Is Haemodynamic Depression during Carotid Stenting a Predictor of Peri-procedural Complications?

Article Outline

• Abstract
• Patients and Methods
  • Pre-operative evaluation
    • Carotid stent procedure
    • Haemodynamic protocol
    • Definitions and peri-operative complications
      • Statistical analysis
• Results
• Discussion
• Conclusions
• Acknowledgements
• References
• Copyright

Objective

The clinical significance of Haemodynamic Depression (HD) during carotid stenting (CAS) remains unclear. The aim of this study was to analyze the frequency and predictors of HD during CAS in a single centre experience.

Methods

A prospective protocol for CAS was applied in a 15-month interval. Patients with restenosis, on betablockers, or with arrhythmias were excluded. A standardized dose of atropine (0.4mg) was given prior to stent deployment. Changes in heart rate, blood pressure, and neurological status were monitored and recorded. HD was defined as systolic pressure <90mmHg and/or heart rate <50 beats/min. Fifteen potential predictors of HD (age, gender, hypertension, smoking, diabetes, coronary artery disease, previous myocardial infarction, symptoms, degree of carotid stenosis contralateral CEA or CAS, calcified/hyperechoic plaque, plaque length, stent oversizing and type of stent) were tested in multivariate analysis.

Results

Two hundred and twenty three consecutive patients were enrolled. HD occurred in 98 cases (44%): in 68 cases HD required additional pharmacological support. At 30 days, any stroke rate was 3.1% (3 major and 4 minor), TIA rate 1.8%, myocardial infarction rate 0.4%. No deaths were recorded. No difference in complication rates were found in patients with or without HD. From regression analysis only the presence of calcified plaque (HR 9.5; 95% CI 5.0 to 18.2; p<0.0001) and the plaque length (HR 1.77; 95% CI 1.03 to 3.06; p=0.038) were associated significantly with HD.

Conclusions

HD during CAS is a common, relatively benign event, without increased risk of peri-operative complications. Careful pharmacological treatment is necessary to decrease HD and the potential complications, especially in patients with more severe calcified lesions. These results require confirmation in a separate, larger cohort.

Keywords: Carotid stenting, Haemodynamic, Complication, Atropine

Although recent randomized trials have questioned the safety of carotid artery stenting (CAS), in comparison to carotid endarterectomy (CEA), CAS is still under clinical investigation as alternative treatment for carotid stenosis, since it is less invasive and patient recovery is faster.¹, ², ³ The main risks of CAS are from cerebral embolic events with consequent neurological deficits. Furthermore, it has been ascertained that relevant haemodynamic changes, such as severe hypotension and bradycardia, may occur more frequently and seriously during CAS than during CEA, as a result of baroreflex stimulation triggered by ballooning and stenting in the region of carotid sinus. These haemodynamic depressions (HD), reported in up to 68% of cases may increase the risk of peri-procedural complications especially when patients have severe comorbidities.⁴, ⁵, ⁶, ⁷, ⁸, ⁹

The aim of the present study was to evaluate the incidence and clinical relevance of HD during CAS with respect to peri-procedural neurological and cardiac events and to investigate factors predicting the development of HD.

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Patients and Methods 

A prospective protocol was applied to assess HD in to patients undergoing CAS from March 2006 to June 2007. The institutional review board approved the study and all patients gave informed consent.

Patients with symptomatic (>60%) or asymptomatic carotid stenosis (>70%) requiring treatment were included. Patients with bilateral carotid stenosis also were included provided that there was at least a 1 month interval between the two staged endoluminal interventions. To avoid interference with spontaneous hemodynamic changes during CAS, patients with carotid restenosis or under treatment for cardiac rhythm disorders (including those with pace-makers) or treated with beta-blockers were excluded. Patients with acute or unstable symptoms also were excluded.

Pre-operative evaluation 

The pre-operative imaging studies consisted of duplex ultrasound scanning (US) and selectively Computed Tomography (CT scan or AngioCT scan). Magnetic resonance or angiography were seldom used. All US measurements were performed by previously validated operators who defined site, degree of stenosis, vessel measurements and plaque morphology, in order to correctly select devices sizes and characteristics.

