Accepted Manuscript Predictors and Consequences of Hemodynamic Instability Following Carotid Artery Stenting Tiffany Y. Wu, M.D., Sung W. Ham, M.D., Steven G. Katz, M.D. PII:
S0890-5096(15)00328-3
DOI:
10.1016/j.avsg.2015.03.035
Reference:
AVSG 2346
To appear in:
Annals of Vascular Surgery
Received Date: 10 November 2014 Revised Date:
5 March 2015
Accepted Date: 6 March 2015
Please cite this article as: Wu TY, Ham SW, Katz SG, Predictors and Consequences of Hemodynamic Instability Following Carotid Artery Stenting, Annals of Vascular Surgery (2015), doi: 10.1016/ j.avsg.2015.03.035. This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
ACCEPTED MANUSCRIPT
Predictors and Consequences of Hemodynamic Instability Following Carotid Artery Stenting Authors: Tiffany Y. Wu1, M.D., Sung W. Ham2, M.D., Steven G. Katz, M.D3.
RI PT
Corresponding author: Steven G. Katz, M.D
Department of Surgery, Huntington Hospital, Keck School of Medicine, University of Southern California. 100 W. California Blvd. Pasadena, CA 91105
SC
e-mail: [email protected]
1
Department of Graduate Medical Education, Huntington Hospital, Pasadena, CA
2
M AN U
Division of Vascular Surgery, Keck School of Medicine, University of Southern California, Los Angeles, CA
3
Division of Vascular Surgery, Keck School of Medicine, University of Southern California, Pasadena, CA
AC C
EP
TE D
Full Presentation at the 29th Annual Meeting of the Western Vascular Society, September 22, 2014. Coronado, CA.
ACCEPTED MANUSCRIPT
Objective: The purpose of this study is to determine the predictors and consequences of hemodymamic instability (HI) following carotid artery stenting (CAS).
SC
RI PT
Methods: The records of all patients undergoing CAS in a single institution were reviewed. Patient demographics and risk factors were recorded. Indications for CAS, medications including statins, atropine, and beta blockers, anatomic risk factors, balloon and stent length and diameter, as well as degree of stenosis were noted. The presence of peri-procedural hypertension (SBP>160), hypotension (SBP160 mmHg), hypotension (SBP 0.35 for each). None of the hemodynamic factors alone (hypertension, hypotension, bradycardia, SBP drop greater than 30mmHg, or HR drop greater than 20 bpm) were associated with a higher incidence of TIA, stroke, or death (Table 5). Discussion
First introduced in the 1950’s, CEA has become the gold standard for the treatment of extra-cranial carotid stenosis. Even though its safety and efficacy were called into question in the 1980’s and 1990’s, its efficacy in stroke prevention was validated by the NASCET and ACAS studies. Recently, CAS has been proposed as an alternative to CEA, but concerns over its safety remain. Recent advances in embolic protection with flow reversal and avoidance of arch pathology by utilizing trans-cervical approaches have been advocated as methods of lessening morbidity. While the results of ongoing trials with these
ACCEPTED MANUSCRIPT
techniques are pending, all require balloon dilatation and stent deployment in the carotid vessels. Hemodynamic instability, which frequently occurs during CAS, has been associated by some with an increase in peri-procedural major adverse events4,9,11. It is therefore important to delineate the factors that are predictive of its occurrence, and also to determine the consequences of its presence.
M AN U
SC
RI PT
The frequency of HI in several large series has varied between 42% and 84%9,11. The finding of a 65% incidence in our cohort falls well within this range. While some have found that patients with coronary artery disease were more likely to develop HI6, we could not corroborate this finding. We, like others demonstrated an increased risk of HI in octogenarians4,6,12,13,14. This may be accounted for by the age related diastolic ventricular dysfunction and diminished cardiac reserve often seen in this group of patients which would diminish their capacity to respond to the hemodynamic changes associated with carotid baroreceptor stimulation. In our series as in others, female sex has been associated with an increase rate of HI13. Some have also documented an increased need for vasopressor infusion in women following CAS13. The fact that 39% of our patient cohort was female may have allowed us sufficient power to make this association. In several studies, symptomatic patients, especially those with previous stroke were more likely to develop HI12. We could find no such correlation in our patient series. The association between preoperative beta-blocker usage and an increase in the incidence of bradycardia is not surprising. It is interesting to note that in our group of patients, a history of angina, contralateral occlusion, and prior neck irradiation were protective for HI. While one might postulate that radiation might injure the baroreceptors making them less susceptible to the stimulation that occurs during CAS, the protective effect of angina and contralateral occlusion remain obscure.
