Acta Neurochirurgica

, Volume 159, Issue 11, pp 2081–2087 | Cite as

Prolonged hypotension after carotid artery stenting: incidence, predictors and consequences

  • Elif Gökçal
  • Elvin Niftaliyev
  • Çiğdem Deniz
  • Mehmet Ergelen
  • Vildan Güzel
  • Ömer Göktekin
  • Talip Asil
Original Article - Vascular



Hemodynamic changes frequently occur after carotid artery stenting (CAS), and in some patients these changes, particularly hypotension, may be prolonged. There are discrepant results for predicting patients at high risk for these prolonged hemodynamic changes and identifying the effect on clinical outcome. In this study, we aimed to determine the frequency, predictors and consequences associated with prolonged hypotension (PH) after CAS in our center.


We retrospectively analyzed the demographics, risk factors, nature of carotid disease, degree of stenosis of both internal carotid arteries, stent diameter and site of dilatation during stenting in 137 CAS procedures. After CAS, duration of hospital stay, complications during hospital stay and major vascular events or death in a 3-month period were evaluated. PH was defined as a systolic blood pressure <90 mmHg lasting more than 1 h despite adequate treatment after CAS.


PH occured in 23 (16.8%) patients. The presence of contralateral stenosis ≥70% and absence of diabetes mellitus were significantly associated with PH. Duration of hospital stay was significantly longer in patients with PH. No patients with PH had a periprocedural complication or major vascular events in the follow-up period.


PH was more prevalent in patients with contralateral high-degree carotid stenosis and patients without diabetes mellitus after CAS. PH did not cause any post-procedural complications or major vascular events at follow-up, but it resulted longer hospital stays. Further studies are needed to better define the pathophysiologic mechanisms underlying these hemodynamic alterations.


Carotid artery stenting Prolonged hypotension Predictive factors Consequences 


Carotid angioplasty and stenting (CAS) have been increasingly used in the treatment of extracranial internal carotid artery (ICA) stenosis with the advantage of offering less invasiveness compared to carotid endarterectomy (CEA). However, hemodynamic changes may occur frequently during CAS [8]. Baroreceptors located in the carotid sinuses play a significant role in the regulation of blood pressure and heart rate [14]. Stretching of the baroreceptors during CAS may lead to the development of hypotension and bradycardia as a result of reduced sympathetic tonus and increased parasympathetic output [17]. Studies exploring the predictive factors for hemodynamic depression during or after CAS and its association with post-procedural complications and major vascular events at follow-up have discrepant results [2, 13, 27, 30].

In this study, we aimed to investigate the frequency, predictors and consequences of prolonged hypotension [PH, defined as systolic blood presure (SBP) below 90 mmHg >1 h despite the adequate intravenous fluid and/or vasopressor treatment] after CAS.

Methods and materials

Between April 2012 and April 2015, we retrospectively identified patients who underwent a CAS between 2012 and 2015 at the Neurology and Cardiology Departments of Bezmialem Vakıf University.

Carotid stenting was performed for symptomatic patients (having a history of stroke attributed to the relevant carotid artery) with a stenosis ≥50% and to asymptomatic patients (without any stroke history) with a stenosis ≥70%. Among those patients with symptomatic carotid disease, subjects with a history of transient ischemic attack (TIA) or ischemic stroke were identified. The National Institute Health Stroke Scale (NIHSS) scores were estimated based on the findings of the pre-stenting neurologic examination in those with ischemic stroke. Also, the duration of time (days) from the clinical presentation to CAS procedure was calculated in patients with symptomatic carotid stenosis. Demographics and vascular risk factors of all patients were recorded. The following criteria were considered for the presence of vascular risk factors: a history of hypertension (HT) or an observed SBP >140 mmHg and/or diastolic BP >90 mmHg, presence of a history of diabetes mellitus (DM) or a fasting glucose exceeding 126 mg/dl out of the acute phase, a positive history of hyperlipidemia (HL) or a fasting total cholesterol >200 mg/dl, low density lipoprotein (LDL) >130 mg/dl and/or a triglyceride (TG) >180 mg/dl. Data for the presence of coronary artery disease (CAD), coronary artery bypass grafting (CABG), smoking and previous history of stroke were retrieved from patients’ clinical charts.

