JNS-11955; No of Pages 4

Journal of the Neurological Sciences xxx (2011) xxxxxx

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Journal of the Neurological Sciences

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Intraoperative hypotension, new onset atrial brillation, and adverse outcome after carotid endarterectomy
Luciano A. Sposato a, b, c, e,, Andrs Surez a, Agustn Juregui b, Patricia M. Riccio b, c, Matas Altounian a, Mauro G. Andreoli a, Andrs I. Rodriguez a, Juan F. Ressia a, Gabriela J. Bressan a, Francisco R. Klein b, Hctor Raffaelli d, Gerardo E. Bozovich a
a

Favaloro University School of Medicine, Favaloro University Hospital, Argentina Stroke Center, Institute of Neurosciences at Favaloro University Hospital, Argentina c Vascular Research Institute at INECO Foundation, Argentina d Department of Vascular Surgery at Favaloro University Hospital, Argentina e Universidad Diego Portales, Santiago, Chile
b

a r t i c l e

i n f o

a b s t r a c t
Background: Information regarding predisposing factors, frequency, and prognostic implications of new onset atrial brillation (NOAF) after carotid endarterectomy (CEA) is scarce. We assessed the frequency, risk factors, and the prognostic impact of NOAF after CEA. Methods: We assessed every patient undergoing CEA (n = 186) at our academic hospital between 2006 and 2009. Patients underwent continuous electrocardiographic monitoring during surgery and during the rest of hospital stay. We performed univariate and multivariate analyses for identifying variables associated with NOAF and for individualizing variables related to four perioperative adverse outcome measures: a) ischemic stroke; b) ischemic stroke and myocardial infarction, c) ischemic stroke and death, and d) ischemic stroke, myocardial infarction, and death. Results: The study cohort comprised 186 patients. Overall, NOAF was detected in 7 cases (3.8%). The only variable associated with NOAF was intraoperative hypotension (OR 9.6, 95% CI 1.947.4, P = .006). There were no perioperative deaths. NOAF was associated with perioperative ischemic stroke and with the combined outcome of ischemic stroke and myocardial infarction. Conclusions: We found a low frequency of NOAF after CEA. Intraoperative hypotension was associated to a higher risk of NOAF. In turn, NOAF was related to adverse postoperative outcome. Further research is needed to clarify the pathophysiological relation between intraoperative hypotension, NOAF, and adverse CEA outcome. 2011 Elsevier B.V. All rights reserved.

Article history: Received 17 May 2011 Accepted 28 July 2011 Available online xxxx Keywords: Carotid endarterectomy Carotid artery interventions Carotid artery disease Bypass surgery Atrial brillation Arrhythmias Risk stratication Prognosis Stroke Outcome

1. Introduction Atherosclerotic disease of extracranial internal carotid artery (ICA) is a preventable cause of ischemic stroke and death. Its prevalence varies from 2.2% in women under 70 years to 12.5% in men older than 70 years [1]. On average, 15% of ischemic strokes are caused by ICA disease [2]. Carotid endarterectomy (CEA) is the procedure of choice for symptomatic patients with stenosis 70% of the ICA and for selected cases with ICA stenosis ranging from 50 to 69% [3]. CEA has also been recommended for carefully \selected asymptomatic patients with ICA stenosis 60% [4]. Every year, approximately 100,000 patients in the United States undergo a carotid revascularization
Corresponding author at: INECO, Pacheco de Melo 1860, Ciudad de Buenos Aires, C1126AAB, Argentina. Tel.: + 54 911 6859 2803; fax: + 54 11 4812 0010. E-mail addresses: lsposato@ineco.org.ar, lucianosposato@gmail.com, lsposato@ffavaloro.org (L.A. Sposato). 0022-510X/$ see front matter 2011 Elsevier B.V. All rights reserved. doi:10.1016/j.jns.2011.07.052

procedure [5] and up to 2.3% of CEAs are complicated by a periprocedural stroke [6]. One of the rst steps towards preventing this complication is to identify patients at higher risk. New onset atrial brillation (NOAF) is found in 30% of patients undergoing coronary artery by-pass grafting and is related to worse outcome [7]. This nding is of major importance since patients with NOAF discharged on warfarin experience reduced mortality during long-term follow-up [8]. Despite this knowledge, the relation between NOAF and CEA has been poorly studied. The aim of our study was to assess the frequency, risk factors, and the prognostic impact of NOAF after CEA. 2. Methods 2.1. Study population We retrospectively assessed every patient 18 years undergoing CEA at our academic hospital between January 1, 2006, and December