EP
TE D
The association between hemodynamic instability and the rate of major adverse events following CAS has varied substantially in the literature. Several studies have reported an increased incidence of major adverse events or stroke in those patients who experienced prolonged HI4,11. As in other studies we were able to demonstrate only an increased incidence of TIA in those experiencing prolonged HI while the incidence of stroke, myocardial infarction or death were not significantly impacted. This may be in part explained by our low rates of significant hypotension (10.6%) and severe bradycardia (2.5%), the components of HI that would be most likely to have a profound physiologic effect on the patient.
AC C
It has been well established that stimulation of baroreceptors during CAS causes a temporary rise in medullary parasympathetic impulses leading to decreased vasomotor tone and resultant bradycardia and hypotension. In spite of this, the routine use of parasympatholytic drugs during CAS has been controversial. Some have postulated that the prophylactic use of atropine would result in an increased incidence of cardiac events or confusion in those undergoing carotid stenting, while others have demonstrated a decreased incidence of HI and its resultant complications8. Our data would tend to support the latter. Only one patient in our series suffered a myocardial infarction, and severe hypotension and bradycardia were rare following the routine use of atropine. We were unable to determine whether there was any association between atropine use or non-use and HI given the low number of patients in our series who did not receive atropine. We acknowledge that our manuscript is someone limited since it is a retrospective case review rather than a prospective randomized study.
ACCEPTED MANUSCRIPT
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M AN U
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We conclude that hemodynamic instability is a frequent occurrence following CAS. Female patients and those over 80 years of age are particularly susceptible. However, patients with prolonged HI do not appear to suffer an increased incidence of permanent neurological deficits, myocardial infarction, or death. When atropine is used on a routine basis, severe hypotension and bradycardia can for the most part be averted, and untoward complications of its use are rare. In addition, the use of vasopressors and prolonged hemodynamic monitoring in an ICU setting can be minimized.
ACCEPTED MANUSCRIPT
References
6.
7.
8.
9. 10.
11.
12. 13.
14. 15.
RI PT
SC
5.
M AN U
4.
TE D
3.
EP
2.
Brott TG, Hobson RW, Howard G, Roubin GS, Clark WM, Brooks W, et al; CREST Investigators. Stenting versus endarterectomy for treatment of carotid-artery stenosis. N Engl J Med 2010;363:11-23. Dangas G, Laird JR Jr, Satler LF, Mehran R, Mintz GS, Larrain G, et al. Postprocedural hypotension after carotid artery stent placement: predictors and short- and long-term clinical outcomes. Radiology 2000;215:677-83. Leisch F, Kerschner K, Hofmann R, Steinwender C, Grund M, Bibl D, et al. Carotid sinus reactions during carotid artery stenting: predictors, incidence, and influence on clinical outcome. Catheter Cardiovasc Interv 2003;58:516-23. Lin PH, Zhou W, Kougias P, El Sayed HF, Barshes NR, Huynh TT. Factors associated with hypotension and bradycardia after carotid angioplasty and stenting. J Vasc Surg 2007;46:846-53; discussion: 853-4. Mendelsohn FO, Weissman NJ, Lederman RJ, Crowley JJ, Gray JL, Phillips HR, et al. Acute hemodynamic changes during carotid