All patients undergoing CAS received 100 mg of acetylsalicylic acid (ASA) and 75 mg of clopidogrel for a minimum duration of 7 days before the procedure. Regular anti-hypertensive therapy was continued. The procedure was performed by an interventional cardiologist or an interventional neurologist. Atropine sulfate at a dose of 100 mg was given to all patients during the procedure. Also 4000 to 5000 U of heparin (70 U/kg) was administered after femoral artery puncture, followed by an additional heparin dose of 2000 U during the procedure. After the procedure, BP of patients was measured hourly for at least 24 h. Patients having an SBP below 90 mmHg were initially given intravenous fluids. Intravenous vasopressor therapy such as dopamine or vasopressin was administered in those with persistence of hypotension despite intravenous fluids. All patients were treated with 100 mg of ASA and 75 mg of clopidogrel at least for 3 months after CAS.

The severity of stenosis of ICA was evaluated by catheter angiography before the procedure and defined on the basis of NASCET (North American Symptomatic Carotid Endarterectomy Trial) criteria [19]. The severity of the stenosis in the contralateral carotid artery was assessed by using computed tomography (CT) angiography if the evaluation of the contralateral carotid artery was not performed by catheter angiography. The diameter of the stent used and the site of dilatation during CAS were identified.

Persistence of SBP below 90 mmHg for more than 1 h despite adequate treatment after the procedure was considered PH. Post-procedural complications, duration of hospital stay and major vascular events such as myocardial infarction (MI), peripheral vascular disease, stroke or death within the first 3 months of follow-up were retrieved from patient records. In patients with inadequate data retrieval, phone calls were made to gather information on de novo occurrence of vascular conditions.

A total of 206 CAS procedures were identified between 2012 and 2015. Patients were excluded if they had significant missing data in clinical charts, received intravenous antihypertensive treatment before the procedure due to the presence of severe hypertension or were given general anesthesia during the procedure.

Patients with or without PH were compared regarding demographic, clinical and technical variables as well as major vascular events during the follow-up period. SPSS (Statistical Package for Social Sciences) for Windows Version 23 software was used for statistical analyses. Mean, minimum, maximum and percentage values were calculated for descriptive data. The Pearson chi-square test was used to compare the differences in categorical variables. Student’s t-test or Fischer’ exact test was used for numerical variables. Multivariate analyses were performed with multiple logistic regression to determine the independent factors (p < 0.1 in the univariate analysis) associated with PH. Statistical significance was set at p <0.05.


The mean age of 137 patients was 67.79 ± 8.2 years (range: 47–82). There were 107 male (78.1%), and 30 female (21.9%) patients. HT, DM, CAD, CABG and HL were present in 84.7%, 33.6%, 44.5%, 19% and 50.4% of the patients, respectively; 26.3% of patients were smokers.

Stenting was performed for asymptomatic carotid stenosis in 34 patients (24.8%), for TIA in 22 (16.1%) and for ischemic stroke in 81 (59.1%). NIHSS scores of patients with ischemic stroke ranged between 0 and 8, with a mean value of 2.78 ± 1.9. In patients having TIA or ischemic stroke, the procedure was performed within 1 to 2 weeks after the index event in 20 patients (14.6%), 2 to 4 weeks in 28 (20.4%), 4 to 8 weeks in 20 (14.6%) and after 8 weeks in the remaining 35 patients (25.5%). Twenty patients (14.6%) had a past history of stroke, and of these four patients had undergone endarterectomy or CAS before.

Stenting was performed on the right ICA in 72 (52.6%) and on the left ICA in 65 (47.4%) patients. The mean degree of stenosis on the ipsilateral ICA was 87.1 ± 10, whereas it was 49.2 ± 34 on the contralateral side. In 20 patients (14.6%), the contralateral ICA was completely occluded.

Prolonged hypotension was present in 23 patients (16.8%). The mean of the duration of PH was 19.8 ± 12.6 h (range between 4 and 44 h). Table 1 depicts the demographic characteristics of patients with or without PH. The incidence of PH was significantly lower in patients with DM than in those without DM (p < 0.04). Of 46 diabetic patients, the mean of HbA1c was 7.25 ± 1.5. 33 patients (71.7%) who were being treated with oral antidiabetic medications and 8 (17.4%) with insulin. The remaining five diabetic patients (10.9%) were not using any medication for DM regularly. Only three patients (6.5%) had PH in diabetic patients. Of these, two were being treated with OAD and one with insulin, and the mean of HbA1c was 6.79 ± 1.0.
Table 1