Please cite this article as: Sposato LA, et al, Intraoperative hypotension, new onset atrial brillation, and adverse outcome after carotid endarterectomy, J Neurol Sci (2011), doi:10.1016/j.jns.2011.07.052

L.A. Sposato et al. / Journal of the Neurological Sciences xxx (2011) xxxxxx

31, 2009. The study cohort is described in the supplemental le. For the present analysis we excluded patients with known paroxysmal or chronic atrial brillation on the basis of patient recall or by documentation of atrial brillation or atrial utter on a previous electrocardiogram (ECG). Participants were also excluded if the arrhythmia was detected on the admission ECG. Atrial brillation was dened by the absence of p waves or evidence of atrial utter with irregular ventricular response. Patients underwent transesophageal or transthoracic Doppler echocardiography (TEE or TTE) as part of the preoperative assessment when considered appropriate by the treating physician. We assessed data related to baseline ICA disease (grade of stenosis, left vs. right, and symptomatic vs. asymptomatic), risk factor proles, left ventricular ejection fraction, atrial area, and procedural aspects such as types of anesthesia, duration of procedure, use of shunt and patch graft, intraoperative hypotension, postoperative hypertension, plasmatic lactate concentrations within 24 and 48 h after surgery, and CEA with or without concomitant CABG. Intraoperative hypotension was dened as a systolic blood pressure b80 mmHg during 15 min [9]. ICA stenosis was measured according to NASCET method [10]. We decided to exclude 22 patients undergoing combined CEA + CABG with the intention of avoiding a potential effect of CABG on NOAF risk and on surgical outcome [11]. 2.2. New onset atrial brillation Patients underwent continuous electrocardiographic monitoring during surgery and throughout hospital stay. The detailed electrocardiographic monitoring protocol is described elsewhere [12] and can be found in the supplementary data appendix. We documented every episode of NOAF during hospital stay. We determined the frequency of NOAF after CEA. NOAF was dened as any atrial brillation diagnosed after CEA in a patient with no history of chronic or paroxysmal atrial brillation. We recorded the following data related to NOAF: time from surgery to diagnosis of the atrial brillation, number of episodes, duration (stratied into b1 or 1 h), and discharge with or without atrial brillation. 2.3. Outcome measures We documented periprocedural strokes, acute myocardial infarction, and death. We established four outcome measures: a) ischemic stroke; b) ischemic stroke and myocardial infarction; c) ischemic stroke and death; and d) ischemic stroke, myocardial infarction, and death. Events were considered as periprocedural if they occurred within 30 days after surgery. Every patient suspected of having experienced a cerebrovascular event underwent complete neurological evaluation and either a computed tomography scan or a magnetic resonance imaging of the brain, or both. Neurological assessment was performed at baseline, during hospital stay until discharge, and at our outpatient clinic 30 days after the event. Stroke severity was determined by using the National Institutes of Health Stroke Scale (NIHSS) [13]. Strokes were adjudicated by two certied neurologists (P.R. and L.A.S.) based on the clinical presentation and results of neuroimaging studies. 2.4. Statistical analysis

