Periprocedural Monitoring with Regional Cerebral Oxygen Saturation in Carotid Artery Stenting

Summary

Hemodynamic instability during and after carotid artery stenting (CAS) may reduce cerebral blood flow (CBF), leading to cerebral ischemia. To investigate changes in CBF in the periprocedural period, we continuously recorded the regional cerebral oxygen saturation (rSO2) using near-infrared spectroscopy.

In 46 consecutive patients with carotid artery stenosis, rSO2 was continuously recorded during and after CAS. In addition, the patients underwent SPECT to evaluate a change in CBF on the next day after CAS.

Introprocedural bradycardia (heart rate <50 bpm) occurred in 21 patients (46%) including one transient cardiac arrest. Intraprocedural hypotension (systolic blood pressure <80 mmHg) occurred in 18 patients (39%), and 16 of them showed prolonged hypotension. The rSO2 in patients with bradycardia/hypotension during CAS was significantly less than that in patients without them (p<0.01). Moreover, the SPECT on the next day after CAS demonstrated that the ipsilateral CBF in patients with bradycardia/hypotension during CAS significantly more than that in patients without them (p<0.05).

Intraprocedural hemodynamic instability resulted in a significant decrease in rSO2, leading to a possible severe cerebral ischemia. In addition, intraprocedural bradycardia/hypotension might be related with postprodedural hyperperfusion, causing the morbidity and mortality after CAS.

Introduction

Carotid artery stenting (CAS) has been introduced as an alternative to carotid endarterectomy for the treatment of carotid artery stenosis^1-4. Although the safety of CAS has been supported by the recent SAPPHIRE trial³, bradycardia and hypotension often occur during and after CAS ^5-11, and they might cause severe cerebral ischemia, leading to the morbidity and mortality⁶. However, there have been not enough informations about cerebral blood flow on such an occasion as bradycardia/hypotension during CAS procedures. Therefore, we continuously recorded the regional cerebral oxygen saturation (rSO2) using nearinfrared spectroscopy to investigate changes in cerebral blood flow in the periprocedural period of CAS.

Material and Methods

Between January 2004 and December 2005, CAS procedures were attempted at our hospital in 46 consecutive patients (40 men, six women, ranging in age from 48 to 82 years; mean age 70.7 years). Blood pressure and heart rate were monitored continuously throughout the procedure. The blood pressure was measured at five-minute intervals by an automated-cuff-inflation sphygmomanometer. Bradycardia was defined as heart rate less than 50 beats per minutes, and was treated with intravenous atropine sulfate. Hypotension was defined as systolic blood pressure less than 80 mmHg, and was treated with intravenous ephedrine hydrochloride.

The rSO2 was continuously recorded using INVOS 4100 near-infrared spectrophotometers (Somanetics Corporation, Troy, MI, USA) during and after CAS. The rSO2 sensor was attached on the forehead of a surgical side to evaluate cerebral oxygen saturation, which can reflect cerebral blood flow (CBF) when the cerebral metabolism is stable ^12,13. In addition, single photon emission computed tomography (SPECT) was performed to evaluate a change in CBF on the next day after CAS.

In the interventional neuroradiology suite, CAS was performed using a transfemoral approach under cerebral protection afforded by a PercuSurge GuardWire (Medtronic Inc., Santa Rosa, CA, USA) balloon occlusion device. After the occlusion balloon was inflated in the distal ICA, the lesion was pre-dilated, and a self-expandable stent was deployed. Then, the blood was aspirated through the aspiration catheter, and the protection balloon was deflated. After evaluating a diameter of the lesion with intravascular ultrasound sonography, the protection balloon was inflated again, and post-dilatation was cautiously performed. A final angiogram was obtained to confirm that the dilatation was adequate and no local complications such as dissection occurred.

Results

During CAS, HR significantly decreased from 82.8 ± 2.7 to 59.6 ± 3.8 (bpm, mean ± SE) (n = 46, p<0.001), and SBP significantly decreased from 137.8 ± 3.3 to 95.2 ± 4.7 (mmHg) (n=46, p<0.001) (figure 1A, 1B). Bradycardia (<50 bpm) occurred in 21 cases (46%) of the patients, including a case of cardiac arrest, and hypotension (<80 mmHg) occurred in 18 cases (39%) of them. Moreover, in 16 cases of them, the hypotension prolonged after CAS, and intravenous norepinephrine was continuously injected to maintain blood pressure.

Figure 1.

Changes in HR (A) and SBP (B) during CAS. HR significantly decreased from 82.8 ± 2.7 to 59.6 ± 3.8 (bpm) (n = 46, p<0.001), and SBP significantly decreased from 137.8 ± 3.3 to 95.2 ± 4.7 (mmHg) (n= 46, p<0.001).

