| | Multistate population-based outcomes of combined carotid endarterectomy and coronary artery bypass☆☆☆★★★♢♢♢Presented at the Fiftieth Annual Meeting of the American Association for Vascular Surgery, Boston, Mass, Jun 9-12, 2002. Received 18 June 2002; accepted 26 August 2002. Abstract Objectives: The management of combined carotid and coronary disease is controversial, and the outcomes of combined carotid endarterectomy (CEA) and coronary artery bypass grafting (CABG) have not been determined on a community-wide basis. This study was undertaken to evaluate the community-wide outcomes of combined CEA and CABG and to evaluate the risk for adverse events. Methods: A complete medical record review of 10,561 CEA procedures randomly selected from Medicare patients undergoing CEA in 10 states was performed. In this sample, 226 procedures were performed in combination with CABG in the same operative event. Results: Recent ipsilateral stroke or transient ischemic attack was the indication for the CEA in only 12% of patients undergoing CEA/CABG, and 56% were asymptomatic with respect to the carotid lesion. The combined stroke and death rate was 17.7% (25 nonfatal strokes, two fatal strokes, and 13 nonstroke deaths). Eighty percent of the nonfatal strokes were disabling. Proximal aortic arch atherosclerosis and symptomatic carotid stenosis were associated with stroke (P < .05). Female gender, emergent operation, redo CABG, blood pressure on pump, total pump time, presence of left main disease, and number of diseased coronaries were associated with mortality (P < .05). The strokes appeared to be associated with the operative event, but diagnosis was delayed and postevent carotid patency was not documented. Most strokes were not limited to the hemisphere ipsilateral to the CEA. Conclusion: The community-wide outcomes of combined CEA/CABG in the Medicare population are inferior to those reported in many single-institution reviews. Diagnosis of postoperative stroke is often delayed, and most strokes are not limited to the hemisphere ipsilateral to the CEA operative site. (J Vasc Surg 2003;37:32-9.)
The management of concomitant severe atherosclerotic disease in the carotid and coronary circulation is difficult and controversial. Advanced coronary disease is common in patients undergoing evaluation for carotid endarterectomy (CEA). Hertzer et al1 have shown that 28% of these patients have severe correctable coronary disease. In addition, coronary artery disease is the leading cause of both early and late mortality after CEA.2, 3, 4 Similarly, one of the most concerning complications after coronary artery bypass grafting (CABG) is stroke. Although all strokes after CABG cannot be attributed to carotid disease, a significant proportion of patients for CABG are found to have severe carotid disease. It is estimated that up to 22% of patients who undergo evaluation for CABG have >50% stenosis of one or both carotid arteries and that 12% have stenoses >80%.5
Carotid endarterectomy for high-grade carotid lesions is beneficial in reducing stroke,6, 7 and CABG is effective in reducing mortality from symptomatic coronary artery disease.8 However, the management of severe disease in both the coronary and carotid circulations continues to be controversial. Many reports in the literature support combined CEA/CABG, reporting both low morbidity and low mortality rates.9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21 These reports tend to involve multiyear case series from centers of excellence. These centers are to be commended; however, these reports do not necessarily reflect community-wide outcomes of the combined procedure. This report focuses on the outcomes of combined CEA/CABG in a multistate population-based sample of patients. In addition, the anatomic distribution of the strokes and risk factors for stroke and mortality are defined.
