[Skip to Content]
Access to paid content on this site is currently suspended due to excessive activity being detected from your IP address 54.159.129.152. Please contact the publisher to request reinstatement.
Sign In
Individual Sign In
Create an Account
Institutional Sign In
OpenAthens Shibboleth
[Skip to Content Landing]
Download PDF
Table 1. 
Arterial Distribution of Stroke on Brain Imaging
Arterial Distribution of Stroke on Brain Imaging
Table 2. 
Distribution of Postoperative Stroke in Patients With Significant Carotid Stenosis
Distribution of Postoperative Stroke in Patients With Significant Carotid Stenosis
Table 3. 
Significant Carotid Stenosis and Stroke in 3942 Patients Undergoing Preoperative Carotid Evaluation
Significant Carotid Stenosis and Stroke in 3942 Patients Undergoing Preoperative Carotid Evaluation
Table 4. 
Incidence of Postoperative Stroke by Categories of Carotid Intervention
Incidence of Postoperative Stroke by Categories of Carotid Intervention
Table 5. 
Risk Factor Comparison in Patients With Severe Carotid Stenosis Undergoing Combined Carotid and Cardiac vs Cardiac Operations Alonea
Risk Factor Comparison in Patients With Severe Carotid Stenosis Undergoing Combined Carotid and Cardiac vs Cardiac Operations Alonea
1.
Libman  RBWirkowski  ENeystat  MBarr  WGelb  SGraver  M Stroke associated with cardiac surgery: determinants, timing, and stroke subtypes. Arch Neurol 1997;54 (1) 83- 87
PubMedArticle
2.
Likosky  DSMarrin  CACaplan  LR  et al. Northern New England Cardiovascular Disease Study Group, Determination of etiologic mechanisms of strokes secondary to coronary artery bypass graft surgery. Stroke 2003;34 (12) 2830- 2834
PubMedArticle
3.
Selim  M Perioperative stroke. N Engl J Med 2007;356 (7) 706- 713
PubMedArticle
4.
Chaturvedi  SBruno  AFeasby  T  et al. Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology, Carotid endarterectomy–an evidence-based review: report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Neurology 2005;65 (6) 794- 801
PubMedArticle
5.
Naylor  ARMehta  ZRothwell  PMBell  PR Carotid artery disease and stroke during coronary artery bypass: a critical review of the literature. Eur J Vasc Endovasc Surg 2002;23 (4) 283- 294
PubMedArticle
6.
Dubinsky  RMLai  SM Mortality from combined carotid endarterectomy and coronary artery bypass surgery in the US. Neurology 2007;68 (3) 195- 197
PubMedArticle
7.
Hill  MDShrive  FMKennedy  JFeasby  TEGhali  WA Simultaneous carotid endarterectomy and coronary artery bypass surgery in Canada. Neurology 2005;64 (8) 1435- 1437
PubMedArticle
8.
Castaldo  JENicholas  GGee  WReed  J Duplex ultrasound and ocular pneumoplethysmography concordance in detecting carotid stenosis. Arch Neurol 1989;46 (5) 518- 522
PubMedArticle
9.
Adams  HP  JrBendixen  BHKappelle  LJ  et al.  Classification of subtype of acute ischemic stroke: definitions for use in a multicenter clinical trial; TOAST–Trial of Org 10172 in Acute Stroke Treatment. Stroke 1993;24 (1) 35- 41
PubMedArticle
10.
North American Symptomatic Carotid Endarterectomy Trial Collaborators, Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis. N Engl J Med 1991;325 (7) 445- 453
PubMedArticle
11.
Brener  BJBrief  DKAlpert  J  et al.  A four-year experience with preoperative noninvasive carotid evaluation of two thousand twenty-six patients undergoing cardiac surgery. J Vasc Surg 1984;1 (2) 326- 338
PubMedArticle
12.
Executive Committee for the Asymptomatic Carotid Atherosclerosis Study, Endarterectomy for asymptomatic carotid artery stenosis. JAMA 1995;273 (18) 1421- 1428
PubMedArticle
13.
Jones  ELCraver  JMMichalik  RA  et al.  Combined carotid and coronary operations: when are they necessary? J Thorac Cardiovasc Surg 1984;87 (1) 7- 16