Plaque morphology was recorded at the time of examination and classified, as echolucent plaques, [defined as low echogenic or non calcified plaques appearing fully black or with spotty white areas representing less than 25% of the total (Type 1 and 2 of Gray-Weale)¹⁰], or hyperechoic/calcified plaques [defined as high echogenic or calcified plaques, appearing white or almost white with anechoic areas representing less than 25% of the total (Type 3 and 4 of Gray-Weale)¹⁰]. The vessel lumen was used as the reference structure for defining echolucency; the bright echo zone produced by the media-adventitia interface was used as the reference for defining echogenicity.

Two carotid measurements were recorded on US: common carotid artery (CCA: 2cm below the bulb) and internal carotid diameter (ICA: 2cm above the carotid bulb or in the case of longer plaques distal to the plaque end). The degree of stenosis, measured by US was always confirmed with angiography at the time of CAS procedure using the North American Symptomatic Carotid Endarterectomy Trial measurements criteria.¹¹ All patients scheduled for CAS received antiplatelet therapy consisting of acetylsalicylic acid (mean dosage of 125mg/d) and clopidogrel (75mg/d) after a 300mg loading dose administered 12hours before CAS.

CAS was performed in an endovascular operating room with high quality fixed imaging system (Axiom Artis FA, Siemens). Patient neurological status was continuously monitored. Transcranial Doppler (TCD 4040 Pyoneer EME) was utilized when possible. Percutaneous transfemoral or transbrachial approaches under local anesthesia were used in all cases. Mild sedation was seldom used and general anesthesia never.

Cerebral protection devices (CPD) and self expandable stent of different models were applied in all procedures, tailored to vessel and lesion characteristics according to operator evaluation and experience. Distal filters were preferred in cases of contralateral occlusion or severe external carotid disease and endoluminal clamping systems in cases of vessel tortuosity. Pre-dilation was used selectively.

Stent size and length were chosen according to preoperative measurements of the target vessel by US examination, or by computer assisted tri-dimensional vessel reconstruction through rotational angiography. Stents were routinely post-dilated using a balloon sized for the ICA (5 to 6mm diameter balloon catheter at a pressure of 8 to 10 atmospheres for 5 seconds). A selective control angiography in at least 2 projections was performed to evaluate local and intracranial results.

Closure devices were used during the last period of the study for access control.

All patients received intrarterial pressure, cardiac and neurological monitoring throughout the procedure. According to the haemodynamic protocol, routine prophylactic atropine at a standardized dose of 0.4mg/iv was given to all the patients before stent deployment.

All haemodynamic changes were recorded. When HD became symptomatic or did not spontaneously reverse within 10”, additional haemodynamic pharmacologic treatment was applied. When additional atropine and fluid administration were not sufficient, vasopressors or inotropes were used: ethylephrine or metaraminol as a first-line drug at increased doses, and dopamine when needed.

Cardiac morbidity, based on cardiac enzymes and electrocardiographic changes or clinical evidence of congestive heart failure (CHF), were recorded.

During the first two hours after the procedure, heart rate, non invasive oxygen saturation, pressure measurements with a non invasive automated system and neurological status were continuously monitored in all patients. Subsequently these parameters were checked on an hourly basis. Enzymes and ECG were checked immediately and on the following morning. The same external audit of neurologists and cardiologists evaluated evident or suspected symptoms regardless of the occurrence of intraprocedural hemodynamic instability. When no complications occurred, patients were discharged on the first postoperative day under a standardized dual antiplatelet therapy for at least 30 days, followed by a single, lifelong antiplatelet regimen. Clinical and US examination were repeated before discharge, at 1 month, and every six months thereafter. In the case of symptoms or uncertainty after discharge, all patients were instructed to inform their practitioner or the Vascular and Endovascular Centre neurological or cardiological consultation.

Any symptomatic or asymptomatic hypotension (systolic blood pressure <90mmHg) or bradycardia (heart rate<50 beats/min), regardless of the need for adjunctive atropine, fluid support or vasopressor agents, was defined HD.