Methods  Population and data collection A random sample of 10,561 CEA procedures (International Classification of Diseases, Ninth Revision, Clinical Modification procedure code of 38.12-endarterectomy of vessels of head and neck) performed on patients with discharge dates between June 1, 1995, and May 31, 1996, was identified with the Medicare Provider Analysis and Review part A claims files from Arkansas, Georgia, Illinois, Indiana, Iowa, Kentucky, Michigan, Nebraska, Ohio, and Oklahoma. The sampling procedure used to identify these 10,561 cases is described elsewhere.22 Requests for copies of the entire medical record for the primary admission and any readmissions were sent to the hospitals. Compliance with these requests is mandated by federal statute as part of participation in the Medicare program. A data collection tool was created for medical record abstraction by trained abstractors. Each medical record was comprehensively reviewed to determine patient demographics, the indication for the procedure, perioperative care process, and postoperative outcomes. The records were initially reviewed by trained abstractors at a Centers for Medicare and Medicaid Services Clinical Data Abstraction Center (DynKePRO, York, Pa). Data were abstracted from medical records directly into a computerized data entry system with an online edit check and data definitions to improve accuracy of data collection. In addition, the abstraction process underwent an extensive validation procedure that is described elsewhere.22 The medical records of all patients with strokes were independently reviewed by two clinicians with expertise in CEA or stroke to confirm the stroke and severity. Within this sample of 10,561 patients, 226 patients that had undergone both a CEA and a CABG procedure with the same anesthetic were identified. The data from these 226 patients are analyzed for this report. In addition, the medical records from 184 of these patients were available and were rereviewed by one of the authors (KRB) for further data abstraction. The additional data collected from these 184 charts included information on comorbidities (unstable angina, stable angina), anatomy (distribution of coronary disease, percent carotid stenosis, proximal aortic arch atherosclerosis), operative characteristics (urgent or emergent indication, bypass pump time, lowest temperature and lowest mean blood pressure on pump, number of coronary bypasses), and postoperative complications (anatomic location of stroke, timing of stroke). Definitions Indications for CEA were classified into four mutually exclusive categories. Patients were considered to have stroke as the indication for the procedure only if they had documented ipsilateral hemispheric symptoms that persisted for more than 24 hours within 90 days before the procedure. Similarly, patients were considered to have transient ischemic attack (TIA) as the indication only if transient (<24 hours) ipsilateral hemispheric symptoms occurred within 90 days before the procedure and they did not have a stroke within that same time period. Patients were considered to be asymptomatic if there was no history at any time before the procedure of cerebrovascular symptoms in either the anterior or posterior circulation. All other patients (eg, those with remote ipsilateral symptoms, global or vertebrobasilar symptoms, contralateral hemispheric symptoms) were classified in a nonspecific category. These definitions were used to create distinct stroke, TIA, and asymptomatic indication groups with high reproducibility, given the limitations of retrospective medical record review. Patients were considered to have peripheral vascular disease if a diagnosis of vascular disease in an arterial system other than the coronary and carotid territories was recorded. Stable and unstable angina were considered to be present if they were documented in the preoperative history. Coronary arteries were considered to be diseased if a stenosis ≥70% was documented. The left main coronary artery was considered diseased if ≥50% stenosis was documented. Patients were considered to have proximal aortic arch atherosclerosis if a finding of an atherosclerotic proximal aorta was noted on preoperative transesophogeal echocardiogram or in the operative report. The operation was said to be urgent or emergent if specifically stated such by the operating surgeon or if the operation occurred within 24 hours of cardiac catheterization for unstable angina. Postreconstruction imaging included angiogram, duplex scan, or continuous wave Doppler interrogation of the CEA operative site. For the purpose of outcome classification, a postoperative stroke was considered to have occurred if any new or worsening central nervous system deficit developed during the postoperative period and persisted for more than 24 hours. Postoperative strokes were classified as major or minor by looking at a point in time 5 days after the stroke or at hospital discharge, whichever occurred sooner. If the patient had a new persistent deficit that resulted in a need for assistance with ambulation or eating or had significant difficulty with speaking, the patient was considered to have had a major stroke. Patients without disability at 5 days after the event were considered to have had a minor stroke. Deaths were considered stroke related if the death was associated with a major stroke. If there was no evidence of major stroke associated with the death, the death was classified as non-stroke-related. The timing of the stroke was defined by the earliest documentation of a new postoperative deficit noted in the physician, nursing, or ancillary care notes. Data analysis Simple descriptive statistics were used to initially examine the data, including means and standard deviations. The relationships between comorbid, anatomic, or technical variables and the outcome variables of stroke, mortality, and combined stroke and mortality were examined with χ2 tests and t tests where appropriate. For variables that were significantly associated with stroke or death in the univariate analysis, logistic regression controlling for CEA indication was undertaken. An adjusted odds ratio was obtained and compared with the unadjusted odds ratio obtained without controlling for CEA indication. Because of the small number of outcomes, more extensive multivariate logistic regression was not used. Results Sixty-three percent of the patients were male, and the average age of the population was 72.2 years. Sixty-six percent of the patients had a history of tobacco use, and 76% had hypertension. Diabetes was present in 33%, and peripheral vascular disease (other than carotid disease) was present in 34%. A history of atrial fibrillation was present in 11%. Unstable angina was the presenting cardiac symptom in 65%, and stable angina was the presenting symptom in an additional 16%. Fig 1 shows the indications for CEA.