Demographics and vascular risk factors of patients with and without hypotension


Patients with hypotension (n = 23)

Patients with normal blood pressure (n = 114)


Age, mean ± SD

68 6.3

67 8.5




3, 13%

27, 23.7%



20, 87%

87, 76.3%



19, 82.6%

97, 85.1%


Diabetes mellitus

3, 13%

43, 37.7%



13, 56.5%

56, 49.1%


Coroner artery disease

8, 34.8%

53, 46.5%



6, 26.1%

20, 17.5%



7, 34.9%

29, 254%


Clinical and technical variables were compared in Table 2. In patients with a contralateral stenosis of ≥70%, PH occurred significantly more frequently (p = 0.02). No significant differences were detected regarding the site of the procedure, degree of stenosis, indications for the procedure, timing of the procedure in those with symptomatic carotid disease, past history of stroke and presence of contralateral occlusion. Also the groups were comparable in terms of stent diameter and site of dilatation. The total length of hospital admission was significantly longer among those with PH (p = 0.000).
Table 2

Clinical characteristics, technical variables, degree of stenosis and hospital stay in days in patients with hypotension and normal blood pressure


Patients with hypotension (n = 23)

Patients with normal blood pressure (n = 114)


Nature of carotid disease


6, 26.1%

28, 24.6%



3, 13%

19, 16.7%

 Symptomatic stroke

14, 60.9%

67, 58.8%

Stroke history

3, 13%

17, 14.9%


Site of stenting


14, 60.9%

58, 50.9%



9, 39.1%

56, 49.1%

Degree of ipsilateral stenosis, mean ± SD

87 ± 11

87 ± 10


Contralateral stenosis ≥70%

12, 54.5%

32, 28.3%


Contraleral occlusion

5, 21.7%

15, 13.2%


Time to stenting

 1–4 weeks

7, 41.2%

41, 47.7%


 >4 weeks

10, 58.8%

45, 52.3%

NIHSS before stenting, mean ± SD

3 ± 1.9

2.77 ± 1.9


Hospital stay, days, mean ± SD

4.8 ± 2.5

2.6 ± 2.4


Site of dilatation


16, 69.6%

74, 64.9%



2, 8.7%

17, 14.9%


2, 8.7%

11, 9.6%

Stent diameter

 ≤8 mm

14, 60.9%

73, 64%


 >8 mm

9, 39.1%

41, 36%

Contralateral stenosis ≥70% (p: 0.037, odds ratio: 1.017, 95% confidence interval: 1.001–1.032) and absence of DM (p: 0.012, odds ratio: 0.107, 95% confidence interval: 0.019–0.607) emerged as independent risk factors for the development of PH in the logistic regression analysis.

Re-occlusion occurred in three patients during the procedure, which required a repeated intervention to re-establish the flow. During the 3-month follow-up period, ischemic stroke, TIA, MI and femoral thrombus formation occurred in 3, 1, 2 and 2 patients, respectively. In the overall patient group, 8% of the subjects had peri-procedural complications or major vascular events at follow-up. Only one patient had died during the follow-up period because of a new ischemic stroke. None of the patients who had complications peri-procedurally or during the follow-up period had had PH.


In our study, PH occurred in 16.8% of our patients. In the literature, the rate of PH after CAS varies between 11% and 35% according to the criteria used [4, 7, 13, 27]. As in many previous studies, PH was defined on the basis of the occurrence of an SBP of less than 90 mmHg for more than 1 h despite adequate treatment in our study [7, 13, 22, 24, 28].

Baroreceptors of the carotid sinus are stretch receptors that adjust the BP through the modulation of the sympathetic and parasympathetic activity. Stretching of these baroreceptors during the CAS procedure may lead to hypotension or bradycardia, although these hemodynamic alterations are temporary and self-limiting in most cases [15, 16, 21]. Studies investigating the pathophysiologic mechanisms of hemodynamic changes after CAS have focused on baroreceptor sensitivity (BRS), and it has been reported that BRS and consequently parasympathetic activity increases after CAS [1, 5, 31]. Compression of the atheromatous plaque and also continuous radial force exerted by the stent itself into the vessel wall have been suggested as the cause of alteration in baroreceptor activity in CAS [5]. Some reports have suggested an association between hemodynamic depression and the degree of ipsilateral carotid stenosis as well as the presence of contralateral occlusion [12, 30]. In our patient group, presence of ≥70% contralateral carotid stenosis was significantly associated with the risk of PH. Consistent with our observation, another previous study reported an association between PH and contralateral carotid stenosis [10]. To the best of our knowledge, no study investigating the BRS in CAS has focused on the status of contralateral ICA. However, in a study investigating the effect of CEA in the baroreflex mechanism, patients with contralateral stenosis showed greater baroreflex dysfunction and hemodynamic instability after CEA [20]. The investigators also used the intraluminal rub test to stimulate the lumen of the operated carotid artery, which results in a more significant hypotensive response in patients with contralateral carotid stenosis. The authors hypothesized that there is a physiologic baroreceptor reserve in humans, and this reserve decreases and fails to compensate hemodynamic changes in patients with contralateral stenosis.

