CASE REPORT
Prolonged Hypotension Following Innominate and Left Common Carotid Artery Bypass Geoffrey Hobika, MD, and Jahan Porhomayon, MD, FCCP
T
HE AUTONOMIC NERVOUS system and carotid sinus baroreceptor activities play an important role in the regulation of arterial blood pressure and cardiovascular homeostasis. When these peripheral baroreceptors are exposed to a low-or high-pressure state, the changes in carotid sinus tension wall lead to reduced or increased baroreceptor discharge and, subsequently, to altered sympathetic and vagal tone.1–4 In clinical practice, this reflex is manipulated in the form of carotid massage for the treatment of supraventricular tachycardia. After carotid endarterectomy (CEA) or carotid artery stenting (CAS), carotid baroreceptors may be exposed to a relative increase in blood flow or wall tension, which can result in postoperative systemic hypotension (baroreceptor hyperactivity).5 The authors present a case of prolonged postoperative hypotension after innominate and left common carotid artery bypass for severe common brachiocephalic trunk stenosis in a patient with an aortic arch anomaly. They postulated that his prolonged postoperative hypotension was due to bilateral carotid baroreceptor dysfunction. CASE REPORT
A 55-year-old man with a past medical history of hyperlipidemia and a 46-pack-year smoking history sought medical attention with symptoms of right arm claudication and amaurosis fugax involving his right eye. In his initial evaluation, the right arm pain during exertion raised concern for angina, and coronary ischemia was evaluated with a normal treadmill stress test, and echocardiography revealed normal left ventricular systolic function, wall motion, and no valvular issues. Then after an episode of amaurosis fugax, his vascular anatomy was studied, revealing an aortic arch variant in which both the innominate artery and the left common carotid artery had a common origin from the aorta (also referred to as a “common brachiocephalic trunk”) (Fig 1). The patient had a significant flow-limiting proximal stenosis involving the common brachiocephalic trunk, in effect causing significant reduction of blood flow to his left and right common carotid arteries as well as his right subclavian artery. His carotid arteries were without other flow-limiting atherosclerotic lesions. His left subclavian artery takeoff from the aorta was in a normal location and without significant atherosclerotic disease. Physical examination revealed a diminished right radial pulse and a significant discrepancy in his upper extremity blood pressure recordings (left: 121/83 mmHg, right: 61/37 mmHg). Home medication included clopidogrel, simvastatin, and loratadine. He came for elective bypass, and preoperatively, largebore peripheral intravenous access was secured and a left radial
arterial catheter was placed. The patient then was brought to the operating room and general anesthesia was induced; invasive arterial pressure monitors, including a pulmonary artery catheter and a right radial arterial catheter, were placed. Bilateral radial artery catheters were placed to assess the success of revascularization of the innominate artery. Through a median sternotomy, the patient underwent an ascending aorta-to-innominate artery and left common carotid artery bypass. This was accomplished with a bifurcated Dacron graft anastomosed in an end-to-side manner from the ascending aorta to his right innominate and left common carotid arteries, which were each anastomosed each in an end-to-end manner (Fig 2). After the completion of the bypass, the bilateral upper extremity blood pressures were equivalent to within 10 mmHg. Immediately, the post-bypass patient required multiple intravenous boluses of phenylephrine to maintain mean arterial pressure (MAP) above 65 mmHg (Fig 3). A strategy of lowdose inhalation anesthesia as well as infusion of low-dose propofol plus maintenance of baseline hemodynamics provided the necessary mechanisms for brain protection against cerebral ischemia.6 Additionally, healthy young individuals can tolerate temporary partial occlusion of the innominate artery because of sufficient collateral flow from the contralateral carotid and vertebral arteries. Upon arrival to the intensive care unit, the patient was intubated and became hemodynamically unstable, with systolic blood pressure decreasing to the 70 mmHg-to-80 mmHg range. Oxygenation, filling pressures, and cardiac output remained within normal parameters; however, systemic vascular resistance was reduced. Bleeding from the 2 mediastinal tubes that were placed intraoperatively was minimal. Hypotension was refractory to crystalloid boluses, and vasopressor therapy was initiated. Norepinephrine was started at 4 μg/min and titrated up to 16 μg/min. A vasopressin infusion was started at 0.04 U/min to maintain MAP above 65 mmHg. Vasopressin was discontinued on postoperative day (POD) 1. Electrocardiogram showed
From the Department of Anesthesiology, VA Western New York Healthcare System, State University of New York at Buffalo School of Medicine and Biomedical Sciences, Buffalo, NY. Address reprint requests to Jahan Porhomayon, MD, FCCP, VA Medical Center, Room 203C, 3495 Bailey Avenue, Buffalo, NY 14215. E-mail: [email protected] © 2014 Elsevier Inc. All rights reserved. 1053-0770/2602-0033$36.00/0 http://dx.doi.org/10.1053/j.jvca.2014.12.002 Key words: innominate artery, carotid sinus/body, bypass, hypotension, carotid artery, baroreceptors
Journal of Cardiothoracic and Vascular Anesthesia, Vol ], No ] (Month), 2014: pp ]]]–]]]
1
2
HOBIKA AND PORHOMAYON
IA LSCA
Le carod artery
Fig. 1. Variant anatomy. There is a common origin of the left common carotid artery and innominate artery (bovine arch). IA, innominate artery; LSCA, left subclavian artery.