PubMed
14.
Gardner  TJHorneffer  PJManolio  TA  et al.  Stroke following coronary artery bypass grafting: a 10-year study. Ann Thorac Surg 1985;40 (6) 574- 581
PubMedArticle
15.
Brener  BJBrief  DKAlpert  JGoldenkranz  RJParsonnet  V The risk of stroke in patients with asymptomatic carotid stenosis undergoing cardiac surgery: a follow-up study. J Vasc Surg 1987;5 (2) 269- 279
PubMedArticle
16.
Blossom  GBFietsam  R  JrBassett  JSGlover  JLBendick  PJ Characteristics of cerebrovascular accidents after coronary artery bypass grafting. Am Surg 1992;58 (9) 584- 589
PubMed
17.
Frye  RLKronmal  RSchaff  HVMyers  WOGersh  BJ Stroke in coronary artery bypass graft surgery: an analysis of the CASS experience; the participants in the Coronary Artery Surgery Study. Int J Cardiol 1992;36 (2) 213- 221
PubMedArticle
18.
Ricotta  JJFaggioli  GLCastilone  AHassett  JM Risk factors for stroke after cardiac surgery: Buffalo Cardiac Cerebral Study Group. J Vasc Surg 1995;21 (2) 359- 364
PubMedArticle
19.
D’Agostino  RSSvensson  LGNeumann  DJBalkhy  HHWilliamson  WAShahian  DM Screening carotid ultrasonography and risk factors for stroke in coronary artery surgery patients. Ann Thorac Surg 1996;62 (6) 1714- 1723
PubMedArticle
20.
Roach  GWKanchuger  MMangano  CM  et al. Multicenter Study of Perioperative Ischemia Research Group and the Ischemia Research and Education Foundation Investigators, Adverse cerebral outcomes after coronary bypass surgery. N Engl J Med 1996;335 (25) 1857- 1863
PubMedArticle
21.
Dashe  JFPessin  MSMurphy  REPayne  DD Carotid occlusive disease and stroke risk in coronary artery bypass graft surgery. Neurology 1997;49 (3) 678- 686
PubMedArticle
22.
Gott  JPThourani  VHWright  CE  et al.  Risk neutralization in cardiac operations: detection and treatment of associated carotid disease. Ann Thorac Surg 1999;68 (3) 850- 857
PubMedArticle
23.
Likosky  DSLeavitt  BJMarrin  CA  et al. Northern New England Cardiovascular Disease Study Group, Intra- and postoperative predictors of stroke after coronary artery bypass grafting. Ann Thorac Surg 2003;76 (2) 428- 435
PubMedArticle
24.
Ricotta  JJWall  LPBlackstone  E The influence of concurrent carotid endarterectomy on coronary bypass: a case-controlled study. J Vasc Surg 2005;41 (3) 397- 402
PubMedArticle
25.
Barbut  DGrassineau  DLis  EHeier  LHartman  GSIsom  OW Posterior distribution of infarcts in strokes related to cardiac operations. Ann Thorac Surg 1998;65 (6) 1656- 1659
PubMedArticle
26.
Katz  ESTunick  PARusinek  HRibakove  GSpencer  FCKronzon  I Protruding aortic atheromas predict stroke in elderly patients undergoing cardiopulmonary bypass: experience with intraoperative transesophageal echocardiography. J Am Coll Cardiol 1992;20 (1) 70- 77
PubMedArticle
27.
Barbut  DHinton  RBSzatrowski  TP  et al.  Cerebral emboli detected during bypass surgery are associated with clamp removal. Stroke 1994;25 (12) 2398- 2402
PubMedArticle
28.
van der Linden  JCasimir-Ahn  H When do cerebral emboli appear during open heart operations? a transcranial Doppler study. Ann Thorac Surg 1991;51 (2) 237- 241
PubMedArticle
29.
Páramo  JARifon  JLlorens  RCasares  JPaloma  MJRocha  E Intra- and postoperative fibrinolysis in patients undergoing cardiopulmonary bypass surgery. Haemostasis 1991;21 (1) 58- 64
PubMed
30.
Filsoufi  FRahmanian  PBCastillo  JGBronster  DAdams  DH Incidence, imaging analysis, and early and late outcomes of stroke after cardiac valve operation. Am J Cardiol 2008;101 (10) 1472- 1478
PubMedArticle
31.
Borger  MAFremes  SEWeisel  RD  et al.  Coronary bypass and carotid endarterectomy: does a combined approach increase risk? a metaanalysis. Ann Thorac Surg 1999;68 (1) 14- 21
PubMedArticle
Original Contribution
September 2009