In our study, absence of DM was found to be associated with PH. Studies examining the relationship between DM and hemodynamic depression have generally yielded controversial results. In one study, DM was found to represent an independent risk factor for hemodynamic depression [11]. On the other hand, another study found that DM could actually provide protection against hemodynamic depression, similar to our results [7]. DM is known to be one of the factors decreasing BRS [25]. Also, an impairment of the baroreflex functions, particularly in the cardiovagal extension, has been demonstrated in diabetic individuals [28]. It has been reported that diabetic neuropathy is a more significant determinant of baroreflex sensitivity than carotid artery elasticity in patients with type 2 diabetes [26]. Studies have shown that the early stages of diabetic autonomic neuropathy involve reduction of parasympathetic activity, which results in sympathetic predominance, followed by sympathetic denervation in later stages [6]. However, no study, including ours, investigating hemodynamic changes in CAS have considered the pesence or absence of diabetic neuropathy in patients with DM, and this may account for these discordant results. We analyzed the mean of HbA1C levels and the treatments used in our diabetic patients, but there were only three diabetic patients with PH, obstructing the comparison with diabetics having normal BP after CAS. New prospective studies should include the use of electrophysiologic studies for staging of DM and diabetic neuropathy if present before the CAS procedure to better understand the effect of DM in the development of postprocedural hemodynamic changes.

Previously reported risk factors for persistent hemodynamic depression include plaques located at the bulb, calcifications at the plaque and bifurcation, severity of the calcification, presence of ulceration in the plaque, the distance between the bifurcation and the site of maximum stenosis, and the type of stenting [7, 11, 18]. One limitation of our study was the absence of these angiographic data. However, of the angiographic variables tested, i.e., the site of dilatation and stent diameter, none was associated with the occurrence of PH. In a recent study, there was no association between post-dilation and the risk of hemodynamic depression [2]. Besides, another report found an association between post-dilatation and hemodynamic depression [23].

Despite many studies suggesting an association between hemodynamic instability and major vascular events, a meta-analysis failed to detect such an association [17]. On the other hand, studies conducted in recent years have suggested that such alterations, particularly when prolonged, may lead to complications such as peri-procedural MI, ischemic stroke or TIA [11, 13, 22, 29]. With this knowledge, we do not discharge patients undergoing CAS and having hypotension after the procedure until maintining normotension without any intervention for at least 6 h. In the present study, for this reason, although PH did not play a significant role in the development of major vascular events, it was associated with prolongation of the hospital stay, consistent with previous studies [2, 9, 22].

In our study, the rate of any complication was 8%, being a rather good result when compared with a previous study reporting a rate of 13.3% for CAS [3]. In the aferomentioned study, the results of CEA and CAS procedures performed in 2003–2007 and 2008–2012 were compared and found that the rate of any complications of the CAS procedure significantly decreased over the years, and they concluded that the CAS procedure has undergone some developments over the years. In our patient group having a lower rate of any complications, CAS procedures were performed between 2012 and 2015. This topic is beyond the scope of our study design, but changes in the patient population, updates in pharmacologic treatments, improvement of procedural techniques and an increase in experience may improve the outcome of CAS procedures over time.

The current study is subject to certain limitations. First, it was a retrospective study with a modest sample size. However, we strictly defined the inclusion criteria and did not enroll patients with inadequate data to avoid under- or overestimating the rate of PH. We also did not evaluate the rate of bradycardia. In clinical practice, bradycardia is a relatively rare complication we experience, and we suggest that the routine use of prophylactic atropine before stenting avoids prolonged bradycardia. Another limitation is not evaluating concomitant medications, which may also affect hemodynamic changes after CAS. However, we did not discontinue the medications used before or not prescribed medications such as beta-blockers or oral antidiabetic medications just before the CAS.