(i.e. left ventricular ejection fraction and left atrial area). A two-tailed P value b .05 was deemed statistically signicant for the multivariable model. In order to assess effect modication by the interaction of relevant biological factors, we tested the interaction term intraoperative hypotension duration of surgery. The association between covariates and NOAF detection was expressed as odds ratios (OR) and 95% condence intervals (CI). We carried out univariable (not shown) and multivariable analyses for each of the three outcome measures by using the same methodology above mentioned. We also tested the following interaction terms for the outcome measures: NOAFintraoperative hypotension, NOAFcontralateral ICA occlusion, and intraoperative hypotension contralateral ICA occlusion. We used SPSS 13.0 for Windows (SPSS Inc, Chicago, IL) for all statistical analyses. The study was approved by the Institutional Review Board and the Institutional Ethics Committee. 3. Results A total of 186 patients underwent CEA during the study period. CEA were performed by the same surgical team, which comprised ve surgeons. All procedures were done by longitudinal arteriotomy and with general anesthesia. One hundred and forty nine patients (80.1%) underwent TEE or TTE. Demographic characteristics, risk factor proles, and data about surgical procedures and baseline carotid artery disease are shown in Table 1. Length of stay was 3.8 2.9 days. We evidenced a NOAF in 7 patients (3.8%, 95% CI 1.87.6). The median time from CEA to detection of NOAF was 4 days, interquartile range 2.54.5 (mean 4.0 2.1). No NOAFs were diagnosed within 24 h after CEA, two cases were detected on the second day after surgery (28.6%). NOAF was paroxysmal in the 7 participants. Six (85.7%) of these patients experienced only 1 episode, while 1 (14.3%) suffered 2. The minimal duration of a NOAF episode was 1 h in 5 patients (71.4%) and b1 h in the remainder 2 participants (28.6%). Five patients returned to sinus rhythm spontaneously (71.4%), although one of them required further pharmacological cardioversion due to recurrent episodes. The remaining 2 patients were treated with pharmacologic cardioversion. One patient required the correction of hypokalemia (14.3%). The 7 patients were discharged on sinus rhythm. The univariate analysis for NOAF is shown in Table 1. Intraoperative hypotension (OR 9.6. 95% CI 1.947.4, P = .006) was the only variable associated with NOAF in the multivariable analysis, after adjusting for age, gender, left atrial area, left ventricular ejection fraction, duration of surgery, previous myocardial infarction, and coronary heart disease. The interaction term intraoperative hypotension duration of surgery was not associated with NOAF diagnosis. Outcome measures are shown in Table 2. Seven patients suffered a minor periprocedural ischemic stroke (5 ipsilateral to the operated ICA), three participants experienced a myocardial infarction, and there were no periprocedural deaths. Multivariable analyses for ischemic stroke and the combined outcome of ischemic stroke and myocardial infarction are shown in Table 3. The Interaction term NOAF intraoperative hypotension was associated with a higher risk of periprocedural ischemic stroke (OR 3.3, 95% CI 1.57.0, P = .002). 4. Discussion

We used the 2 test or the Mann-Whitney U test to compare dichotomous or categorical variables and the Student t test for continuous variables. We performed a univariate analyses for identifying variables associated with NOAF. Age, gender and those variables with a level of signicance of two-tailed P b .1 in the univariate analysis were included in a multivariable regression model along with other factors considered biologically important, despite their level of signicance

Our study specically reports on the frequency, risk factors, and prognostic implications of NOAF after CEA. We found that NOAF was relatively uncommon after CEA (3.8%, 95% CI 1.87.6), but it was consistently associated with myocardial infarction and stroke. There is a lack of reports specically assessing the frequency of postoperative NOAF in patients undergoing CEA. A study investigating risk factors and outcome of CEA, found a 2.7% of perioperative atrial

Please cite this article as: Sposato LA, et al, Intraoperative hypotension, new onset atrial brillation, and adverse outcome after carotid endarterectomy, J Neurol Sci (2011), doi:10.1016/j.jns.2011.07.052