artery stenting. Am J Cardiol 1998;82:1077-81. Mlekusch W, Schillinger M, Sabeti S, Nachtmann T, Lang W, Ahmadi R, et al. Hypotension and bradycardia after elective carotid stenting: frequency and risk factors. J Endovasc Ther 2003;10:851-9. Qureshi AI, Luft AR, Sharma M, Janardhan V, Lopes DK, Khan J, et at. Frequency and determinants of postprocedural hemodynamic instability after carotid angioplasty and stenting. Stroke 1999; 30: 2086-2093. Cayne NS, Faries PL, Trocciola SM, Saltzberg SS, Dayal RD, Clair D, et al. Carotid angioplasty and stent-induced bradycardia and hypotension: impact of prophylactic atropine administration and prior carotid endarterectomy. J Vasc Surg 2005;41:956-61. Gupta R, Abou-Chebl A, Bajzer CT, Schumacher HC, Yadav JS. Rate, predictors, and consequences of hemodynamic depression after carotid artery stenting. J Am Coll Cardiol 2006;47:1538-43. Howell M, Krajcer Z, Dougherty K, Strickman N, Skolkin M, Toombs B, et al. Correlation of periprocedural systolic blood pressure changes with neurological events in high-risk carotid stent patients. J Endovasc Ther 2002;9:810-6. Ullery BW, Nathan DP, Shang EK, Wang GJ, Jackson BM, Murphy EH, Fairman RM, Woo EY. Incidence, predictors, and outcomes of hemodynamic instability following carotid angioplasty and stenting. J Vasc Surg. 2013;58(4):917-25. Taha M, Naoki T, Hiroshi S, Kotaro H, Masayuki M, Fumio A, et al. Periprocedural hemodynamic instability with carotid angioplasty and stenting. Sur Neuro 2008; 70: 279-285. Trocciola SM, Chaer RA, Lin SC, Ryer EJ, De Rubertis B, Morrissey NJ, et al. Analysis of parameters associated with hypotension requiring vasopressor support after carotid angioplasty and stenting. J Vasc Surg 2006;43:714-20. Allison S, Lee W, Gur I, Katz S. Carotid Stent: A Surgeons Prospective. J Am Coll Surg 2011;213:173178. Hobson RW, Howard VJ, Roubin GS, Brott TG, Ferguson RD, Popma JJ, et al. Carotid artery stenting is associated with increased complications in octogenarians: 30-day stroke and death rates in the CREST lead-in phase. J Vasc Surg 2004; 40: 1106-1111.
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1.
ACCEPTED MANUSCRIPT
Tables Table I. Risk Factors Prevalence n=191 Male 61% HTN 87% Smoker 49% CAD 48% DM 38% Asymptomatic 56% Symptomatic 44% - TIA 24% - Stroke 20% Statin 63% Beta-blocker 41% Previous ipsilateral CEA 15% Previous neck radiation 4% Peri-procedural atropine 92% HTN=hypertension, CAD=coronary artery disease, DM= diabetes mellitus, TIA=transient ischemic attack, CEA=carotid endarterectomy Table II. Hemodynamic Instability (HI)
Incidence n=199 Any HI 65.3% (n=130) Transient HI 31.7% (n=63) Prolonged HI 33.7% (n=67) SBP >160 mm Hg 30.2% (n=60) SBP < 90 mm Hg 10.6% (n=21) HR < 60 bpm 17.6% (n=35) SBP drop >30mmHg 36.1% (n=72) HR drop >20 bpm 2.5% (n=5) HI= hemodynamic instability SBP=systolic blood pressure, bpm=beats per minute
TE D
Outcome
M AN U
SC
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Risk Factor
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Table III. Factors Predictive of HI
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p value Risk Factor Type of HI *Angina Any HI .010 Age >80 Transient HI .046 Age >80 Prolonged HI .037 Female Prolonged HI .023 HI= hemodynamic instability. *Angina was found to be protective in univariate analysis but this finding was not significant in multivariate analysis. Table IV. Factors Protective for HI Risk Factor Previous Neck Radiation Previous Neck Radiation Contralateral occlusion
Type of HI Any HI Prolonged HI Any HI
p value .013 .039 .050