Intervention was considered successful when the procedure was completed and the residual diameter reduction from the final angiogram was <30%.

The primary outcome measure was the occurrence of any peri-procedural (within 30 days) stroke. The peri-procedural occurrence of HD, disabling strokes, death, transient ischemic attack (TIA), or myocardial infarction (MI) were secondary outcomes.

Stroke was defined as a new neurological event persisting >24hours and classified as fatal, disabling (modified Rankin Score ≥3) or non-disabling (modified Rankin Score <3). TIA was defined as any new neurological focal event with complete recovery within 24hours. MI was diagnosed in the occurrence of persistent ST changes and/or new Q wave in 2 leads or the presence of elevated enzymes (including troponin>0.1 ng/mL).

Statistical analysis 

Statistical analyses were performed using SPSS/PC version 12.00 Win package (SPSS for Windows Chicago, IL, USA 2003). Results were considered to be statistically significant at p<0.05. Baseline characteristics of patients with and without HD were compared using χ² and t tests. Patients were stratified according to the presence of HD and outcome differences were measured as Odds Ratio (OR) with corresponding 95% Confidence Interval (CI). Patients with HD requiring pharmacological support were compared to those without HD.

Logistic regression analysis was used to determine the variables that independently predicted patients developing HD and HD requiring pharmacological support. The following risk factors for HD were included in the model: age, gender, hypertension, smoking, diabetes, coronary artery disease, previous myocardial infarction, previous symptoms, degree of carotid stenosis, contralateral CEA, contralateral CAS, calcified/hyperchoic plaque, plaque length, stent oversizing and type of stent (open versus closed design). Backward stepwise logistic regression analysis was applied to selected variables in the multivariate models. Results were reported as hazard ratios (HR) with corresponding 95% CI.

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Results 

Of a total of 387 consecutive patients undergoing CAS during the study period, 223 primary carotid stenoses were eligible for inclusion in the prospective protocol for haemodynamic assessment and represent the study population.The mean age was 71±7.4 years and 69% were men. The study included both symptomatic (N=63; 28%) and asymptomatic patients (N=160; 72%).

The following CPDs were used: FilterWire EZ system, Boston Scientific, Natick, MA,USA (n 179, 80.3%); MO.MA system, Invatec, Brescia, Italy (n 19, 8.5%); Angioguard RX Filter, Johnson and Johnson-Cordis, Warren, NJ, USA (n 12, 5.3%); Emboshield Filter, Abbott Laboratories, Abbott Park, Illinois, USA, (n 5, 2.3%); Rx Accunet Filter, Guidant, Santa Clara, CA, USA (n 3, 1.3%); Rubicon Filter, Rubicon Medical Inc., Salt Lake City, UT, USA (n 3, 1.3%); SpideRX Filter, EV3, Plymouth, MN, USA (n 2, 1%). Pre-dilation was performed in 49 vessels (22%).

Self-expandable stents were close cell design/elgiloy fabric in 177 cases (79.3%) [Carotid Wallstents (Boston Scientific Corp., Natick, MA, USA)] and open cell/nitinol made in 45 (20.3%) [Precise stents (Johnson and Johnson-Cordis, Warren, NJ, USA)]. Furthermore, 1 (0.4%), multidesigned nitinol stent was used (Cristallo Ideale stent; Invatec, Brescia, Italy).

The procedure was technically successful in all 223 cases. Adverse peri-procedural events occurred in 8 patients (3.6%). There were 3 disabling (1.3%), and 4 non-disabling (1.8%) strokes, 4 TIAs and 1 MI. No deaths and no episodes of CHF were recorded within 30 days.

The overall incidence of HD was 98/223 (44%). Hypotension occurred in 68 (30.5%), bradycardia developed during 95 (42.6%) procedures, and isolated bradycardia without hypotension in 30 (13.4%). Asystole occurred in 20 patients (8.9%). In 68 of the 98 patients developing HD (69.4%) adjunctive atropine or vasopressor treatment was required.

