD (PI), Kathy Garrison (Coordinator); Erasmus University, Rotterdam: Patrick Serruys, MD, PhD (PI), P.J. de Feyter, MD, Victor Umans (Coordinator); St Vincent’s Medical Center, Bridgeport, Conn: Edward Kosinski, MD (PI), Maria Capasso (Coordinator); John Hopkins Hospital, Baltimore: Jeffrey Brinker, MD (PI), Mark Midei, MD, Jon R. Resar, MD, Vicki J. Coombs, RN (Coordinator); St Francis Hospital, Beech Groove, Ind: Mark Cohen, MD (PI), Horance Hickman, MD, Paula Cross (Coordinator); St Joseph’s Hospital, Atlanta: William Knopf, MD (PI), Christopher Cates, MD, Jan Shaftel (Coordinator); Washington DC Cardiology Center: Kenneth Kent, MD (Co-PI), Martin Leon, MD (Co-PI), Augusto Pichard, MD, Lowell Satler, MD, Jeff Popma, MD, Pam Shotts (Coordinator); Maine Medical Center, Portland: Mirle Kellett, Jr, MD (PI), Joshua Cutler, MD, Jane Kane (Coordinator); Boston University Medical Center, Boston: Alice Jacobs, MD (PI), David P. Faxon, MD, Mary Mazur (Coordinator); Minneapolis Heart Institute, Minneapolis: Michael Mooney, MD (PI), James Madison, MD, Ellen Sawicki (Coordinator); Mayo Foundation, Rochester: David R. Holmes, Jr, MD (PI), K. Garratt, MD, J. Bresnahen, MD, Jeanette Ramaker (Coordinator); Ochsner Foundation Hospital, New Orleans: Christopher J. White, MD, Steven Ramee, MD, Bryan Leasure (Coordinator); Riverside Methodist Hospitals, Columbus: Anthony Chapekis, MD (Co-PI), N. Howard Kander, MD (Co-PI), Christine Gilliland (Coordinator); Southwest Cardiology Presbyterian Hospital, Albuquerque: Harvey White, MD (PI), Roann Sexson (Coordinator); Georgetown University, Washington: Stephen N. Oesterle, MD (PI), Leni Barry (Coordinator); Rhode Island Hospital, Providence: David O. Williams (PI), Barry Shariff, MD, Mary Grogan (Coordinator); University of Louisville: David J. Talley, MD (PI), ZoeAnn Yussman (Coordinator); Sequoia Hospital, Redwood City: Tomoaki Hinohara, MD (PI), Lissa Braden (Coordinator); Emory University Hospital, Atlanta: Spencer King, MD (PI), Sue Mead (Coordinator); St Vincent Hospital, Portland: Phillip Au, MD (PI), Henry Garrison, MD, Terry Glickman (Coordinator); University of Washington, Seattle: Douglas K. Stewart, MD (PI), Joseph Chambers, MD, Joy Dalquist (Coordinator); Beth Israel Hospital, Boston: Richard Kuntz, MD (PI), Donald Baim, MD, Cynthia Senerchia (Coordinator); Christ Hospital, Cincinnati: Dean Kereiakes, MD (PI), Charles Abbottsmith, MD, David Lausten (Coordinator); Good Samaritan, Phoenix: Marvin Padnick, MD (PI), James Schumacher, MD, Angie Stephens (Coordinator); Medical College of Virginia, Richmond: Michael Cowley, MD (PI), Kim Kelly (Coordinator).
Robert M. Califf, MD (Clinical Director), Lisa G. Berdan, PA-C (Coordinator), Kerry L. Lee, PhD (Statistical Director), Gordon Keeler, MS (Statistician), Tammy Allen, RN (Monitor), Maggie Liu, RN (Monitor), Kathi Lucas, RN (Monitor), Karen Pieper MS (Statistician), John Snapp, MS (Data Manager), Pamela L. Monds (Secretary/Assistant).
Angiography Core Laboratory
Stephen G. Ellis, MD (Medical Director), Darrell Debowey, MS (Technical Director), Timothy D. Crowe, Thomas B. Ivanc, Holly B. Vilsack, Julie A. Merriam, Damian J. Green, Deborah L. Fisher, Sara Brant.
Jeffrey M. Isner, MD (Chairman), Marianne Kearney, BS (Coordinator), Kellie Wills, BS, Carrie Loushin, BS, Scott Bortman, MD.
Data and Safety Monitoring Committee
Hugh C. Smith, MD (Chairman), Robert M. Califf, MD, Alan Guerci, MD, Neal S. Kleiman, MD, Kerry Lee, PhD, Daniel B. Mark, MD, Jimmy Tcheng, MD, W. Douglas Weaver, MD.
Economics and Quality of Life Coordinating Center
Daniel B. Mark, MD, MPH (Principal Investigator), Linda Davidson-Ray (EQOL Coordinator), Lai Choi Lam, MS (Statistician), Charles Moore (Data Manager), Lura Larson (Data Technician), Courtney Smith (Administrative Support).
Eric J. Topol (Chairman), Spencer King, MD, Michael Cowley, MD, David O. Williams, MD, Tomoaki Hinohara, MD, Patrick Serruys, MD, Kenneth Kent, MD, Robert M. Califf, MD.
Val Stosik, MBA, Debra Shyne, Donna Passmore.
This study was supported by grants from Devices for Vascular Interventions and Eli Lilly. Dr Elliott was supported by a White-Parsons Fellowship of the National Heart Foundation of New Zealand.
↵1 The remaining CAVEAT investigators and study sites are listed in the “Appendix.”
- Received August 29, 1994.
- Revision received November 7, 1994.
- Accepted November 26, 1994.
- Copyright © 1995 by American Heart Association
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