Asymptomatic carotid disease was the indication in 126 of the patients (56%), and only 12% had a clear ipsilateral TIA or stroke as the indication for CEA. The degree of stenosis in both carotid arteries is seen in Fig 2.
These data come from the 184 charts that were reabstracted. Eighty-seven percent of these patients had an ipsilateral stenosis of ≥80%, and 20% of patients had bilateral stenoses ≥80%. Fig 3, which is also derived from the reabstracted data, shows that most of these patients did not have severe or symptomatic disease as the indication for CEA.
Only 9% of these patients underwent operation for a recent TIA or stroke, and only an additional 22% had bilateral severe disease or a contralateral occlusion. The overall combined stroke and mortality rate was 17.7%. This included 25 nonfatal strokes, two fatal strokes, and 13 nonstroke deaths, for an overall stroke rate of 12% and a mortality rate of 6.6%. Eighty percent of the nonfatal strokes were disabling, meaning that the patient had a persistent new deficit that significantly interfered with walking, talking, or eating 5 days after surgery or at discharge, whichever came first. The factors assessed for association with adverse outcome are seen in Table I.
| | |  | | | Stroke | Mortality | Combined stroke/mortality | |
|---|
| | No. (%) | Rate (%) | RR (P value) | Rate (%) | RR (P value) | Rate (%) | RR (P value) | |
|---|
| Comorbidities | | | | | | | | |
|  Female gender | 83 (36.7) | 15.7 | 1.59 (.19) | 12.0 | 3.45 (.01) | 25.3 | 1.90 (.02) | |
| Smoking history | 149 (65.9) | 11.4 | 0.88 (.73) | 6.7 | 1.03 (.95) | 16.8 | 0.86 (.61) | |
| Diabetes | 75 (33.2) | 13.3 | 1.18 (.65) | 5.3 | 0.73 (.58) | 16.0 | 0.86 (.64) | |
| History of MI | 126 (55.8) | 11.1 | 0.85 (.66) | 9.5 | 3.17 (.05) | 19.8 | 1.32 (.34) | |
| History of HTN | 172 (76.1) | 14.0 | 2.51 (.10) | 6.4 | 0.86 (.79) | 19.2 | 1.48 (.30) | |
| History of AFIB | 23 (10.2) | 13.0 | 1.10 (.86) | 8.7 | 1.35 (.68) | 21.7 | 1.26 (.59) | |
| History of CHF | 47 (20.8) | 12.8 | 1.09 (.85) | 6.4 | 0.95 (.94) | 19.1 | 1.11 (.77) | |
| Unstable angina* | 120 (65.2) | 10.8 | 1.15 (.76) | 6.7 | 4.27 (.13) | 16.7 | 1.52 (.30) | |
| Stable angina* | 30 (16.3) | 6.7 | 0.60 (.47) | 3.3 | 0.64 (.66) | 10.0 | 0.64 (.43) | |
| Carotid indication | | | | | | | | |
| Asymptomatic (reference) | 126 (55.8) | 6.3 | 1.00 | 8.7 | 1.00 | 13.5 | 1.00 | |
| Nonspecific symptoms | 72 (31.9) | 15.3 | 2.43 (.04) | 2.8 | 0.32 (.10) | 18.1 | 1.34 (.40) | |
| Ipsilateral TIA | 17 (7.5) | 23.5 | 3.73 (.02) | 11.8 | 1.35 (.68) | 35.3 | 2.62 (.02) | |
| Ipsilateral stroke | 11 (4.8) | 36.4 | 5.78 (.001) | 0 | - | 36.4 | 2.70 (.04) | |
| Carotid stenosis (≥80%) | | | | | | | | |
| Ipsilateral stenosis† | 151 (86.8) | 9.3 | 0.53 (.23) | 4.6 | 0.53 (.41) | 13.2 | 0.51 (.11) | |