The characteristics of patients with and without HD are shown in Table 1. Atherosclerotic hyperechoic/calcific and longer plaques were significantly more frequent in HD and HD requiring further pharmacologic support. None of the remaining clinical baseline and morphologic factors were significantly associated with HD. In particular, the rates of cardiac risk factors (history of myocardial infarction, unstable angina, or coronary disease) were similar in HD and non HD patients.

Table 1. Characteristics of patients with and without HD

HD: hemodynamic depression; MI: myocardial infarction; CEA: caratid endarterectomy; CAS: carotid artery stenting.

The distribution of clinical outcomes for patients with and without HD is shown in Table 2. There were no significant differences between patients with and without HD (or HD requiring pharmacological support) in the rates of stroke, MI, or any major adverse clinical event (Table 2). In particular, no MI or CHF occurred in the HD group. Four of 98 patients with HD showed protracted HD (persistant and requiring further support after the end of the procedure), no complications occurred in these patients. Furthermore, patients with HD did not have a longer post-operative stay due to protracted or severe HD (1.22 days for HD vs. 1.09 days for non HD group; p=0.6).

Table 2. Clinical Outcomes n patients with and without HD

HD: hemodynamic depression; TIA: transient ischemic attack; MI: myocardial infarction.

MACE: major adverse clinical events.

In multivariate analysis, the presence of hyperechoic/calcified plaque was a predictor for both HD (HR 9.5; 95% CI 5.0 TO 18.2; p<0.0001) and HD requiring further support (HR 8.1; 95% CI 3.9 to 16.92; p<0.0001). Plaque length was a more marginal predictor of HD (HR 1.77; 95% CI 1.03 to 3.06; p=0.038). There were no other significant predictors for HD or HD with support (Table 3).

Table 3. Multivariate analysis of predictors on HD and HD requiring support (Backward method)

HD: hemodynamic depression.

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Discussion 

In this study, about half (44%) of patients experienced bradycardia or hypothension during the procedure. It has been suggested that more one factor is able to trigger the baroreflex in the carotid sinus region causing haemodynamic instability during CAS. Stretch applied to carotid artery by balloon dilatation generally is accepted as transient and easily resolved. However, stents may cause prolonged pressure transmission against the carotid sinus resulting in a more pronounced baroreflex response, which may not be prevented with atropine. Furthermore, other local factors (e.g., oversizing and length of carotid stent, higher radial force from different stent design) are suggested as adjuncts able to influence the unpredictability of baroreflex response.

In our experience two types of acute HD were identifiable. The first involved transient and self-resolving episodes not requiring pharmacological adjunct to the prophylactic dose of 0.4mg/i.v. of atropine. The second pattern, that most frequently encountered (68/98), showed a prolonged and more severe course requiring vasopressors or additional atropine. Both of these patterns appeared to be unrelated to the patients' underlying cardiac condition. Other studies have suggested that patients with a history of significant cardiac risk factors may have increased baroreceptor sensitivity and are more likely to develop HD.⁷, ¹², ¹³ Others have reported age or local variables (plaque length, site, calcification, stent size and contralateral stenosis) as predictors of increased dysfunction of baroreceptors.¹⁴, ¹⁵, ¹⁶, ¹⁷

Our data suggest that only local factors (highly calcified and longer plaque) are associated with a higher probability of HD (HR 9.59; 95% CI 5.0 to 18.26; P<0.0001 and HR 1.77; 95% CI 1.0 to 3.0; P<0.038). Presumably, heavily calcified plaques are more prone to HD because the baroreceptors, usually exposed to dampened pressure waves, receive a sudden and extraordinary stimulation by radial force due to balloon dilation.¹⁸ The longer the plaque, the higher the number of baroreceptors dampened. It has also been suggested that calcified plaques require more aggressive balloon inflation, triggering an amplified baroreflex response. However, in this study inflation pressure ranges were too narrow (6-8 atmospheres for a maximum of 5 seconds) to justify such an hypothesis. Nevertheless,, even in severe HD there was no increased risk of adverse cerebrovascular or cardiac events. Other local factors (oversizing of stented artery, higher radial force from close cell elgiloy fabric, contralateral occlusion) were not associated to higher probability of HD in our study. It could be that the effect of these variables on baroreflex response is minor and may be easily controlled with prophylactic doses of atropine and accuracy in deployment manoeuvres.