Strokes After Cardiac Surgery and Relationship to Carotid Stenosis

Author Affiliations

Author Affiliations: Division of Neurology, Department of Medicine (Drs Y. Li, Isayev, and Castaldo and Mss Walicki, Mathiesen, and Jenny), and Departments of Radiology (Dr Q. Li) and Health Studies (Dr Reed), Lehigh Valley Hospital and Health Network, Allentown, Pennsylvania.

Arch Neurol. 2009;66(9):1091-1096. doi:10.1001/archneurol.2009.114
Abstract

Objective  To critically examine the role of significant carotid stenosis in the pathogenesis of postoperative stroke following cardiac operations.

Design  Retrospective cohort study.

Setting  Single tertiary care hospital.

Participants  A total of 4335 patients undergoing coronary artery bypass grafting, aortic valve replacement, or both.

Main Outcome Measures  Incidence, subtype, and arterial distribution of stroke.

Results  Clinically definite stroke was detected in 1.8% of patients undergoing cardiac operations during the same admission. Only 5.3% of these strokes were of the large-vessel type, and most strokes (76.3%) occurred without significant carotid stenosis. In 60.0% of cases, strokes identified via computed tomographic head scans were not confined to a single carotid artery territory. According to clinical data, in 94.7% of patients, stroke occurred without direct correlation to significant carotid stenosis. Undergoing combined carotid and cardiac operations increases the risk of postoperative stroke compared with patients with a similar degree of carotid stenosis but who underwent cardiac surgery alone (15.1% vs 0%; P = .004).

Conclusions  There is no direct causal relationship between significant carotid stenosis and postoperative stroke in patients undergoing cardiac operations. Combining carotid and cardiac procedures is neither necessary nor effective in reducing postoperative stroke in patients with asymptomatic carotid stenosis.

Cerebrovascular complications following cardiac surgical procedures are a major source of morbidity and mortality. The etiology for postoperative stroke is multifactorial and may include carotid artery stenosis, hypotension, cardiac arrhythmia, aortic atherosclerosis, and transient hypercoagulable state.13 The presence of multiple coexisting causes makes studying the mechanism of stroke challenging.

Significant carotid stenosis has been recognized as a positive predictor of postoperative stroke in patients receiving cardiac surgical procedures.2 However, studies directly addressing the role of severe carotid stenosis are lacking. To date, no randomized clinical trials have addressed this important topic,4 and few retrospective trials have investigated the lateralization and territorial distribution of postoperative stroke to determine whether there is a correlation between stroke distribution and carotid stenosis. Therefore, the evidence for carotid stenosis as a cause for postoperative stroke is mostly indirect.5

Despite this lack of evidence, combined carotid and cardiac surgical procedures are performed frequently in an effort to reduce the incidence of postoperative stroke. It is estimated that approximately 5000 such procedures were performed in the United States in 2001 alone.6 More recent analyses, however, have consistently revealed an increased incidence of adverse events, including stroke or death, following combined procedures.6,7

This retrospective analysis was undertaken to analyze the relationship between stroke and carotid stenosis in patients after cardiac operation. This study aimed to answer 2 simple but critical questions: Does severe carotid stenosis increase the risk of ipsilateral anterior circulation stroke in patients undergoing cardiac surgical procedures? Conversely, does concomitant carotid repair reduce the risk of perioperative stroke?

METHODS

The study was approved by the institutional review board of Lehigh Valley Hospital and Health Network, and individual consent was waived. Two complementary computerized hospital databases were compared and combined. Patients receiving nonurgent coronary artery bypass grafting and/or valve replacement were included. Urgent cardiac surgical procedures (ie, those performed within 24 hours of admission) were excluded because there was insufficient time for carotid evaluation and preoperative consultation by vascular or neurology services. Members of the Division of Cardiothoracic Surgery performed the cardiac procedures for recognized indications. Patients with carotid stenosis of more than 70% in diameter were evaluated by members of the divisions of Vascular Surgery and Neurology to determine the need for prophylactic carotid endarterectomy based on clinical presentation. When combined carotid and cardiac procedures were recommended, members of the Division of Vascular Surgery performed carotid endarterectomy as the initial procedure under the same general anesthesia.

Carotid arteries were initially assessed with high-resolution carotid duplex sonography, mostly performed within the month preceding the surgical date. More than 90% of the studies were performed in our facility, where unified criteria for interpretation have been in place with 96% sensitivity for detecting severe carotid stenosis when compared with percutaneous cerebral arteriography.8 Significant carotid disease was defined as 50% stenosis or greater, including carotid occlusion. For patients with stenosis of more than 70% on carotid duplex scanning, a second type of imaging such as magnetic resonance angiography, computed tomographic (CT) angiography, or conventional percutaneous angiography was usually performed to verify the degree of stenosis.