| Contralateral stenosis‡ | 39 (25.5) | 15.4 | 1.35 (.52) | 2.6 | 0.42 (.39) | 17.9 | 1.08 (.85) | |
| Contralateral occlusion‡ | 20 (13.1) | 25.0 | 2.38 (.07) | 0 | - | 25.0 | 1.58 (.31) | |
| Bilateral stenosis§ | 31 (20.7) | 12.9 | 1.10 (.86) | 3.2 | 0.55 (.56) | 16.1 | 0.96 (.93) | |
| CEA technique | | | | | | | | |
| Patch | 77 (34.1) | 7.8 | 0.55 (.17) | 5.2 | 0.70 (.53) | 11.7 | 0.56 (.09) | |
| Shunt | 118 (52.2) | 12.7 | 1.14 (.71) | 6.8 | 1.05 (.93) | 17.8 | 1.01 (.97) | |
| Monitor | 47 (20.8) | 17.0 | 1.60 (.23) | 2.1 | 0.27 (.16) | 19.1 | 1.11 (.77) | |
| No monitor/no shunt | 74 (32.7) | 9.5 | .72 (.42) | 8.1 | 1.37 (.54) | 17.6 | 0.99 (.97) | |
| Proximal aortic atherosclerosis* | 31 (16.8) | 29.0 | 4.44 (.0002) | 9.7 | 2.47 (.18) | 35.5 | 3.39 (.0003) | |
| Left main disease* | 65 (35.3) | 10.8 | 1.07 (.88) | 9.2 | 3.66 (.04) | 18.5 | 1.46 (.28) | |
| Redo operations | | | | | | | | |
| Carotid | 5 (2.2) | 20.0 | 1.70 (.57) | 0 | - | 20.0 | 1.13 (.89) | |
| CABG | 15 (6.6) | 6.7 | 0.54 (.51) | 26.7 | 5.12 (.001) | 33.3 | 2.01 (.10) | |
| Emergent operation* | 15 (8.2) | 20.0 | 2.11 (.20) | 20.0 | 5.63 (.005) | 33.3 | 2.56 (.03) | |
| Postreconstruction imaging | 49 (21.7) | 10.2 | 0.82 (.67) | 2.0 | 0.26 (.14) | 12.2 | 0.64 (.26) | |
| *N = 184. These data come from reabstraction. There were only 184 charts available for review, including 19 strokes and nine deaths. †N = 174. ‡N = 153. §N = 150. These data come from reabstraction, and there were some missing data in records. | | | | |
Female gender, presence of left main coronary artery disease, history of myocardial infarction, redo CABG, and emergent operation were significantly associated with mortality. CEA indication was significantly associated with stroke. Patients with nonspecific symptoms had a relative risk of 2.4 for stroke after the combined procedure compared with asymptomatic patients. Patients with ipsilateral TIA as an indication had a relative risk of 3.7, and patients with ipsilateral stroke as an indication had a relative risk of 5.7 compared with asymptomatic patients. In addition, the presence of proximal aortic arch atherosclerosis conveyed a 4.4 times increased risk of stroke. The severity of ipsilateral or contralateral stenosis (≥80%) was not significantly associated with stroke. Bilateral severe stenosis (≥80%) also was not significantly associated with a poor outcome. Occlusion contralateral to the side of CEA trended toward a significant association with stroke ( P = .07). The use of a patch, a shunt, or an intraoperative assessment of need for a shunt was not shown to be protective against stroke or death in our series, although there was a trend toward a benefit from patching with the combined stroke/mortality outcome (relative risk, .56; P = .09). CABG operative factors are seen in Table II.