In summary, PH is commonly observed after CAS and is traditionally thought to arise from the stretching of baroreceptors. In our study, we found that a high degree of stenosis of the contralateral carotid artery and absence of DM were associated with PH after CAS. Considering our results and the provided literature, we suggest that not only stretching of the baroreceptors but also some other pathophysiologic processes of the autonomic nervous system and baroreflex sensitivity may play a role in the development of hemodynamic depression after CAS. Further prospective studies are warranted to better define the pathophysiologic mechanisms underlying these hemodynamic alterations.



E.G. provided the concept, literature search, analysis and writing of the manuscript. E.N. provided the data collection design and processing. V.G. and Ç.D. provided technical help. T.A. provided critical review and supervision. M.E and Ö.G. provided general support.

Compliance with ethical standards


The authors declare that no funding was received for this research.

Conflict of interest


Human and animal rights and informed consent

All procedures performed in studies involving human participants were in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Helsinki Declaration and its later amendments or comparable ethical standards.

For this retrospective study, formal consent is not required.


  1. 1.
    Acampa M, Guideri F, Marotta G, Tassi R, D’Andrea P, Giudice GL, Gistri M, Rocchi R, Bernardi A, Bracco S, Venturi C, Martini G (2011) Autonomic activity and baroreflex sensitivity in patients submitted to carotid stenting. Neurosci Lett 491:221–226. doi:10.1016/j.neulet.2011.01.044 CrossRefPubMedGoogle Scholar
  2. 2.
    Borhani Haghighi A, Kokabi S, Yousefi S, Emami M, Shariat A, Nikseresht A, Ashjazadeh N, Izadi S, Petramfar P, Poursadegh M, Jaberi AR, Emami S, Agheli H, Nemati R, Yaghoubi E, Kashani K, Panahandeh M, Heidari-Khormizi SM, Cruz-Flores S, Edgell R (2015) The prevalence and factors contributing to hemodynamic depression in patients undergoing carotid angioplasty and stenting. J Vasc Interv Neurol 8:5–10PubMedGoogle Scholar
  3. 3.
    Bradac O, Mohapl M, Kramar F, Netuka D, Ostry S, Charvat F, Lacman J, Benes V (2014) Carotid endarterectomy and carotid artery stenting: changing paradigm during 10 years in a high-volume centre. Acta Neurochir 156:1705–1712. doi:10.1007/s00701-014-2166-x CrossRefPubMedGoogle Scholar
  4. 4.
    Dangas G, Laird JR Jr, Satler LF, Mehran R, Mintz GS, Larrain G, Lansky AJ, Gruberg L, Parsons EM, Laureno R, Monsein LH, Leon MB (2000) Postprocedural hypotension after carotid artery stent placement: predictors and short- and long-term clinical outcomes. Radiology 215:677–683. doi:10.1148/radiology.215.3.r00jn04677 CrossRefPubMedGoogle Scholar
  5. 5.
    Demirci M, Saribas O, Uluc K, Cekirge S, Boke E, Ay H (2006) Carotid artery stenting and endarterectomy have different effects on heart rate variability. J Neurol Sci 241:45–51. doi:10.1016/j.jns.2005.10.011 CrossRefPubMedGoogle Scholar
  6. 6.
    Dimitropoulos G, Tahrani AA, Stevens MJ (2014) Cardiac autonomic neuropathy in patients with diabetes mellitus. World J Diabetes 5:17–39. doi:10.4239/wjd.v5.i1.17 CrossRefPubMedPubMedCentralGoogle Scholar
  7. 7.
    Gupta R, Abou-Chebl A, Bajzer CT, Schumacher HC, Yadav JS (2006) Rate, predictors, and consequences of hemodynamic depression after carotid artery stenting. J Am Coll Cardiol 47:1538–1543. doi:10.1016/j.jacc.2005.08.079 CrossRefPubMedGoogle Scholar