Postoperative stroke was defined as persistent (>24 hours) focal or multifocal neurological deficits that were best explained by ischemia involving the brain or retina from the surgical procedure until hospital discharge. All patients with stroke were evaluated by a board-certified neurologist. Patients with nonfocal results from neurological examination, such as encephalopathy, memory deficit, or unsteadiness, were excluded from the study if their examination results continued to be nonfocal and a second CT scan of the brain showed no evidence of ischemia.

All brain CT and magnetic resonance imaging scans were reviewed by a neuroradiologist (Q.L.) who was blind to all clinical information except the date of symptom onset. After review of the scans, the neuroradiologist (Q.L.) provided an interpretation, including the presence, size, and arterial distribution of infarction.

Stroke subtypes were classified with modified TOAST (Trial of Org 10172 in Acute Stroke Treatment) criteria.9 Cardioembolism was defined based on the following criteria: (1) cortical or cerebellar lesions, subcortical or brainstem lesions of more than 1.5 cm; (2) lack of large-vessel disease in the corresponding territory (carotid or basilar artery); and (3) lesions in multiple vessel territories (bilateral or anterior and posterior circulation) or at least 1 of the following: atrial fibrillation, acute myocardial infarction, or dilated cardiomyopathy. Large-artery atherosclerosis was defined based on the following criteria: (1) cortical or cerebellar lesions, subcortical or brainstem lesions of more than 1.5 cm; and (2) 50% stenosis or greater or occlusion in the internal carotid or basilar artery. Small-vessel occlusion was defined as the following: (1) no symptoms suggestive of cortical dysfunction, such as visual loss or aphasia; (2) isolated subcortical or brainstem lesion of less than 1.5 cm or normal results on a CT scan; and (3) clinical manifestation of pure motor, pure sensory, ataxic hemiparesis, clumsy-hand, or sensorimotor syndrome.

Analyses were completed using the Pearson χ2 or Fisher exact test for categorical variables and the t test for continuous variables. Significance was set at α <.05.

RESULTS
DEMOGRAPHIC AND OPERATIVE CHARACTERISTICS

From July 1, 2001, to December 31, 2006, 4924 patients underwent cardiac procedures at our institution; 589 patients were excluded because of urgent operational status or the rarity of the procedure performed, such as aortic dissection repair or myxoma removal. A cohort of 4335 patients was identified for this retrospective analysis. Of this cohort, 3196 patients had coronary artery bypass grafting, 557 had aortic valve replacement, and 582 had both. The mean (SD) age of the patients studied was 67.5 (11.0) years. The study included 2930 men and 4232 white participants. A total of 3942 patients (90.9%) underwent preoperative carotid evaluation with noninvasive ultrasonography. In addition, 133 patients (3.1%) underwent magnetic resonance angiography, CT angiography, or conventional percutaneous angiography.

POSTOPERATIVE EVENTS

A total of 76 patients (1.8%) developed postoperative stroke (n = 75) or retinal ischemia (n = 1) (the single patient with retinal ischemia was considered to have a stroke in subsequent analysis). Among these, 55 cases of strokes (72.4%) were detected within 24 hours of operation and 68 (89.5%) within the first 72 hours. The time period for initial recognition of stroke ranged from postoperative day 1 through day 9. All strokes were ischemic, and 1 was associated with hemorrhagic transformation. A total of 65 patients died, among whom 8 deaths were believed to be secondary to stroke.

Applying modified TOAST criteria, 57 patients (75.0%) were classified as having cardioembolic stroke (new onset atrial fibrillation, n = 20; previously existent and persistent atrial fibrillation, n = 14; acute myocardial infarction, n = 11; stroke in multiple artery territories, n = 20; multiorgan embolism, n = 4), 4 patients (5.3%) had large-vessel stroke (carotid artery, n = 1; basilar artery, n = 3), and 10 patients (13.2%) had small-vessel stroke. In 5 patients, stroke could not be categorized owing to multiple coexisting etiologies.

DISTRIBUTION OF INFARCTS ON IMAGING

Of 76 patients with stroke, 75 patients underwent noncontrast CT scanning of the head; 70 patients had a second brain CT scan after 24 hours, and 2 patients also underwent magnetic resonance imaging. A total of 60 patients had evidence of acute infarction, whereas 15 patients had normal results on scanning. Table 1 describes the distribution of stroke on imaging. Of 60 patients with abnormal imaging results, 22 had stroke in unilateral carotid distribution, 1 had a watershed pattern, and 36 had infarctions in the bilateral anterior distribution or posterior circulation that were not confined to 1 carotid artery. The remaining patient had a basal ganglia stroke, the territory of which could not be precisely determined.