L.A. Sposato et al. / Journal of the Neurological Sciences xxx (2011) xxxxxx Table 1 Risk factor proles, periprocedural aspects, baseline carotid artery disease, and univariate analysis for NOAF. Overall (n = 186) Risk factor prole Age, years, mean SD Male gender, n (%) Hypertension, n (%) Diabetes mellitus, n (%) Hyperlipidemia, n (%) Smoking habit, n (%) COPD, n (%) CHD, n (%) Left atrial area N 20 cm2, n (%) LVEF b30%, n (%) LVEF, mean SD Previous myocardial infarction, n (%) Previous TIA, n (%) Previous stroke, n (%) Periprocedural aspects Intraoperative shunting, n (%) Patch utilization, n (%) Duration of surgery, minutes, mean SD Duration of surgery N 120 min, n (%) Intraoperative hypotension, n (%) Postoperative hypertension, n (%) Highest lactate within rst 24 h, mg/dl, mean SD Highest lactate within rst 48 h, mg/dl, mean SD Baseline carotid artery disease Left ICA, n (%) Stenosis 70% of operated ICA, n (%) Symptomatic stenosis of operated ICA, n (%) Contralateral ICA stenosis 70%, n (%) Contralateral ICA stenosis 95%, n (%) 68.6 8.6 134 (72.0) 163 (87.6) 59 (31.7) 139 (74.7) 115 (61.8) 32 (17.2) 106 (57.0) 59/140 (42.1) 4/145 (2.8) 56.8 9.5 61 (32.8) 40 (21.5) 52 (28.0) With NOAF (n = 7) 74.7 6.9 7 (100.0) 6 (85.7) 3 (42.9) 5 (71.4) 4 (57.1) 0 (0.0) 6 (85.7) 3/4 (75.0) Without NOAF (n = 179) P Table 3 Regression model for outcome measures. OR (95% CI) Multivariate analysis for ischemic stroke NOAF 19.2 (2.3162.5) Previous stroke 8.5 (1.452.1) Multivariate analysis for myocardial infarction and ischemic stroke NOAF 19.0 (1.1315.0) P .007 .020

68.3 8.6 .062 127 (70.9) .99 157 (87.7) .88 56 (31.3) .52 134 (74.9) .84 111 (62.0) .80 32 (17.9) .22 100 (55.9) .12 56/136 .18 (41.2) 2/5 (40.0) 2/140 (1.4) b.001 42.5 20.2 57.3 8.7 .002 3 (42.9) 58 (32.4) .56 2 (28.6) 2 (28.6) 38 (21.2) 50 (27.9) .64 .97

.040

NOAF: new onset atrial brillation. CEA: carotid endarterectomy. ICA: internal carotid artery. *Adjusted for age, gender, and variables with P b .1 in the multivariate analysis (not shown): diabetes mellitus, intraoperative hypotension, duration of surgery, contralateral ICA stenosis 95%, and contralateral ICA occlusion. As there were no periprocedural deaths, regression models for the combined outcome of ischemic stroke and death are not shown. Adjusted for age, gender, and variables with P b .1 in the multivariate analysis (not shown): left ventricular ejection fraction, previous stroke, duration of surgery, surgery of left ICA, highest plasmatic lactate levels within 48 h after CEA, contralateral ICA stenosis 95%, and contralateral ICA occlusion.

179 (96.2) 169 (90.9) 119 31 73 (39.2) 16 (8.6) 160 (86.0) 15.5 7.6 12.2 4.8

7 (100.0) 6 (85.7) 153 64 5 (71.4) 3 (42.9) 7 (100.0) 18.8 7.8 11.8 1.0

172 (96.1) 163 (91.1) 132 28 68 (38.0) 13 (7.3) 153 (85.5) 15.3 7.6 12.3 5.1

.59 .63 .016 .08 .001 .28 .32 .83

95 (51.1) 170 (91.4) 28 (15.1) 41 (22.0) 13 (7.0)

5 (71.4) 6 (85.7) 2 (28.6) 2 (28.6) 2 (28.6)

90 (50.3) 164 (91.6) 26 (14.5) 39 (21.8) 11 (6.1)

.27 .59 .31 .67 .022

SD: standard deviation. COPD: chronic obstructive pulmonary disease. CHD: coronary heart disease. LVEF: left ventricular ejection fraction. TIA: transient ischemic attack. CABG: coronary artery bypass grafting. ICA: internal carotid artery.

brillation, though is not clear whether those cases had a history of paroxysmal atrial brillation or not [14]. Intraoperative hypotension was the single variable associated with NOAF. Villarreal et al. found that postoperative hypotension after CABG was more frequent among patients experiencing NOAF than among those with sinus rhythm [15]. Based on this nding, it could be hypothesized that atrial brillation could have triggered intraoperative hypotension in our patients, though no case of NOAF was detected

