Prevention of Hemodynamic Instability in Extra-Cranial Carotid Angioplasty and Stenting Using Temporary Transvenous Cardiac Pacemaker
Hemodynamic instability is a common condition during extra-cranial carotid angioplasty and stenting (CAS). We evaluated the safety and efficacy of prophylactic placement of temporary cardiac pacemaker during extra-cranial CAS for the prevention of hemodynamic instability. For this, forty-seven carotid artery stents were deployed in 41 high-risk patients. Temporary transvenous cardiac pacemakers were inserted before CAS procedure. The pacers were set to capture a heart rate <60 bpm. Clinical symptoms, blood pressure, heart rate, and pacing activation were monitored and data were collected. We found that pacing occurred in 25 carotid lesions during balloon predilatation; pacemakers were activated transiently in 25 patients. The longest pacing continued for 1 day. Among cases with pacemaker activation, 1 patient developed post-procedural symptomatic hypotension that lasted for 4 days. No related complications were observed. It was, therefore, concluded that pacing was technically effective in producing electrical ventricular responses and was hemodynamically effective in 25 carotid lesions which underwent balloon predilatation. The prophylactic use of a temporary transvenous cardiac pacemaker during CAS was rapid and effective in controlling peri-operative hemodynamic instability and preventing stroke and other complications. The prophylactic use of temporary pacemaker is particularly recommended for patients at high risk for developing hemodynamic instability.
KeywordsPacemaker Carotid artery Angioplasty Stent Bradycardia CAS
Carotid angioplasty and stenting (CAS) is widely recognized as a minimally invasive, safe, and effective therapeutic strategy for carotid stenosis [1, 2, 3]. Bradycardia, hypotension, and subsequent hemodynamic depression frequently occur during and after the CAS procedures. Pre-medication with atropine before and during the procedure cannot effectively correct hemodynamic instability. Prophylactic placement of temporary transvenous cardiac pacemaker is a feasible adjunct therapy to control peri-procedural hemodynamic changes [4, 5, 6]. At our department, 41 patients undergoing CAS procedures were enrolled in this study during the time period from January 2009 to July 2011. Temporary transvenous pacemakers were inserted before CAS procedure. Herein, we report that the prophylactic use of a temporary transvenous cardiac pacemaker during CAS was rapid and effective in controlling peri-operative hemodynamic instability and preventing stroke and other related complications.
Subjects and Methods
Study Design and Patients
Baseline characteristics of patients
Age: >70 years
Right/left side carotid stenting
Internal carotid artery TIA
Coronary artery disease
Lesions underwent balloon predilatation
Straight self-expanding stent
Tapered self-expanding stent
Inclusion Criteria for CAS
Patients with symptomatic carotid stenosis of ≥50 % and symptomatic or asymptomatic stenosis of ≥70 % were included in this study according to the NASCET criteria . Carotid artery stenosis was documented by color Doppler ultrasound, computed tomography angiography, and digital subtraction angiography (DSA). A written informed consent was obtained from each patient or from the next of kin in the family. The study was approved by the institutional ethics committee.
All patients were subjected to complete medical examination (including chest X-ray, electrocardiogram, blood test, biochemical test, renal function, blood lipids, blood glucose, coagulation function test, and routine urine/fecal examinations) to exclude severe cardiovascular, liver, pulmonary, or renal insufficiency. Carotid artery stenosis was evaluated and verified by Doppler ultrasound, computed tomography angiography, and DSA. Patients received oral administration of aspirin (325 mg/day) and clopidogrel (75 mg/day) for 3–5 days before the procedure. Intramuscular injection of 0.1 g phenobarbital sodium was given to patient 0.5 h before the procedure.
Temporary Pacemaker Placement
The pacemaker insertion was performed under local anesthesia using 1 % Lidocaine HCl injection at sterile groin area with the patient in supine position. The access was made into the left femoral vein via Seldinger technique. The electrode of temporary pacemaker (Viitatron, MEP2000) was advanced to the right ventricular apex. The pacing electrodes were connected. The pacemaker was set to demand mode in which pacing is initiated when the patient’s intrinsic heart rate becomes slower than 60 beats per min.