  8. 8.
    Gupta R, Horowitz M, Jovin TG (2005) Hemodynamic instability after carotid artery angioplasty and stent placement: a review of the literature. Neurosurg Focus 18:e6CrossRefPubMedGoogle Scholar
  9. 9.
    Kiani H, Haghighi A, Rostami A, Azargashb E, Tabaei SJ, Solgi A, Zebardast N (2016) Prevalence, risk factors and symptoms associated to intestinal parasite infections among patients with gastrointestinal disorders in Nahavand, western Iran. Rev Inst Med Trop Sao Paulo 58:42. doi:10.1590/S1678-9946201658042 CrossRefPubMedPubMedCentralGoogle Scholar
  10. 10.
    Leisch F, Kerschner K, Hofmann R, Steinwender C, Grund M, Bibl D, Leisch FA Jr, Bergmann H (2003) Carotid sinus reactions during carotid artery stenting: predictors, incidence, and influence on clinical outcome. Catheter Cardiovasc Interv 58:516–523. doi:10.1002/ccd.10483 CrossRefPubMedGoogle Scholar
  11. 11.
    Lian X, Lin M, Liu M, Huang J, He X (2014) Complications and predictors associated with persistent hemodynamic depression after carotid artery stenting. Clin Neurol Neurosurg 124:81–84. doi:10.1016/j.clineuro.2014.06.008 CrossRefPubMedGoogle Scholar
  12. 12.
    Lian X, Lin M, Zhu S, Liu W, Li M, Sun W, Yin Q, Xu G, Zhang R, Liu X (2011) Risk factors associated with haemodynamic depression during and after carotid artery stenting. J Clin Neurosci 18:1325–1328. doi:10.1016/j.jocn.2011.01.030 CrossRefPubMedGoogle Scholar
  13. 13.
    Lin PH, Zhou W, Kougias P, El Sayed HF, Barshes NR, Huynh TT (2007) Factors associated with hypotension and bradycardia after carotid angioplasty and stenting. J Vasc Surg 46:846–853; discussion 853-844. doi:10.1016/j.jvs.2007.07.020 CrossRefPubMedGoogle Scholar
  14. 14.
    Mancia G, Ferrari A, Gregorini L, Parati G, Ferrari MC, Pomidossi G, Zanchetti A (1979) Control of blood pressure by carotid sinus baroreceptors in human beings. Am J Cardiol 44:895–902CrossRefPubMedGoogle Scholar
  15. 15.
    McKevitt FM, Sivaguru A, Venables GS, Cleveland TJ, Gaines PA, Beard JD, Channer KS (2003) Effect of treatment of carotid artery stenosis on blood pressure: a comparison of hemodynamic disturbances after carotid endarterectomy and endovascular treatment. Stroke 34:2576–2581. doi:10.1161/01.STR.0000097490.88015.3A CrossRefPubMedGoogle Scholar
  16. 16.
    Mlekusch W, Schillinger M, Sabeti S, Nachtmann T, Lang W, Ahmadi R, Minar E (2003) Hypotension and bradycardia after elective carotid stenting: frequency and risk factors. J Endovasc Ther 10:851–859; discussion 860-851. doi:10.1583/1545-1550(2003)010%3C0851:HABAEC%3E2.0.CO;2 CrossRefPubMedGoogle Scholar
  17. 17.
    Mylonas SN, Moulakakis KG, Antonopoulos CN, Kakisis JD, Liapis CD (2013) Carotid artery stenting-induced hemodynamic instability. J Endovasc Ther 20:48–60. doi:10.1583/12-4015.1 CrossRefPubMedGoogle Scholar
  18. 18.
    Nonaka T, Oka S, Miyata K, Mikami T, Koyanagi I, Houkin K, Yoshifuji K, Imaizumi T (2005) Prediction of prolonged postprocedural hypotension after carotid artery stenting. Neurosurgery 57:472–477 discussion 472-477 CrossRefPubMedGoogle Scholar
  19. 19.
    North American Symptomatic Carotid Endarterectomy Trial (1991) Methods, patient characteristics, and progress. Stroke 22:711–720CrossRefGoogle Scholar
  20. 20.
    Nouraei SA, Al-Rawi PG, Sigaudo-Roussel D, Giussani DA, Gaunt ME (2005) Carotid endarterectomy impairs blood pressure homeostasis by reducing the physiologic baroreflex reserve. J Vasc Surg 41:631–637. doi:10.1016/j.jvs.2005.01.009 CrossRefPubMedGoogle Scholar