INFARCTS AND SIGNIFICANT CAROTID DISEASE

All 76 patients with stroke had preoperative carotid evaluation. Of these, 18 patients (23.7%) had significant carotid stenosis. Two patients had bilateral significant carotid stenosis, and both had an infarction in the posterior circulation. Table 2 shows the incidence and distribution of stroke in these patients based on clinical and radiographic data. In 14 of 18 patients (77.8%), stroke occurred outside the territory of diseased carotid artery. Of 4 patients with infarcts found exclusively within the diseased carotid artery, 3 had ipsilateral occlusion and 1 patient had an ipsilateral 60% stenosis.

INCIDENCE OF SIGNIFICANT CAROTID STENOSIS

Of 3942 patients who received preoperative carotid evaluation, 239 (6.1%) had significant carotid stenosis (Table 3). Based on North American Symptomatic Carotid Endarterectomy Trial criteria, 5 were symptomatic and 234 asymptomatic.10

Compared with the entire cohort, the subgroup of patients with significant carotid stenosis had a higher incidence of postoperative stroke (7.5% vs 1.8%; P = .001). Table 3 summarizes the incidence of postoperative stroke based on the severity of carotid stenosis. The stroke risk was higher (15.6%) among patients with carotid occlusion when compared with those patients with significant carotid stenosis, but this did not reach statistical significance (P = .22).

Table 4 summarizes the incidence of postoperative stroke by categories of carotid intervention. Eight strokes occurred in subgroups of 53 patients (15.1%) who underwent combined procedures. No postoperative stroke occurred in the group of 51 patients with an equal degree of carotid stenosis (≥70%) who underwent cardiac surgical procedures without any preoperative carotid revasculization. Table 5 shows a comparison of multiple risk factors between these 2 groups. No significant difference was found other than the incidence of postoperative stroke (0% vs 15.1%; P = .004).

COMMENT

A randomized trial to explore the relationship between carotid stenosis and postoperative stroke following cardiac operations was proposed many years ago but has never been attempted because of the extraordinarily large number of patients needed for statistical power and the prohibitively high cost of completing such a study.11 Using carotid duplex and CT scanning as the major detection methods, this retrospective study provided a detailed analysis of the distribution of stroke and its relationship with significant carotid disease at the bifurcation in patients undergoing routine cardiac procedures.10,12 Only clinically significant strokes were considered, and patients who had transient ischemic attacks were excluded. This study did not enroll patients at multiple centers, and therefore bias toward the surgical, anesthetic, and medical practices specific to a single center could not be minimized.

In this cohort, the incidence of postoperative stroke (1.8%) corresponds well with most of the previously published large trials, which report stroke risks from 0.9% to 3.2%.1,2,1324 The incidence appeared to be slightly higher among patients undergoing combined valve replacement and coronary artery bypass grafting, but it did not alter our analysis of carotid stenosis in the pathogenesis of postoperative stroke (data not shown). It was observed that the incidence of stroke after cardiac procedures could be as much as 4 times higher among patients with significant carotid stenosis vs those without.5 Comparably, our analysis suggested a 4-fold increased relative risk (7.5% vs 1.8%).

However, this study strongly suggests there is no direct causal relationship between postoperative stroke and severe carotid stenosis. First, only 5.3% of postoperative strokes were in the large-vessel category, based on TOAST criteria. Second, 76.3% of postoperative strokes occurred in the absence of significant carotid disease at the bifurcation. Third, 60.0% of strokes on CT scanning had a distribution that was not confined to a single carotid artery (Table 1). Most strokes occurred in the vertebrobasilar artery, contralateral carotid artery, or multivessel territory. Only 4 patients with significant carotid stenosis developed stroke in the diseased carotid territory (Table 2). Of 76 strokes, 72 are not related to significant carotid stenosis at the bifurcation. Therefore, most of these postoperative strokes had alternate causes.