ACCEPTED MANUSCRIPT
HI= hemodynamic instability Table V. Logistic Regression Type of HI
Odds Ratio
p value
4.194 3.750 3.870 0.750
.031 .029 .036 .027
AC C
EP
TE D
M AN U
SC
Age >80 Prolonged HI 1.073 Female Prolonged HI 1.073 OR >120min Transient HI 1.046 Angina Overall HI 0.009 HI=hemodynamic instability, OR= operating room time
Odds Ratio
RI PT
Risk Factor
ACCEPTED MANUSCRIPT
Tables Table I. Risk Factors Prevalence n=191 Male 61% HTN 87% Smoker 49% CAD 48% DM 38% Asymptomatic 56% Symptomatic 44% - TIA 24% - Stroke 20% Statin 63% Beta-blocker 41% Previous ipsilateral CEA 15% Previous neck radiation 4% Peri-procedural atropine 92% HTN=hypertension, CAD=coronary artery disease, DM= diabetes mellitus, TIA=transient ischemic attack, CEA=carotid endarterectomy Table II. Hemodynamic Instability (HI)
Incidence n=199 Any HI 65.3% (n=130) Transient HI 31.7% (n=63) Prolonged HI 33.7% (n=67) SBP >160 mm Hg 30.2% (n=60) SBP < 90 mm Hg 10.6% (n=21) HR < 60 bpm 17.6% (n=35) SBP drop >30mmHg 36.1% (n=72) HR drop >20 bpm 2.5% (n=5) HI= hemodynamic instability SBP=systolic blood pressure, bpm=beats per minute
TE D
Outcome
M AN U
SC
RI PT
Risk Factor
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Table III. Factors Predictive of HI
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p value Risk Factor Type of HI *Angina Any HI .010 Age >80 Transient HI .046 Age >80 Prolonged HI .037 Female Prolonged HI .023 HI= hemodynamic instability. *Angina was found to be protective in univariate analysis but this finding was not significant in multivariate analysis. Table IV. Factors Protective for HI Risk Factor Previous Neck Radiation Previous Neck Radiation Contralateral occlusion
Type of HI Any HI Prolonged HI Any HI
p value .013 .039 .050
ACCEPTED MANUSCRIPT
HI= hemodynamic instability Table V. Logistic Regression Type of HI
Odds Ratio
p value
4.194 3.750 3.870 0.750
.031 .029 .036 .027
AC C
EP
TE D
M AN U
SC
Age >80 Prolonged HI 1.073 Female Prolonged HI 1.073 OR >120min Transient HI 1.046 Angina Overall HI 0.009 HI=hemodynamic instability, OR= operating room time
Odds Ratio
RI PT
Risk Factor
S0890-5096(15)00328-3
DOI:
10.1016/j.avsg.2015.03.035
Reference:
AVSG 2346
To appear in:
Annals of Vascular Surgery
Received Date: 10 November 2014 Revised Date:
5 March 2015
Accepted Date: 6 March 2015
Please cite this article as: Wu TY, Ham SW, Katz SG, Predictors and Consequences of Hemodynamic Instability Following Carotid Artery Stenting, Annals of Vascular Surgery (2015), doi: 10.1016/ j.avsg.2015.03.035. This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
ACCEPTED MANUSCRIPT
Predictors and Consequences of Hemodynamic Instability Following Carotid Artery Stenting Authors: Tiffany Y. Wu1, M.D., Sung W. Ham2, M.D., Steven G. Katz, M.D3.
RI PT
Corresponding author: Steven G. Katz, M.D
Department of Surgery, Huntington Hospital, Keck School of Medicine, University of Southern California. 100 W. California Blvd. Pasadena, CA 91105
SC
e-mail: [email protected]
1
Department of Graduate Medical Education, Huntington Hospital, Pasadena, CA
2
M AN U
Division of Vascular Surgery, Keck School of Medicine, University of Southern California, Los Angeles, CA
3
Division of Vascular Surgery, Keck School of Medicine, University of Southern California, Pasadena, CA
AC C
EP
TE D
Full Presentation at the 29th Annual Meeting of the Western Vascular Society, September 22, 2014. Coronado, CA.
ACCEPTED MANUSCRIPT
Objective: The purpose of this study is to determine the predictors and consequences of hemodymamic instability (HI) following carotid artery stenting (CAS).