Table 2 Outcome measures. Overall NOAF (n = 186) (n = 7) Myocardial infarction, 3 (1.6) n (%) Ischemic stroke, n (%) 7 (3.8) Periprocedural death, 0 (0.0) n (%) Myocardial infarction 10 (5.4) and stroke, n (%) No NOAF OR (95% CI) (n = 179) P

1 (14.3) 2 (1.1) 2 (28.6) 5 (2.8) 0 (0.0) 0 (0.0) 3 (42.9) 7 (3.9)

14.8 (1.2180.0) .007 13.9 (2.289.9) 18.4 (3.598.6) b.001 b.001

CEA: carotid endarterectomy. CABG: coronary artery by-pass grafting.

during surgery. In contrast, intraoperative hypotension could have been caused by general anesthesia. In this scenario, signicant decreases in systolic blood pressure could have been the predisposing factor for the development of NOAF [16]. Systolic blood pressures below 90 mmHg are not uncommon among patients undergoing CEA under general anesthesia [17] due to the vasodilating effects of anesthetics and, in some cases, because of surgically induced abnormalities of carotid baroreceptor sensitivity (i.e. damage to the vagus nerve or the carotid sinus during dissection of the common carotid artery). Previous stroke and NOAF were associated with periprocedural ischemic stroke. History of stroke has been shown to be associated with periprocedural ischemic stroke after CEA [18,19]. Despite the clear association between atrial brillation and ischemic stroke, we cannot infer a causal relationship between NOAF and stroke in our study because the arrhythmia was detected after the cerebrovascular event in the 2 cases. NOAF was associated with the combined outcome of periprocedural myocardial infarction and ischemic stroke. Other authors have found a relation between NOAF and cardiovascular adverse events after different vascular surgeries [20]. Several mechanisms may explain the relation between NOAF and adverse prognosis after vascular procedures. Atrial brillation results in loss of synchronized atrial contraction, abnormal ventricular response, elevated ventricular rates, and a decrease in myocardial blood ow. Long-term alterations such as atrial and ventricular cardiomyopathy may occur after prolonged periods of diminished left ventricular output [21]. Intraoperative hypotension itself may enhance several of these phenomena. Our study has limitations that need to be acknowledged. In the rst place, despite the prospective documentation of mostly predened variables, its retrospective nature may have resulted in bias; thus our ndings should only be considered as generators of hypotheses to be explored in future prospective investigations. The same concept is also applicable to the single-center design, which may limit the generalizability of our results. However, surgical techniques and complication rates of vascular surgeons participating in our study were within recommended international standards [3,4] and are similar to those of large randomized controlled trials [22]. Second, the frequency of NOAF was low when compared with other types of vascular surgeries despite having demonstrated that our electrocardiographic monitoring protocol has a very good sensitivity [12]. Finally, the small sample size may have limited the precision of the estimates, as can be noted by the wide condence intervals of the multivariate analyses. In conclusion, our study showed a relatively low frequency of NOAF after CEA. Intraoperative hypotension was associated with a

Please cite this article as: Sposato LA, et al, Intraoperative hypotension, new onset atrial brillation, and adverse outcome after carotid endarterectomy, J Neurol Sci (2011), doi:10.1016/j.jns.2011.07.052

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higher risk of perioperative NOAF. In turn, NOAF was directly associated with adverse cardiovascular outcomes, though we cannot imply a causal association. Our ndings may have important implications regarding the prevention of cardiovascular complications after CEA and highlight the need for future trials assessing the pathophysiological relation between intraoperative hypotension, NOAF, and adverse outcome after CEA. Sources of funding The study was partially funded by an unrestricted research grant from INECO Foundation. Conicts of interest/disclosures None of the authors has nancial associations that might pose a conict of interest in connection with the submitted manuscript. Acknowledgments None. Appendix A. Supplementary data Supplementary data to this article can be found online at doi:10. 1016/j.jns.2011.07.052. References
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Please cite this article as: Sposato LA, et al, Intraoperative hypotension, new onset atrial brillation, and adverse outcome after carotid endarterectomy, J Neurol Sci (2011), doi:10.1016/j.jns.2011.07.052