| | | | | Stroke (n = 19) | No stroke (n = 165) | P value | Death (n = 9) | No death (n = 175) | P value | |
|---|
| No. of diseased coronaries | 3.39 | 2.87 | .056 | 3.67 | 2.89 | .035 | |
| No. of bypasses | 3.79 | 3.42 | .15 | 3.33 | 3.46 | .72 | |
| Pump characteristics | | | | | | | |
| Total time on pump | 116.8 | 103.2 | .17 | 130.6 | 103.3 | .053 | |
| Crossclamp time | 71.3 | 62.5 | .22 | 68.6 | 63.2 | .59 | |
| Lowest temperature | 28.93 | 29.65 | .40 | 30.11 | 29.55 | .66 | |
| Lowest blood pressure | 53.83 | 54.99 | .65 | 48.0 | 55.20 | .053 | |
| | | | | |
The number of diseased coronary arteries was higher in those patients who died and trended towards a significant association with stroke. None of the other operative factors were significant, although the total time on pump and the lowest blood pressure on pump trended towards significance, with a P value of .053 in both cases. Table III shows the results of the logistic regression for those variables that were associated or possibly associated with stroke in the univariate analysis.
| | | | Variable | OR stroke | P value | Adjusted OR stroke | P value | |
|---|
| Carotid stenosis (≥80%) | | | | | |
| Ipsilat stenosis | 0.49 | .24 | 0.55 | .35 | |
| Contralateral stenosis | 1.41 | .52 | 1.08 | .89 | |
| Bilateral stenosis | 1.15 | .81 | 0.81 | .74 | |
| Contralateral occlusion | 2.83 | .07 | 2.48 | .13 | |
| Carotid techniques | | | | | |
| Patch | 0.52 | .17 | 0.48 | .13 | |
| Shunt | 1.17 | .37 | 1.17 | .70 | |
| Monitor | 1.73 | .23 | 1.7 | .26 | |
| No monitor/no shunt | 0.69 | .42 | 0.69 | .43 | |
| Redo CEA | 1.88 | .58 | 1.75 | .63 | |
| Proximal aortic atherosclerosis | 5.85 | .001 | 5.35 | .001 | |
| Postreconstruction imaging | 0.80 | .67 | 0.77 | .62 | |
| | | | | |
None of the odds ratios changed significantly after adjustment for CEA indication, but the P value for contralateral occlusion becomes somewhat larger, which removed the trend toward significance. Indepth analysis of the 19 strokes that had charts available for review revealed that four were limited to the side ipsilateral to the CEA, three were limited to the side contralateral to the CEA, seven were limited to the posterior circulation, and five were multifocal. These results are seen in Fig 4.