SC
RI PT
Methods: The records of all patients undergoing CAS in a single institution were reviewed. Patient demographics and risk factors were recorded. Indications for CAS, medications including statins, atropine, and beta blockers, anatomic risk factors, balloon and stent length and diameter, as well as degree of stenosis were noted. The presence of peri-procedural hypertension (SBP>160), hypotension (SBP160 mmHg), hypotension (SBP 0.35 for each). None of the hemodynamic factors alone (hypertension, hypotension, bradycardia, SBP drop greater than 30mmHg, or HR drop greater than 20 bpm) were associated with a higher incidence of TIA, stroke, or death (Table 5). Discussion
First introduced in the 1950’s, CEA has become the gold standard for the treatment of extra-cranial carotid stenosis. Even though its safety and efficacy were called into question in the 1980’s and 1990’s, its efficacy in stroke prevention was validated by the NASCET and ACAS studies. Recently, CAS has been proposed as an alternative to CEA, but concerns over its safety remain. Recent advances in embolic protection with flow reversal and avoidance of arch pathology by utilizing trans-cervical approaches have been advocated as methods of lessening morbidity. While the results of ongoing trials with these
ACCEPTED MANUSCRIPT
techniques are pending, all require balloon dilatation and stent deployment in the carotid vessels. Hemodynamic instability, which frequently occurs during CAS, has been associated by some with an increase in peri-procedural major adverse events4,9,11. It is therefore important to delineate the factors that are predictive of its occurrence, and also to determine the consequences of its presence.
M AN U
SC
RI PT
The frequency of HI in several large series has varied between 42% and 84%9,11. The finding of a 65% incidence in our cohort falls well within this range. While some have found that patients with coronary artery disease were more likely to develop HI6, we could not corroborate this finding. We, like others demonstrated an increased risk of HI in octogenarians4,6,12,13,14. This may be accounted for by the age related diastolic ventricular dysfunction and diminished cardiac reserve often seen in this group of patients which would diminish their capacity to respond to the hemodynamic changes associated with carotid baroreceptor stimulation. In our series as in others, female sex has been associated with an increase rate of HI13. Some have also documented an increased need for vasopressor infusion in women following CAS13. The fact that 39% of our patient cohort was female may have allowed us sufficient power to make this association. In several studies, symptomatic patients, especially those with previous stroke were more likely to develop HI12. We could find no such correlation in our patient series. The association between preoperative beta-blocker usage and an increase in the incidence of bradycardia is not surprising. It is interesting to note that in our group of patients, a history of angina, contralateral occlusion, and prior neck irradiation were protective for HI. While one might postulate that radiation might injure the baroreceptors making them less susceptible to the stimulation that occurs during CAS, the protective effect of angina and contralateral occlusion remain obscure.
EP
TE D
The association between hemodynamic instability and the rate of major adverse events following CAS has varied substantially in the literature. Several studies have reported an increased incidence of major adverse events or stroke in those patients who experienced prolonged HI4,11. As in other studies we were able to demonstrate only an increased incidence of TIA in those experiencing prolonged HI while the incidence of stroke, myocardial infarction or death were not significantly impacted. This may be in part explained by our low rates of significant hypotension (10.6%) and severe bradycardia (2.5%), the components of HI that would be most likely to have a profound physiologic effect on the patient.
AC C
It has been well established that stimulation of baroreceptors during CAS causes a temporary rise in medullary parasympathetic impulses leading to decreased vasomotor tone and resultant bradycardia and hypotension. In spite of this, the routine use of parasympatholytic drugs during CAS has been controversial. Some have postulated that the prophylactic use of atropine would result in an increased incidence of cardiac events or confusion in those undergoing carotid stenting, while others have demonstrated a decreased incidence of HI and its resultant complications8. Our data would tend to support the latter. Only one patient in our series suffered a myocardial infarction, and severe hypotension and bradycardia were rare following the routine use of atropine. We were unable to determine whether there was any association between atropine use or non-use and HI given the low number of patients in our series who did not receive atropine. We acknowledge that our manuscript is someone limited since it is a retrospective case review rather than a prospective randomized study.
ACCEPTED MANUSCRIPT
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EP
TE D
M AN U
SC
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We conclude that hemodynamic instability is a frequent occurrence following CAS. Female patients and those over 80 years of age are particularly susceptible. However, patients with prolonged HI do not appear to suffer an increased incidence of permanent neurological deficits, myocardial infarction, or death. When atropine is used on a routine basis, severe hypotension and bradycardia can for the most part be averted, and untoward complications of its use are rare. In addition, the use of vasopressors and prolonged hemodynamic monitoring in an ICU setting can be minimized.