  21. 21.
    Pappada G, Beghi E, Marina R, Agostoni E, Cesana C, Legnani F, Parolin M, Petri D, Sganzerla EP (2006) Hemodynamic instability after extracranial carotid stenting. Acta Neurochir 148:639–645. doi:10.1007/s00701-006-0752-2 CrossRefPubMedGoogle Scholar
  22. 22.
    Park BD, Divinagracia T, Madej O, McPhelimy C, Piccirillo B, Dahn MS, Ruby S, Menzoian JO (2009) Predictors of clinically significant postprocedural hypotension after carotid endarterectomy and carotid angioplasty with stenting. J Vasc Surg 50:526–533. doi:10.1016/j.jvs.2009.05.005 CrossRefPubMedGoogle Scholar
  23. 23.
    Qazi U, Obeid TE, Enwerem N, Schneider E, White JR, Freischlag JA, Perler BA, Malas MB (2014) The effect of ballooning following carotid stent deployment on hemodynamic stability. J Vasc Surg 59:756–760. doi:10.1016/j.jvs.2013.09.027 CrossRefPubMedGoogle Scholar
  24. 24.
    Qureshi AI, Luft AR, Sharma M, Janardhan V, Lopes DK, Khan J, Guterman LR, Hopkins LN (1999) Frequency and determinants of postprocedural hemodynamic instability after carotid angioplasty and stenting. Stroke 30:2086–2093CrossRefPubMedGoogle Scholar
  25. 25.
    Rowaiye OO, Jankowska EA, Ponikowska B (2013) Baroreceptor sensitivity and diabetes mellitus. Cardiol J 20:453–463. doi:10.5603/CJ.2013.0130 CrossRefPubMedGoogle Scholar
  26. 26.
    Ruiz J, Monbaron D, Parati G, Perret S, Haesler E, Danzeisen C, Hayoz D (2005) Diabetic neuropathy is a more important determinant of baroreflex sensitivity than carotid elasticity in type 2 diabetes. Hypertension 46:162–167. doi:10.1161/01.HYP.0000169053.14440.7d CrossRefPubMedGoogle Scholar
  27. 27.
    Taha MM, Toma N, Sakaida H, Hori K, Maeda M, Asakura F, Fujimoto M, Matsushima S, Taki W (2008) Periprocedural hemodynamic instability with carotid angioplasty and stenting. Surg Neurol 70:279–285; discussion 285-276. doi:10.1016/j.surneu.2007.07.006 CrossRefPubMedGoogle Scholar
  28. 28.
    Trocciola SM, Chaer RA, Lin SC, Ryer EJ, De Rubertis B, Morrissey NJ, McKinsey J, Kent KC, Faries PL (2006) Analysis of parameters associated with hypotension requiring vasopressor support after carotid angioplasty and stenting. J Vasc Surg 43:714–720. doi:10.1016/j.jvs.2005.12.008 CrossRefPubMedGoogle Scholar
  29. 29.
    Ullery BW, Nathan DP, Shang EK, Wang GJ, Jackson BM, Murphy EH, Fairman RM, Woo EY (2013) Incidence, predictors, and outcomes of hemodynamic instability following carotid angioplasty and stenting. J Vasc Surg 58:917–925. doi:10.1016/j.jvs.2012.10.141 CrossRefPubMedGoogle Scholar
  30. 30.
    Wu TY, Ham SW, Katz SG (2015) Predictors and consequences of hemodynamic instability after carotid artery stenting. Ann Vasc Surg 29:1281–1285. doi:10.1016/j.avsg.2015.03.035 CrossRefPubMedGoogle Scholar
  31. 31.
    Yakhou L, Constant I, Merle JC, Laude D, Becquemin JP, Duvaldestin P (2006) Noninvasive investigation of autonomic activity after carotid stenting or carotid endarterectomy. J Vasc Surg 44:472–479. doi:10.1016/j.jvs.2006.06.004 CrossRefPubMedGoogle Scholar

Copyright information

© Springer-Verlag GmbH Austria 2017

Authors and Affiliations

  • Elif Gökçal
    • 1
  • Elvin Niftaliyev
    • 1
  • Çiğdem Deniz
    • 1
  • Mehmet Ergelen
    • 2
  • Vildan Güzel
    • 1
  • Ömer Göktekin
    • 2
  • Talip Asil
    • 1
  1. 1.Neurology DepartmentBezmialem Vakıf UniversityİstanbulTurkey
  2. 2.Cardiology DepartmentBezmialem Vakıf UniversityİstanbulTurkey

Personalised recommendations