The rSO2 showed significant changes during the periprocedual period (figure 2). In all 46 cases, a baseline of rSO2 before the procedure was 61.6 ± 0.8%. During only test occlusion with a PercuSurge GuardWire, the rSO2 significantly decreased to 58.2 ± 0.9% (p<0.001). Then, just after post-dilatation, the rSO2 significantly dropped to 52.1 ± 1.4% (p<0.001). The decrease in rSO2 after post-dilataion in eight cases with bradycardia and hypotension (13.4 ± 1.5 points) was significantly more than that in nine cases without both of them (4.9 ± 1.1 points) (p<0.01) (figure 3).

Figure 2.

Changes in rSO2 during CAS procedures. In all 46 cases, a baseline of rSO2 before the procedure was 61.6 ± 0.8%. During only test occlusion with a PercuSurge Guard-Wire, the rSO2 significantly decreased to 58.2 ± 0.9% (p<0.001). Then, just after post-dilatation, the rSO2 significantly dropped to 52.1 ± 1.4% (p<0.001).

Figure 3.

Influences of bradycardia/hypotension on rSO2 after post-delation. The decrease in rSO2 after post-dilataion in eight cases with bradycardia and hypotension (13.4 ± 1.5 points) was significantly more than that in nine cases without both of them (4.9 ± 1.1 points) (p<0.01) (p<0.01).

The ipsilateral CBF (%) on the next day after CAS was calculated by a ratio of CBF on the ipsilateral to contralateral side of the CAS. In cases that showed a vascular reserve less than 30% in SPECT before CAS, the ipsilateral CBF in seven cases with bradycardia and hypotension (109.8 ± 4.9%) was significantly more than that in nine cases without both of them (96.5 ± 8.3%) (p<0.05) (figure 4).

Figure 4.

Relationship between intraprocedural bradycardia/hypotention and postprocedural hyperperfusion. In cases that showed a vascular reserve less than 30% in SPECT before CAS, the ipsilateral CBF in seven cases with bradycardia and hypotension (109.8 ± 4.9%) significantly more than that in nine cases without both of them (96.5 ± 8.3%) (p<0.05).

Discussion

Distension of the carotid bulb leads to stimulation of the baroreceptor, which increases parasympathetic stimulation to the heart causing bradycardia, and inhibits sympathetic stimulation to the blood vessels causing hypotension ¹⁰. In previous reports, hemodynamic instability including bradycardia and hypotention often occurred during and after CAS ^5-11. Also in our studies, bradycardia (<50 bpm) and hypotension (<80 mmHg) occurred during CAS in 46% and 39%, respectively. Since patients with the hemodynamic instability are at a significantly increased risk of a periprocedual major adverse clinical events or stroke ⁶, it is important to perform the rapid recovery from bradycardia/hypotension and the prophylactic management avoiding them.

The regional cerebral oxygen saturation (rSO2) indicates a change in the balance between the oxygen supply and demand using near-infrared spectroscopy. In a stable state of cerebral metabolism, therefore, rSO2 demonstrates the oxygen supply, which can reflect CBF, under the sensor^12,13. In our previous studies on rSO2 changes in balloon test occlusion for giant aneurysm surgery¹⁴, we showed that a decrease in rSO2 during the balloon occlusion was significantly related with a decrease in CBF measured by SPECT. Also in CAS, it is believed that a change in rSO2 can indicate a change in CBF. However, no reports have demonstrated intraprocedural monitoring of rSO2 in CAS, although there have been a lot of studies on rSO2 changes in carotid endarterectomy (CEA)¹⁵. In the present study, we showed that the rSO2 during CAS in patients with bradycardia and hypotension significantly less than that in patients without both of them (p<0.01). That is, bradycardia/hypotension can cause a decrease in CBF, which might induce severe cerebral ischemia, resulting in the morbidity and mortality in CAS.

There have been few reports demonstrating a change in CBF after CAS. Henry et Al¹⁶ reported that the incidence of cerebral hyperperfusion syndrome was 3.5% in their series of 57 patients. Meyers et Al ¹⁷ demonstrated the incidence of the syndrome was 5% in 140 patients. In the present study, hyperperfusion syndrome occurred in one (2.8%) of all 46 patients. When ipsilateral hyperperfusion is defined as a state with CBF more than 110% over the contralateral hemisphere in SPECT on the next day after CAS, it occurred in seven (24.1%) out of 29 patients in our series. Interestingly, in patients that showed a vascular reserve less than 30% in SPECT before CAS, the ipsilateral CBF after CAS in patients with bradycardia and hypotension during CAS significantly more than that in patients without both of them (p<0.05). Therefore, intraprocedual bradycardia/hypotension, even if the recovery from them is rapid, may be related with hyperperfusion after CAS. We believe that prevention of bradycardia/hypotension as well as rapid recovery from them during CAS is important to reduce the morbidity and mortality after CAS.

Conclusions

In 46 consecutive patients treated with CAS, we demonstrated that patients with bradycardia/hypotension during CAS showed a significant rSO2 decrease compared with patients without them.

In addition, intraprocedural bradycardia/hypotension might be related with postprodedural hyperperfusion measured by SPECT. It is conceivable that prevention of bradycardia/hypotension as well as rapid recovery from them during CAS is important to reduce the morbidity and mortality after CAS.