ACCEPTED MANUSCRIPT
References
6.
7.
8.
9. 10.
11.
12. 13.
14. 15.
RI PT
SC
5.
M AN U
4.
TE D
3.
EP
2.
Brott TG, Hobson RW, Howard G, Roubin GS, Clark WM, Brooks W, et al; CREST Investigators. Stenting versus endarterectomy for treatment of carotid-artery stenosis. N Engl J Med 2010;363:11-23. Dangas G, Laird JR Jr, Satler LF, Mehran R, Mintz GS, Larrain G, et al. Postprocedural hypotension after carotid artery stent placement: predictors and short- and long-term clinical outcomes. Radiology 2000;215:677-83. Leisch F, Kerschner K, Hofmann R, Steinwender C, Grund M, Bibl D, et al. Carotid sinus reactions during carotid artery stenting: predictors, incidence, and influence on clinical outcome. Catheter Cardiovasc Interv 2003;58:516-23. Lin PH, Zhou W, Kougias P, El Sayed HF, Barshes NR, Huynh TT. Factors associated with hypotension and bradycardia after carotid angioplasty and stenting. J Vasc Surg 2007;46:846-53; discussion: 853-4. Mendelsohn FO, Weissman NJ, Lederman RJ, Crowley JJ, Gray JL, Phillips HR, et al. Acute hemodynamic changes during carotid artery stenting. Am J Cardiol 1998;82:1077-81. Mlekusch W, Schillinger M, Sabeti S, Nachtmann T, Lang W, Ahmadi R, et al. Hypotension and bradycardia after elective carotid stenting: frequency and risk factors. J Endovasc Ther 2003;10:851-9. Qureshi AI, Luft AR, Sharma M, Janardhan V, Lopes DK, Khan J, et at. Frequency and determinants of postprocedural hemodynamic instability after carotid angioplasty and stenting. Stroke 1999; 30: 2086-2093. Cayne NS, Faries PL, Trocciola SM, Saltzberg SS, Dayal RD, Clair D, et al. Carotid angioplasty and stent-induced bradycardia and hypotension: impact of prophylactic atropine administration and prior carotid endarterectomy. J Vasc Surg 2005;41:956-61. Gupta R, Abou-Chebl A, Bajzer CT, Schumacher HC, Yadav JS. Rate, predictors, and consequences of hemodynamic depression after carotid artery stenting. J Am Coll Cardiol 2006;47:1538-43. Howell M, Krajcer Z, Dougherty K, Strickman N, Skolkin M, Toombs B, et al. Correlation of periprocedural systolic blood pressure changes with neurological events in high-risk carotid stent patients. J Endovasc Ther 2002;9:810-6. Ullery BW, Nathan DP, Shang EK, Wang GJ, Jackson BM, Murphy EH, Fairman RM, Woo EY. Incidence, predictors, and outcomes of hemodynamic instability following carotid angioplasty and stenting. J Vasc Surg. 2013;58(4):917-25. Taha M, Naoki T, Hiroshi S, Kotaro H, Masayuki M, Fumio A, et al. Periprocedural hemodynamic instability with carotid angioplasty and stenting. Sur Neuro 2008; 70: 279-285. Trocciola SM, Chaer RA, Lin SC, Ryer EJ, De Rubertis B, Morrissey NJ, et al. Analysis of parameters associated with hypotension requiring vasopressor support after carotid angioplasty and stenting. J Vasc Surg 2006;43:714-20. Allison S, Lee W, Gur I, Katz S. Carotid Stent: A Surgeons Prospective. J Am Coll Surg 2011;213:173178. Hobson RW, Howard VJ, Roubin GS, Brott TG, Ferguson RD, Popma JJ, et al. Carotid artery stenting is associated with increased complications in octogenarians: 30-day stroke and death rates in the CREST lead-in phase. J Vasc Surg 2004; 40: 1106-1111.
AC C
1.