The failure to establish carotid stenosis as a cause of perioperative stroke in patients undergoing cardiac operations has been observed by others. Barbut et al25 reported the presence of infarction in multiple arterial territories and the preponderance of infarction in the posterior circulation in their cohort. Infarction was attributed to high-grade carotid stenosis in only 1 of 24 patients. In an extensive review, Naylor et al5 noted that primary carotid disease alone was only responsible for up to approximately 40% of postoperative strokes. In addition, Libman et al1 determined that 7 of 44 postoperative strokes (16%) in their series fit the criteria for classical lacunar syndromes.

Multiple causes other than carotid stenosis could account for postoperative stroke in patients undergoing cardiac procedures. For example, coexistence of aortic atherosclerosis has been demonstrated to be a significant determinant of postoperative stroke.26 In some studies, clamping and manipulation of the aorta or heart could account for more than 60% of emboli.27 Van der Linden and Casimir-Ahn28 reported that cerebral emboli are most likely to occur during the redistribution of blood from the heart-lung machine to the patient, which supports the idea that release of particles from the cardiopulmonary bypass pump is a major contributor to stroke. Postoperative atrial fibrillation is seen in 30% to 50% of patients.3 There is also evidence that the fibrinolytic shutdown activates postoperatively, which may account for the occurrence of embolic and lacunar infarctions.29 A recent multivariate analysis by Filsoufi et al30 suggested that older age, female sex, and presence of diabetes mellitus, cardiomyopathy, longer bypass time, and aortic calcifications are independent predictors of postoperative stroke. The apparent paradox that carotid stenosis is associated with an increased incidence of stroke but is not a direct cause of postoperative stroke may suggest that it is an epiphenomena indicating an increased underlying cardiovascular risk.

The lack of a causal relationship between carotid stenosis and postoperative stroke raises serious doubts about hypoperfusion as a major mechanism. This finding is in line with data from the Northern New England Cardiovascular Disease Study Group suggesting that fewer than 10% of postoperative strokes were caused by hypoperfusion.2 In our study, the incidences of stroke for patient subgroups with 50% to 79% stenosis, 80% to 99% stenosis, and occlusion were 4.9%, 7.0%, and 15.6%, respectively (Table 3). Although higher incidence of stroke was associated with more severe stenosis, this trend did not reach statistical significance. The most plausible explanation for such a trend might simply be the cardiovascular risk burden, as reflected by the degree of carotid stenosis. The observation that more postoperative strokes occur outside rather than within the territory of diseased carotid arteries was consistent among these subgroups.

The increased incidence of stroke among patients with carotid stenosis has led to the proposal for combining carotid and cardiac procedures in selected patients. However, recent analyses suggest that simultaneous repair of carotid lesions is associated with a higher risk of postoperative stroke and death in patients undergoing cardiac operations.6,7,31 In this sample of 239 patients with significant carotid stenosis, 4 patients had strokes found to be caused by carotid disease, but only the patient with 60% unilateral carotid stenosis would have been considered a candidate for endarterectomy based on results of the Asymptomatic Carotid Atherosclerosis Study.12 Therefore, there is virtually no compelling evidence to suggest that repairing the diseased carotid artery prevents postoperative stroke after cardiac procedures. Could the effect of carotid stenosis be falsely low because a significant portion of patients underwent carotid revascularization procedures before cardiac operations? We do not believe this is the explanation. Instead, the incidence of stroke (15.1%) was significantly higher in the subgroup of patients undergoing combined carotid and cardiac procedures than among patients with similar degrees of carotid stenosis but who underwent cardiac procedures alone (Table 4). Further risk analysis failed to identify any factors that could account for the difference in the incidence of postoperative stroke between the 2 groups (Table 5). Also, the operative risk for combined procedures is higher than the added stroke risks from separate cardiac procedures (1.8%) and carotid endarterectomy (<1% of the 30-day risk of postoperative stroke in our institution; data not shown). Therefore, the occurrence of postoperative stroke in this subgroup is likely related to the combined procedure itself, with a possible correlation to the duration of the operation. As such, our findings strongly support the idea that combined carotid and cardiac procedures are neither necessary nor effective in reducing the risk of postoperative stroke in this population. Assuming that 5000 combined carotid endarterectomies and cardiac operations are performed annually in the United States, avoidance of such procedures alone could prevent nearly 500 postoperative strokes per year.

In conclusion, we examined the relationship between postoperative stroke and carotid stenosis in a large group of patients undergoing common, nonurgent cardiac procedures at a single medical center. We confirmed a higher incidence of stroke in the subgroup of patients with significant carotid stenosis. However, most strokes have no direct causal relationship with the diseased carotid artery. Combined carotid and cardiac procedures result in a significantly higher incidence of postoperative stroke and should be avoided. Preoperative studies such as echocardiography or CT or magnetic resonance imaging of the heart and aorta could identify disease-free areas for manipulation and clamping to prevent postoperative strokes.