The timing of the first documentation of a neurologic deficit was generally delayed. None of the strokes were noted within the first 6 hours after surgery. Six strokes were noted between 6 and 24 hours, and six strokes were noted between 25 and 48 hours after surgery. Seven strokes were not noted until after the second postoperative day. There did not appear to be any association between the anatomy of the stroke (ipsilateral, contralateral, posterior, multifocal) and timing of documentation of the stroke. In addition, there did not appear to be any association between the severity of the stroke and the timing of documentation of the stroke. In only one case was carotid imaging undertaken after the deficit was discovered, and the repair was patent. Discussion Much controversy has been seen with regard to the combined CEA/CABG procedure. Proponents of the combined approach quote low stroke rates (ranging from 0 to 5.8%) and acceptable mortality rates (ranging from 0 to 8.9%),9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21 although much higher stroke and mortality rates, reaching 25% and 13%, respectively,23 have been reported. The stroke and mortality rates in the largest series tend to be lower, and these series are often from single institutions. One reason this study was undertaken was to determine the outcome of combined CEA/CABG in a population-based sample of patients. Our cases were drawn from a large, randomly selected, representative sample of Medicare patients from 10 states, which makes this sample more generalizable to the greater population of all patients undergoing combined CEA than a single institution series would be. In this study, the stroke and mortality rates were 12% and 6.6%, respectively, with a combined stroke and mortality rate of 17.7%. For comparison, the combined stroke and mortality rate for those patients in the larger data set who underwent CEA alone was 5.2%, as previously reported.22 Thus, the stroke and mortality rates associated with the combined procedure are much higher than with CEA alone. These rates are also high when compared with combined CEA/CABG studies in the literature with comparable numbers of patients.9, 10, 12, 13, 16, 17, 20, 24 Our stroke and mortality rates are higher even than Borger et al25 found in a metaanalysis of 844 patients reported in the literature. The high stroke and mortality rates in this study are even more remarkable given the fact that most patients were asymptomatic and had unilateral disease. These findings suggest that surgeons contemplating a combined procedure should determine their own success with the procedure rather than basing risk/benefit analyses on the reported literature. Another goal of this study was to determine those factors that were associated with stroke or mortality. Proximal aortic arch atherosclerosis was found to be significantly associated with stroke even after controlling for CEA indication, which reflects the risk of atheroembolization when clamping a diseased proximal aorta. This risk factor has been previously described, both for isolated CABG and the combined procedure.26, 27, 28, 29 When the indication for the CEA was symptomatic carotid disease, the patient also had an increased risk of stroke. This risk increased with the severity of the previous symptoms, such that previous stroke conferred a higher risk than did TIA and TIA conferred a higher risk than did nonspecific symptomotology. This relationship has also been described previously, both for isolated CEA and for the combined procedure.18, 21, 30, 31 Interestingly, severity of carotid disease and contralateral occlusion were not found to be associated with stroke risk. Our data set had a small number of outcomes, and perhaps with more data, a significant finding would have emerged. In addition, the use of a patch was not found to be protective, although there was a trend towards significance. Only 77 of the 226 patients underwent patching, and it is again possible that with more data a significant finding would have emerged. The factors associated with 30-day mortality in this study included reoperative CABG, urgent or emergent operation, left main disease, number of diseased coronaries, history of myocardial infarction, and female gender. Nonelective surgery and reoperative surgery have long been known to be risk factors for increased mortality, and the findings here are not surprising. The nonelective condition is generally unstable with a poor prognosis. In our study, the nonelective status was always from cardiac instability or the need for urgent cardiac revascularization. Given the high risk associated with emergent CABG, it is advisable to defer CEA for asymptomatic disease to a later operation in this patient population. Left main coronary artery disease, number of diseased vessels, and history of myocardial infarction are all well-described risk factors for mortality after both isolated CABG and the combined procedure.21, 32 It is not surprising that those patients with a history of myocardial infarction, severe left main disease, or diffuse coronary disease are at a higher risk for mortality. Female gender has been found to be a significant risk factor for mortality after CABG and may reflect smaller vessel size or advanced disease at the time of surgery.33, 34 The third reason that this study was undertaken was to determine the cause of strokes that occur after CEA/CABG. We found that most strokes were not confined to the side ipsilateral to the CEA and that five of 19 were multifocal. Although