ACCEPTED MANUSCRIPT
Tables Table I. Risk Factors Prevalence n=191 Male 61% HTN 87% Smoker 49% CAD 48% DM 38% Asymptomatic 56% Symptomatic 44% - TIA 24% - Stroke 20% Statin 63% Beta-blocker 41% Previous ipsilateral CEA 15% Previous neck radiation 4% Peri-procedural atropine 92% HTN=hypertension, CAD=coronary artery disease, DM= diabetes mellitus, TIA=transient ischemic attack, CEA=carotid endarterectomy Table II. Hemodynamic Instability (HI)
Incidence n=199 Any HI 65.3% (n=130) Transient HI 31.7% (n=63) Prolonged HI 33.7% (n=67) SBP >160 mm Hg 30.2% (n=60) SBP < 90 mm Hg 10.6% (n=21) HR < 60 bpm 17.6% (n=35) SBP drop >30mmHg 36.1% (n=72) HR drop >20 bpm 2.5% (n=5) HI= hemodynamic instability SBP=systolic blood pressure, bpm=beats per minute
TE D
Outcome
M AN U
SC
RI PT
Risk Factor
EP
Table III. Factors Predictive of HI
AC C
p value Risk Factor Type of HI *Angina Any HI .010 Age >80 Transient HI .046 Age >80 Prolonged HI .037 Female Prolonged HI .023 HI= hemodynamic instability. *Angina was found to be protective in univariate analysis but this finding was not significant in multivariate analysis. Table IV. Factors Protective for HI Risk Factor Previous Neck Radiation Previous Neck Radiation Contralateral occlusion
Type of HI Any HI Prolonged HI Any HI
p value .013 .039 .050
ACCEPTED MANUSCRIPT
HI= hemodynamic instability Table V. Logistic Regression Type of HI
Odds Ratio
p value
4.194 3.750 3.870 0.750
.031 .029 .036 .027
AC C
EP
TE D
M AN U
SC
Age >80 Prolonged HI 1.073 Female Prolonged HI 1.073 OR >120min Transient HI 1.046 Angina Overall HI 0.009 HI=hemodynamic instability, OR= operating room time
Odds Ratio
RI PT
Risk Factor
ACCEPTED MANUSCRIPT
Tables Table I. Risk Factors Prevalence n=191 Male 61% HTN 87% Smoker 49% CAD 48% DM 38% Asymptomatic 56% Symptomatic 44% - TIA 24% - Stroke 20% Statin 63% Beta-blocker 41% Previous ipsilateral CEA 15% Previous neck radiation 4% Peri-procedural atropine 92% HTN=hypertension, CAD=coronary artery disease, DM= diabetes mellitus, TIA=transient ischemic attack, CEA=carotid endarterectomy Table II. Hemodynamic Instability (HI)
Incidence n=199 Any HI 65.3% (n=130) Transient HI 31.7% (n=63) Prolonged HI 33.7% (n=67) SBP >160 mm Hg 30.2% (n=60) SBP < 90 mm Hg 10.6% (n=21) HR < 60 bpm 17.6% (n=35) SBP drop >30mmHg 36.1% (n=72) HR drop >20 bpm 2.5% (n=5) HI= hemodynamic instability SBP=systolic blood pressure, bpm=beats per minute
TE D
Outcome
M AN U
SC
RI PT
Risk Factor
EP
Table III. Factors Predictive of HI
AC C
p value Risk Factor Type of HI *Angina Any HI .010 Age >80 Transient HI .046 Age >80 Prolonged HI .037 Female Prolonged HI .023 HI= hemodynamic instability. *Angina was found to be protective in univariate analysis but this finding was not significant in multivariate analysis. Table IV. Factors Protective for HI Risk Factor Previous Neck Radiation Previous Neck Radiation Contralateral occlusion
Type of HI Any HI Prolonged HI Any HI
p value .013 .039 .050
ACCEPTED MANUSCRIPT
HI= hemodynamic instability Table V. Logistic Regression Type of HI
Odds Ratio
p value
4.194 3.750 3.870 0.750
.031 .029 .036 .027
AC C
EP
TE D
M AN U
SC
Age >80 Prolonged HI 1.073 Female Prolonged HI 1.073 OR >120min Transient HI 1.046 Angina Overall HI 0.009 HI=hemodynamic instability, OR= operating room time
Odds Ratio
RI PT
Risk Factor