Back to top
Article Information

Correspondence: John E. Castaldo, MD, Department of Medicine, Lehigh Valley Hospital and Health Network, 1250 S Cedar Crest Blvd, Ste 405, Allentown, PA 18103 (John.Castaldo@lvh.com).

Accepted for Publication: January 21, 2009.

Author Contributions: Drs Y. Li and Castaldo had full access to all the data in the study and take responsibility for the integrity of the data and accuracy of the data analysis. Study concept and design: Y. Li and Castaldo. Acquisition of data: Y. Li, Walicki, Jenny, and Q. Li. Analysis and interpretation of data: Y. Li, Walicki, Mathiesen, Q. Li, Isayev, Reed, and Castaldo. Drafting of the manuscript: Y. Li. Mathiesen, Jenny, Q. Li, and Isayev. Critical revision of the manuscript for important intellectual content: Y. Li, Walicki, Isayev, Reed, and Castaldo. Statistical analysis: Reed. Administrative, technical, and material support: Jenny, Q. Li, and Isayev. Study supervision: Y. Li and Castaldo.

Financial Disclosure: None reported.

Additional Contributions: Karen Boutron, RN, and Joanne Rodgers, RN, provided substantial help in data collection. We also thank the Department of Surgery at Lehigh Valley Hospital and Health Network for allowing us access to the databases.