There has been considerable debate in literature with regards to HD as a predictor of adverse events. Some studies have suggested that HD may lead to a greater incidence of peri-procedural complications, and even death.⁶, ⁹, ¹⁴ However, in other studies only few patients developing HD experienced complications from CAS.⁴, ¹⁶ Our results support these latter findings. Patients with HD, a common condition, did not show any increase in cardiac or neurological adverse events. Cayne et al. found an overall 33% incidence of hypotension/bradycardia with no evidence of clinical stroke or death over 75 CAS patients, and cardiac morbidity was reduced by the use of prophylactic atropine.⁴ On the other hand, Gupta et al., on 500 CAS, found an increased probability not only of peri-procedural stroke (OR 3.34; 95%CI 1.13 to 9.90) but also of myocardial infarction and death (OR 3.05; 95%CI 1.35 to 5.23; P<0.02) in patients with “persistent HD” requiring continuous vasopressor infusion.⁸

The differences in study results are obviously due to several factors such as patient selection and the criteria used to define the severity and persistency of HD. Furthermore, haemodynamic changes in CAS patients at higher surgical risk, because of severe coronary or controlaterateral carotid disease, may skew the occurrence of clinically relevant events. The diminished cardiovascular reserve and the comorbidities inherent to this particular patient population mandate the effort to optimize the haemodynamic status prior, during, and after the procedure.

This study did not support intra-operative hypotension as a predictor of post-operative hypotension, as reported by others.⁷, ¹³ Hypotension was protracted in only a few cases (n=4) and did not expose patients to increased post-procedural risk of stroke or longer hospital stay.

The mechanism for stroke in patients who experience periprocedural HD, as reported by other studies, is presumed due to hypotension that decreases the washout of embolic debris (originating from balloon inflation and stent delivery) in the distal intracranial circulation and dampens the appropriate collateral flow from ischemic territories.¹³, ¹⁹ Appropriate experience in preventing embolic events as well as quick intervention of trained anesthesiologists play a crucial role in achieving a good outcome in patients experiencing HD.²⁰

Invasive monitoring of haemodynamic changes was discontinued after the procedure, however non invasive control of haemodynamic and neurological status was maintained throughout the whole postoperative period, giving enough time to detect all the relevant HD changes which might have occurred.

Some kinds of patients (i.e. restenosis, on beta-blockers, etc.) were excluded from the protocol because in this group HD changes may be undetectable or unreliable.¹³ However, the peri-procedural risk found in the study population was comparable to that shown in the entire 387 CAS cohort of the study period: overall major complication rate 15/387 (3.78%); disabling stroke rate 6/387 (1.55%); non-disabling stroke rate 7/387 (1.8%); myocardial infarction 2/387 (0.5%). This could suggest that prophylactic atropine effects the same level of decreased baroreceptors sensitivity as obtained by previous surgical removal (restenosis after CEA) or pharmacological block.

Since all patients received a prophylactic low dose of atropine, we cannot assess the potential effect of this drug in preventing HD in comparison to other treatment regimens. However, the prophylactic use of atropine has been incorporated in many CAS protocols and recommended by AHA Consensus document.²¹

Potential limitations include the small number of recorded adverse outcomes, which reduces the predictive ability in multivariate models, and the lack of a specific calcium score to assess the stiffness of carotid plaque.

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Conclusions 

The incidence of HD during CAS is high, particularly in the presence of calcified and long carotid plaques. No other clinical or technical factors appear to influence the occurrence of HD, Baroreflex response, as a physiologic response, cannot be inhibited by drug treatment. HD (even when severe or long) does not appear to predispose to peri-procedural adverse events. Early recognition of HD (e.g., presence of long, calcified plaque) and prompt treatment play a crucial role in achieving good CAS outcomes.

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Acknowledgements 

We would like to thank Francesca Zannetti and Eileen Mahoney for editorial assistance.

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