Risk Factors and Neurological Consequences of Syncopes Induced by Internal Carotid Artery Angioplasty
Background and Purpose— Syncope and carotid sinus reactions (CSR) occur frequently in patients undergoing carotid angioplasty (CA). We investigated risk factors and the neurological consequences of carotid sinus syncope induced by CA.
Methods— We examined 359 consecutive patients. Patients underwent assessment of cerebrovascular reserve before CA and continuous electroencephalographical monitoring during the procedure. We examined the impact of vascular risk factors, cerebral hemodynamics, characteristics of plaque, and procedural modality on the incidence of CSR and syncope. The effect of syncopes on periprocedural complication rates was also investigated.
Results— CSR and syncope occurred in 62.7% and 18.0% of the procedures, respectively. The occurrence of CSR during angioplasty was significantly associated with the appearance of syncope. The incidence of syncope was significantly higher in longer plaques located in the carotid bifurcation, in the presence of contralateral carotid stenosis, or when protection devices were used. Although TIA during CA was more common in syncopal patients, stroke or death rates were similar in the 2 groups.
Conclusions— Syncope occurs more frequently in patients with long plaques proximal to the carotid bifurcation, but it does not increase the periprocedural complications rate.
Carotid sinus reactions (CSR) may occur acutely during internal carotid angioplasty (CA) and are often accompanied by the appearance of neurally mediated reflex syncope. To our knowledge, the influence of brain hemodynamics on the appearance of syncope during CA has not been yet elucidated. Moreover, the influence of CSR and syncopes on the periprocedural complication rates remains unknown.
We investigated risk factors for CSR and carotid sinus syncope induced by internal CA. We also examined the effect of CSR and syncopes on the periprocedural morbidity and mortality rates.
Materials and Methods
A CA Registry was established in 1992 to provide epidemiological data on the safety and efficacy of CA. Our Institutional Review Board approved the study and written informed consent was obtained. The following patients were prospectively enrolled: (1) symptomatic patients with TIA or noninvalidating stroke; and (2) asymptomatic patients with progression of the stenosis to 85%, positive microemboli detection, exhausted cerebrovascular reserve, or silent lesions on MR. Demographic data and vascular risk factors were recorded.
Before CA, all participants underwent carotid continuous wave evaluation to establish the indication for CA,1 duplex assessment of plaque characteristics, breath-holding test by transcranial Doppler to assess cerebrovascular reserve, and brain MR.
The percentage of artery stenosis was determined by angiography using the NASCET criteria. Morphological data and the functional status of the circle of Willis were investigated.
CA was performed in keeping with institutional guidelines.2 Continuous neurological and electroencephalographical (EEG) monitoring was performed throughout the procedure. Heart rate was monitored continuously and blood pressure measurements were obtained every 5 minutes during the CA procedure and every minute during balloon inflation and stent placement. If asystole occurred during predilation or stent dilation, the balloon was deflated immediately and 1 mg of atropine was administered intravenously. A detailed neurological examination was performed on completion of angioplasty, on a daily basis until discharge, and 30 days after the procedure to rule out cerebral ischemic events.
The primary study end point was the occurrence of CSR or syncope during CA. CSR was defined as the presence of asystole exceeding 3 seconds or decline in systolic blood pressure exceeding 50 mm Hg with or without bradycardia. Syncope was diagnosed based both on clinical grounds (transient loss of consciousness without neurological sequelae) and EEG abnormalities (large amplitude slow waves or EEG flattening plus absence of epileptic discharge).
The rate of procedural complications, cerebral ischemic events, and deaths during CA or within the first month were recorded to calculate CA-related morbidity and mortality.
Continuous variables are expressed as means and SD. Categorical variables are presented by frequency counts. Intergroup comparisons were analyzed by χ2 test and Student t test. Multiple logistic regression analysis was performed to identify the independent predictors of syncope occurring during the procedures. P<0.05 were considered statistically significant.