Carotid Angioplasty and Stenting Protocol
Under local anesthesia by 1 % Lidocaine HCl injection, 8F vascular sheath was placed in the femoral artery. Heart rate, blood pressure, blood oxygen saturation, and respiratory rates were monitored continuously throughout the procedure. An intravenous bolus of heparin (2–3 mg/kg) was given during the procedure and Nimodipine was administered intravenously to prevent vasospasm. The 8F guiding catheters which were exchanged for 300 mm. 018 guiding wires were positioned in the common carotid artery. A cerebral embolic protection device (Angioguard, Cordis, USA; Spide RX, eV3, USA) was placed at the distal part of cervical segment of the internal carotid artery. Appropriate size balloon and stent were selected after measuring the diameters of common carotid artery and internal carotid artery. The balloon predilatation or stent placement was achieved by following the guiding wire of the embolic protection device. Post-stent inflation was performed after the stent insertion if the vascular expansion at the stenosis was not satisfactory. In the case of bilateral stenosis, the CAS was performed by the same procedure on the other side of the carotid artery.
The National Institute of Health Stroke Scale status was routinely performed during the procedure. After completion of the procedure, intracranial angiography was performed to evaluate the local result, to examine the intracranial blood circulation and exclude the major branch vessel embolic occlusions. The temporary pacemakers were removed within 24 h after the procedure.
Blood pressure was measured in one arm using an automated sphygmomanometer at 5-min intervals during the procedure and at every minute during balloon inflation and stent placement. Heart rate and blood pressure were monitored after the procedure and any episodes of hypotension (systolic blood pressure <90 mmHg and/or average blood pressure <50 mmHg) or bradycardia (heart rate <60 bpm) in the post-procedural period were recorded. Oral administration of aspirin (200 mg/day) and clopidogrel (75 mg/day) were prescribed to patients at least 3 months after the procedure.
Pacemaker implantation in carotid angioplasty and stenting (CAS) patients
Pacemaker activation during balloon predilatation
Pacemaker activation during stent implantment
Association with hypotension
Atherosclerotic stenosis of carotid artery is the most common cause of stroke. CAS is widely recognized as a safe and effective treatment available. Hemodynamic complications due to the increased activity of carotid sinus are the most common events observed in response to CAS, occurring in 7–76 % of patients [5, 6, 8, 9, 10, 11, 12]. The hemodynamic change is probably mediated through dysfunction of the adventitial baroreceptors due to balloon dilation and stent placement in the vicinity of carotid sinus during CAS procedures. It may lead to intra- and post-procedural bradycardia and hypotension, often resulting in serious complications such as asystole, cardiac arrhythmias, stroke, and other cardiovascular and cerebrovascular complications . The ability of adjusting blood pressure within the normal range is highly dependent on the function of carotid baroreceptors. Previous studies have demonstrated a decreased sensitivity of carotid baroreceptors in patients with carotid artery atherosclerosis [14, 15]. Under normal circumstances, the adjustment of blood pressure by carotid sinus is temporary and lasts only a few minutes. However, the adaptation of baroreceptors to mechanical changes is slow and incomplete. Therefore, hemodynamic instability may occur during or after CAS procedure and last for over 2 weeks after the CAS procedure [5, 16].
The previous studies investigating the factors associated with hemodynamic depression after CAS reported that old age, eccentric fibrous calcified plaque at a distance within 10 mm from the carotid bifurcation, low baseline heart rate, prior history of coronary heart disease, patients with compromised ejection fraction, and right carotid stenting were involved as the possible risk factors [16, 17, 18, 19]. It was also reported  that Valsalva ratios (VRs) testing autonomic dysfunction could be used as a measure for predicting the hemodynamic instability before CAS. The most recent carotid revascularization endarterectomy versus stenting trial study  showed that the patients over 70 years had higher risk of peri-procedural stroke with CAS than with carotid endarterectomy (CEA). The mechanisms underlying the increased risk with CAS in very elderly patients probably include factors such as aging of vascular and myocardial cells, degeneration of cardiac conduction system, and significant reduction of pacing cells in sinus node. All of these factors pre-dispose to post-CAS hypotension and bradycardia which lead to persistent hypoperfusion of the brain and thus reduce the ability of the blood flow to clear emboli and microemboli from supply arteries which increases the risk of peri-operative stroke [13, 21]. However, post-procedural hypotension and bradycardia occur more commonly with CAS than CEA [22, 23].