the strokes appeared to have occurred during surgery, the diagnosis was delayed because of persistent intubation and sedation after the CABG procedure. This finding, combined with the strong association of proximal aortic arch atherosclerosis with postoperative stroke, suggests that most strokes in this series were not directly related to the CEA. It appears then that the prevention of noncarotid related strokes with the use of epiaortic imaging before clamping, avoidance of aortic clamping or cannulation, and the use of the off-pump technique may be more important than concomitant CEA in limiting adverse neurologic events in this patient population. Another interesting finding was that most patients in this series were asymptomatic relative to their carotid disease. In fact, only 31% of patients in this series had either recent symptoms or severe disease as the indication for the endarterectomy. In addition, most infarcts were not limited to the ipsilateral carotid territory and may have been unrelated to the CEA. It is possible then that many of these patients could have undergone a staged procedure. There are limitations to this study. The study is a retrospective chart review, and therefore, our data collection depended on what was recorded legibly in the medical record. This could possibly have led to an underestimation of the stroke rate if strokes occurred but were not adequately recorded in the medical record. It is unlikely that major or disabling strokes would fail to be documented by either physicians or nurses. Second, the actual number of outcomes in this study was not sufficient to use multivariate logistic regression to determine risk factors for stroke and mortality after controlling for all baseline factors. This leaves the possibility that some of our significant findings are from confounding effects. A much larger study would have to be undertaken to eliminate this limitation. We did use limited multivariate regression to control for CEA indication and found that our results did not change significantly, indicating that there was not a large confounding effect of carotid indication on our results. Conclusion The overall stroke rate of 12% and the mortality rate of 6.6% in this study are higher than most case series with similar numbers of patients. These results may more accurately reflect the outcomes that can be expected in the usual practice situation as opposed to most results reported in the literature from single institution reviews. The low percentage of patients with clear carotid territory symptoms as an indication for CEA in this series suggests that a combined procedure may have been avoided in many of the patients. Most of the strokes were not limited to the ipsilateral carotid territory and therefore may have been unrelated to the CEA. The association of stroke events with aortic arch atherosclerosis may suggest embolism related to the CABG as an important cause, and the implementation of techniques aimed at preventing such embolization may be more important than combined CEA/CABG in limiting the adverse neurologic event rate associated with CABG in patients with both carotid and coronary disease.
Discussion Dr John J. Ricotta (Stony Brook, NY). I think there are couple of points to be made. First, you found 226 patients in 10 states. How many of these patients were located in centers where one would have expected a reasonable annual experience with combined coronary and carotid disease? I think this is something that we tend to see 15 or 20 or even 30 times a year. And like most other procedures, the more often it is done, the better the results are going to be. I think the other comment is, there is another way to look at your data. We have looked at this in a different way, looking at isolated CABG patients versus combined CABG-carotid patients. And all of the risk, both the mortality risk and the stroke risk, can be completely predicted based on the preoperative characteristics of the patient that is coming for CABG. So, there are several models out there that show increased stroke risk with CABG alone using most of these risk factors. So, how do you know whether these patients would have been better staged or whether they just have an inherent stroke risk because of their atherosclerotic burden and whether you do the carotid or whether you do not do the carotid is not going to make a difference? And finally, I am glad you presented this because I have been trying to get people to do a randomized study for about 5 years and maybe somebody will decide that they want to help me out and answer this question. Dr Kellie R. Brown. I cannot tell you how many of these patients were done at a center that does a lot of these, nor can I tell you the volume of these done at the centers in which these patients were done. I do not have those data. But I do agree, and the slide showing the literature results supports this, that high volume centers have better outcomes. And I think that has been shown with virtually almost any surgical procedure. So, that is not really surprising. I also agree that there is a need for a randomized trial in order to answer the question as to whether or not patients should be staged or which patients can be safely staged. Our statement in this study that many of these patients could possibly have been staged was based on the fact that the majority were asymptomatic and the majority did not have either bilateral disease or recent symptoms as an indication for the endarterectomy. The only way, really, to answer which patients