A total of 359 patients undergoing CA were examined. The general and procedural characteristics of the study participants are shown in Table 1.
CSR and syncope occurred in 225 (62.7%) and 66 patients (18.6%), respectively. CSR occurred invariably during balloon dilation, either before or after stent deployment. The presence of plaques close to the carotid bifurcation, the length of carotid plaques, and the presence of ulcerated plaques were the only significant predictors of CSR occurrence. A significant relationship between the occurrence of CSR and syncope was evident. The occurrence of syncope in relation to possible risk factors is presented in Table 2⇓. The incidence of syncope was significantly higher in plaques >1 cm (RR, 2.2; 95% CI, 1.2 to 4.1), located in the carotid bifurcation (RR, 4.1; 95% CI, 1.9 to 8.5), when protection devices were used (RR, 2.3; 95% CI, 1.2 to 4.4), and in patients with contralateral high-grade carotid stenosis (RR, 1.9; 95% CI, 1.1 to 3.4).
After allowance for potential confounders, the appearance of CSR (OR, 3.3; 95% CI, 1.5 to 7.06), contralateral high-grade carotid stenosis (OR, 2.4; 95% CI, 1.3 to 4.4), and the distance from plaque to bifurcation (OR, 0.20; 95% CI, 0.07 to 0.70) were independent predictors of syncope occurrence.
Syncope occurrence was not associated with an increase in procedural complications (Table 3). The incidence of TIA was significantly higher in patients having syncope (RR, 3.6; 95% CI, 1 to 14). However, major stroke or death rates were similar in the 2 groups. No deaths were observed in syncopal patients. Four patients died in the nonsyncopal group (2 of intracranial hemorrhage, 1 of retroperitoneal hemorrhage, and 1 of ischemic stroke).
CSR occurs frequently in patients undergoing CA. Moreover, 18.6% of subjects in the present series experienced syncopal episodes during the procedure. Our data provide evidence that the length of plaques and their proximity to the carotid bifurcation were significantly associated with CSR and syncope occurrence in CA patients. This is not surprising because inflation of the balloon would occur nearest to the carotid sinus in these cases, thus easily evoking carotid sinus reflexes.
Additionally, contralateral high-grade carotid stenosis may impair cerebral blood flow, thereby predisposing to syncope, but not to CSR occurrence. It is thus posited that brain hypoperfusion, regardless of bradycardia and systemic hypotension, should occur during balloon inflation in this patient group. Surprisingly, no association with decreased cerebral reserve was found using breath-holding test. The results could have been different using more accurate methods to assess cerebrovascular reserve.
In line with a previous small study,3 stent placement did not increase the risk of CSR or syncope during CA. However, a significant relationship between the use of protection devices and the appearance of syncope was evident. This finding has not been reported previously and cannot be explained by filter occlusion attributable to excised plaque material.
The benefit of using either conservative or invasive methods to treat CSR in CA patients chiefly depends on their influence on the rates of complications and periprocedural stroke. Controversy still surrounds this issue.3,4 However, no study has yet examined the impact of syncope occurring during CA on angioplasty outcomes. In our series, the appearance of syncope during the procedure was associated with a higher probability of experiencing a procedural TIA (possibly of hemodynamic origin). It should be noted, however, that syncope was not associated with an increase rate of strokes or deaths. Accordingly, all deaths were observed in nonsyncopal patients. Specifically, half of them were attributable to intracranial hemorrhage precipitated by cerebral hyperperfusion syndrome, a complication of arterial hypertension. Of interest is also the observation that the occurrence of syncope was not associated with the appearance of carotid spasm, residual stenosis, and intimal dissection. Altogether, we have shown that syncope does not have a deleterious effect on CA outcomes. Routine aggressive strategies to prevent syncopal episodes possibly could be avoided.
- Received August 9, 2007.
- Accepted August 28, 2007.
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