Atropine is widely used to prevent or treat the intra-procedural and post-procedural CAS-induced bradycardia. Meanwhile, atropine, to some extent, reduces the incidence of hypotension . In the case of patients with afore-mentioned high-risk factors, pharmacological therapy, however, has certain limitations. First, administration of atropine at or before onset of CAS-induced bradycardia requires a lag period to take effect. Second, due largely to individual differences, the medication dosage is difficult to be well-controlled and, thus, heart rate and blood pressure cannot be effectively corrected. Third, other complications, such as confusion, urinary retention, and arrhythmia, have been detected in older patients with comorbidity of coronary artery disease . Temporary cardiac pacemaker can help keep stable heart rate and thus it is an effective supplementary therapy to medication.
Several small sample size studies involving the use of temporary pacemaker during CAS showed that temporary cardiac pacing could effectively reduce the incidence of peri-procedural hemodynamic instability-related complications in high-risk patients [4, 12, 26, 27]. In this retrospective study, we found that 41 out of 452 (9.1 %) patients undergoing CAS received temporary pacemakers. Twenty-eight out of 41 (68.3 %) patients were over 70 years old. Six out of 41 (14.6 %) patients received bilateral CAS. Ten out of 41 (24.4 %) patients had a previous history of coronary artery disease. Three out of 41 (7.3 %) patients developed bradycardia before the procedure. Pre-operative ultrasound evaluation of carotid atherosclerotic plaques showed the prevalence of 51.1 % echo-lucent plaque. Balloon predilatation was performed in 53.2 % of carotid artery lesions. We observed that the pacemakers were activated during balloon predilatation and stent insertion. No pacing was delayed. After the removal of pacemakers, several patients developed asymptomatic bradycardia and hypotension which were treated by administration of atropine and dopamine. No hemodynamic instability-induced cerebral or cardiac complications were observed. Persistent hypotension lasting for 4 days and bradycardia lasting for 3 days occurred in one patient. Analysis shows that a balloon-expandable stent was placed in this patient. The instant expansion of the stent produced sustained stimulation of carotid sinus which led to persistent hypotension and bradycardia. Regarding 3 patients receiving conical-tapered self-expanding stents, the pacemakers were activated transiently upon balloon predilatation. Hemodynamic instability did not occur before or after stenting. The underlying mechanism might relate to the design of the tapered stent which better conforms to the anatomy of the common carotid artery and thus the stent causes less mechanical stimulation to the carotid sinus.
Hemodynamic instability is a common peri-procedural complication of CAS. Persistent hemodynamic damage increases the incidence of post-procedural cardiovascular and cerebrovascular adverse events, especially in high-risk patients. Therefore, pre-operative evaluations as well as interventional and post-operative close monitoring of ECG and blood pressure are particularly important. In view of the previous and present results, we suggest that the following high-risk factors for peri-operative hemodynamic damage may be regarded as possible indications for the placement of temporary pacemaker, e.g., (1) old age; (2) severe bilateral carotid stenosis after bilateral CAS; (3) prior coronary artery disease and compromised ejection fraction; (4) a heart rate of lower than 60 beats per min with existing atrioventricular block or premature ventricular contraction; (5) eccentric fibrous calcified plaque or mixed plaque within 10 mm from the carotid sinus; and (6) a need for balloon predilatation or post-stent balloon inflation during CAS. Atropine and dopamine remain as the major treatment for hemodynamic instability.
In summary, for high-risk patients, prophylactic placement of temporary pacemaker can rapidly and effectively correct the hemodynamic change and prevent the peri-operative stroke and other complications. However, the complications after insertion of temporary pacemaker, such as deep vein thrombosis and infection, will limit its application. Nonetheless, more studies with larger sample size will be required to validate these findings.
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