should be staged and which patients should be done combined is to have a randomized trial. Dr Matthew J. Dougherty (Philadelphia, Pa). Did you have any information on who was performing the carotid procedure? Was this performed by the cardiac surgeon in a majority of cases? And did you have any information about operative time? I would echo Dr Ricotta's comments, since only a minority of these strokes seem to be ipsilateral, it may just be that these patients have diffuse atherosclerosis and are going to have strokes from the cardiac procedure alone. Dr Brown. I agree. No, I do not have the information on who did the procedures in terms of what their training was or what their specialty was. I did not have operative time. I did have time on pump, and time on pump was not significantly associated with stroke or death. Dr James Watson (Seattle, Wash). I had a recent opportunity to do a combined carotid-coronary bypass and was able to actually complete the carotid using a regional anesthesia followed by a general anesthetic for the coronary bypass, and it worked out quite well. I just wonder whether any of your patients had a combined regional-general anesthetic and wonder about your perspective about the advisability of doing it that way? Dr Brown. I read through every one of those operative notes, and I do not recall that any of the patients done in that manner were. I have never done that. The only time that I have done this procedure, it has all been done under general anesthetic, and I think that is a perfectly acceptable way to do it. Dr R. Clement Darling III (Albany, NY). That was an excellent discussion on a very difficult database you presented. The question I have is, do you know what the mortality and the stroke rate is for patients undergoing just the CABG in this group? Are you just identifying a marker for bad outcomes, or are you identifying a problem with the surgery independent of the combined procedure? Since almost a quarter of the patients had ipsilateral strokes, maybe the combined procedure is not the major contributing factor for the bad outcomes. Dr Brown. No, I do not have the information on the CABG patients that were done, the isolated CABG patients that were done, in the same states. Dr Peter R. F. Bell (Leicester, United Kingdom). We, in fact, wrote a paper in the European journal just a few weeks ago that confirms what you say, the risk of getting a stroke and death from not doing a combined procedure is, in fact, very low. And there is no indication at all, looking at the literature, for doing this operation in these patients. And I think your view confirms that. Just two questions. What do you mean by aortic atherosclerosis? In my experience, they have all got it. And secondly, it is not surprising that the strokes were not reported for 6 hours because most of the patients are on a ventilator at that time. Could you confirm that? Dr Brown. Yes, absolutely. My definition for aortic atherosclerosis was it had to be either documented with a preoperative echo or it had to be documented in the surgeon's operative note, that there was aortic atherosclerosis present. In the terms of the delay in diagnosis, it is true, most of these patients are sedated, on a ventilator after surgery, and that is primarily the reason why the strokes are not identified immediately after surgery. Which only speaks to the point that the timeframe in which they are not discovered is the same timeframe in which you would wish to intervene if you thought this was a problem with the carotid. So, postreconstruction imaging may help to identify those patients who might benefit from an intervention within that perioperative period. References 1.
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Circulation. 2001;103:2133–2137. a University of Chicago Robert Wood Johnson Clinical Scholars Progam Iowa City, Iowa b Division of Vascular Surgery, University of Iowa Iowa City, Iowa c Iowa Foundation for Medical Care. Iowa City, Iowa ☆ Supported by the Iowa Foundation for Medical Care and the Robert Wood Johnson Clinical Scholars Program. ☆☆ Analyses on which this publication is based were performed under Contract Number 500-99-IA03, entitled “Utilization and Quality Control Peer Review Organization for the State of Iowa,” sponsored by the Centers for Medicare and Medicaid Services, Department of Health and Human Services. Content of this publication does not necessarily reflect the views or policies of the Department of Health and Human Services, nor does mention of trade names, commercial products, or organization imply endorsement by the US Government. ★ The author assumes full responsibility for the accuracy and completeness of the ideas presented. This article is a direct result of the Health Care Quality Improvement Program initiated by the Centers for Medicare and Medicaid Services, which has encouraged identification of quality improvement projects derived from analysis of patterns of care and therefore required no special funding on the part of this contractor. Ideas and contributions to the author concerning experience in engaging with issues presented are welcomed. ★★ Competition of interest: nil. ♢ Reprint requests: Kellie R. Brown, MD, 9200 W. Wisconsin Ave, Milwaukee, WI 53226 (e-mail: krbrown@mcw.edu). ♢♢ 0741-5214/2003/$30.00 + 0 PII: S0741-5214(02)75201-4 doi:10.1067/mva.2003.60 © 2003 Society for Vascular Surgery and The American Association for Vascular Surgery. Published by Elsevier Inc. All rights reserved. | |
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