References
1.
Libman  RBWirkowski  ENeystat  MBarr  WGelb  SGraver  M Stroke associated with cardiac surgery: determinants, timing, and stroke subtypes. Arch Neurol 1997;54 (1) 83- 87
PubMedArticle
2.
Likosky  DSMarrin  CACaplan  LR  et al. Northern New England Cardiovascular Disease Study Group, Determination of etiologic mechanisms of strokes secondary to coronary artery bypass graft surgery. Stroke 2003;34 (12) 2830- 2834
PubMedArticle
3.
Selim  M Perioperative stroke. N Engl J Med 2007;356 (7) 706- 713
PubMedArticle
4.
Chaturvedi  SBruno  AFeasby  T  et al. Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology, Carotid endarterectomy–an evidence-based review: report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Neurology 2005;65 (6) 794- 801
PubMedArticle
5.
Naylor  ARMehta  ZRothwell  PMBell  PR Carotid artery disease and stroke during coronary artery bypass: a critical review of the literature. Eur J Vasc Endovasc Surg 2002;23 (4) 283- 294
PubMedArticle
6.
Dubinsky  RMLai  SM Mortality from combined carotid endarterectomy and coronary artery bypass surgery in the US. Neurology 2007;68 (3) 195- 197
PubMedArticle
7.
Hill  MDShrive  FMKennedy  JFeasby  TEGhali  WA Simultaneous carotid endarterectomy and coronary artery bypass surgery in Canada. Neurology 2005;64 (8) 1435- 1437
PubMedArticle
8.
Castaldo  JENicholas  GGee  WReed  J Duplex ultrasound and ocular pneumoplethysmography concordance in detecting carotid stenosis. Arch Neurol 1989;46 (5) 518- 522
PubMedArticle
9.
Adams  HP  JrBendixen  BHKappelle  LJ  et al.  Classification of subtype of acute ischemic stroke: definitions for use in a multicenter clinical trial; TOAST–Trial of Org 10172 in Acute Stroke Treatment. Stroke 1993;24 (1) 35- 41
PubMedArticle
10.
North American Symptomatic Carotid Endarterectomy Trial Collaborators, Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis. N Engl J Med 1991;325 (7) 445- 453
PubMedArticle
11.
Brener  BJBrief  DKAlpert  J  et al.  A four-year experience with preoperative noninvasive carotid evaluation of two thousand twenty-six patients undergoing cardiac surgery. J Vasc Surg 1984;1 (2) 326- 338
PubMedArticle
12.
Executive Committee for the Asymptomatic Carotid Atherosclerosis Study, Endarterectomy for asymptomatic carotid artery stenosis. JAMA 1995;273 (18) 1421- 1428
PubMedArticle
13.
Jones  ELCraver  JMMichalik  RA  et al.  Combined carotid and coronary operations: when are they necessary? J Thorac Cardiovasc Surg 1984;87 (1) 7- 16
PubMed
14.
Gardner  TJHorneffer  PJManolio  TA  et al.  Stroke following coronary artery bypass grafting: a 10-year study. Ann Thorac Surg 1985;40 (6) 574- 581
PubMedArticle
15.
Brener  BJBrief  DKAlpert  JGoldenkranz  RJParsonnet  V The risk of stroke in patients with asymptomatic carotid stenosis undergoing cardiac surgery: a follow-up study. J Vasc Surg 1987;5 (2) 269- 279
PubMedArticle
16.
Blossom  GBFietsam  R  JrBassett  JSGlover  JLBendick  PJ Characteristics of cerebrovascular accidents after coronary artery bypass grafting. Am Surg 1992;58 (9) 584- 589
PubMed
17.
Frye  RLKronmal  RSchaff  HVMyers  WOGersh  BJ Stroke in coronary artery bypass graft surgery: an analysis of the CASS experience; the participants in the Coronary Artery Surgery Study. Int J Cardiol 1992;36 (2) 213- 221
PubMedArticle
18.
Ricotta  JJFaggioli  GLCastilone  AHassett  JM Risk factors for stroke after cardiac surgery: Buffalo Cardiac Cerebral Study Group. J Vasc Surg 1995;21 (2) 359- 364
PubMedArticle
19.
D’Agostino  RSSvensson  LGNeumann  DJBalkhy  HHWilliamson  WAShahian  DM Screening carotid ultrasonography and risk factors for stroke in coronary artery surgery patients. Ann Thorac Surg 1996;62 (6) 1714- 1723
PubMedArticle
20.
Roach  GWKanchuger  MMangano  CM  et al. Multicenter Study of Perioperative Ischemia Research Group and the Ischemia Research and Education Foundation Investigators, Adverse cerebral outcomes after coronary bypass surgery. N Engl J Med 1996;335 (25) 1857- 1863
PubMedArticle
21.
Dashe  JFPessin  MSMurphy  REPayne  DD Carotid occlusive disease and stroke risk in coronary artery bypass graft surgery. Neurology 1997;49 (3) 678- 686
PubMedArticle
22.
Gott  JPThourani  VHWright  CE  et al.  Risk neutralization in cardiac operations: detection and treatment of associated carotid disease. Ann Thorac Surg 1999;68 (3) 850- 857
PubMedArticle
23.
Likosky  DSLeavitt  BJMarrin  CA  et al. Northern New England Cardiovascular Disease Study Group, Intra- and postoperative predictors of stroke after coronary artery bypass grafting. Ann Thorac Surg 2003;76 (2) 428- 435
PubMedArticle
24.
Ricotta  JJWall  LPBlackstone  E The influence of concurrent carotid endarterectomy on coronary bypass: a case-controlled study. J Vasc Surg 2005;41 (3) 397- 402
PubMedArticle
25.
Barbut  DGrassineau  DLis  EHeier  LHartman  GSIsom  OW Posterior distribution of infarcts in strokes related to cardiac operations. Ann Thorac Surg 1998;65 (6) 1656- 1659
PubMedArticle
26.
Katz  ESTunick  PARusinek  HRibakove  GSpencer  FCKronzon  I Protruding aortic atheromas predict stroke in elderly patients undergoing cardiopulmonary bypass: experience with intraoperative transesophageal echocardiography. J Am Coll Cardiol 1992;20 (1) 70- 77
PubMedArticle
27.
Barbut  DHinton  RBSzatrowski  TP  et al.  Cerebral emboli detected during bypass surgery are associated with clamp removal. Stroke 1994;25 (12) 2398- 2402
PubMedArticle
28.
van der Linden  JCasimir-Ahn  H When do cerebral emboli appear during open heart operations? a transcranial Doppler study. Ann Thorac Surg 1991;51 (2) 237- 241
PubMedArticle
29.
Páramo  JARifon  JLlorens  RCasares  JPaloma  MJRocha  E Intra- and postoperative fibrinolysis in patients undergoing cardiopulmonary bypass surgery. Haemostasis 1991;21 (1) 58- 64
PubMed
30.
Filsoufi  FRahmanian  PBCastillo  JGBronster  DAdams  DH Incidence, imaging analysis, and early and late outcomes of stroke after cardiac valve operation. Am J Cardiol 2008;101 (10) 1472- 1478
PubMedArticle
31.
Borger  MAFremes  SEWeisel  RD  et al.  Coronary bypass and carotid endarterectomy: does a combined approach increase risk? a metaanalysis. Ann Thorac Surg 1999;68 (1) 14- 21
PubMedArticle
×