normal sinus rhythm with no ischemic changes or current of injury, and transthoracic echocardiogram did not reveal any new wall motion abnormality, cardiac tamponade, significant valvular abnormality, or reduced left ventricular end-diastolic/end-systolic volume. Dexamethasone, 4 mg, was given intravenously without improvement in MAP, suggesting adrenal insufficiency was not the etiology. Sepsis was ruled out after all culture results were negative. He was extubated on POD 1. The patient failed attempts to be weaned completely from vasopressor therapy, and he was maintained on norepinephrine infusion until POD 2, at which point he was transitioned to oral midodrine (an
Fig 2.
α1-adrenergic agonist). He was discharged to home on POD 6 with a 10-day taper of midodrine (10 mg BID for 5 days followed by 5 mg BID for 5 days), and he was without neurologic deficits. The patient was seen in follow-up on POD 20, which was 2 days after completion of his midodrine taper, and his blood pressure remained low at 83/62 mmHg. DISCUSSION
This case highlights the role of baroreceptors in cardiovascular homeostasis and the way in which their function may
Schematic diagram of aortic arch bifurcated graft.
PROLONGED HYPOTENSION FOLLOWING BYPASS
3
Fig 3. Time graph represents a trend for mean arterial pressure (MAP) and heart rate (HR). Intraoperative time events are in minutes recorded in different time interval by an assigned number, and postoperative time events are in hours assigned also by a number (covering a total of 3 days). PE, phenylephrine.
be altered by disease processes and surgery. Hypotension and hypertension are known complications that can occur after either CEA or CAS for carotid artery stenosis.7 It has been speculated widely that this is secondary to baroreceptor dysfunction. While these hemodynamic alterations may not be preventable, it is important to be aware that they can occur after these procedures, and are associated with increased morbidity and mortality. In a database review of more than 7,500 patients undergoing CEA, the use of intravenous vasoactive medications for postoperative hypotension was associated with increased myocardial infarction, stroke, congestive heart failure, perioperative mortality, and 1-year death or stroke.8 Similarly, patients who developed persistent hypotension after CAS were at increased risk of both in-hospital complications as well as long-term risk of death.9 The authors’ case is interesting specifically because of the patient’s aortic arch anomaly and the duration of his postoperative hypotension requiring vasopressor therapy. They hypothesized that because the patient had severe stenosis of a common brachiocephalic trunk, which gave rise to the innominate and left common carotid arteries, the left and right
carotid baroreceptors were exposed chronically to low pressures. After the bypass, however, both carotid baroreceptors were exposed to higher pressures than they had been acclimated to preoperatively. The resulting feedback from these conditioned baroreceptors likely affected an increased vagal tone and decreased sympathetic tone, which would explain this patient’s postoperative hypotension. Since both carotid baroreceptors were involved, there was the absence of the attenuating influence of the unaffected, contralateral baroreceptor that normally is present after a standard unilateral CEA or CAS. In that sense, the surgery the authors’ patient underwent is similar to bilateral CEA or CAS. Using a small sample size, Govindarajan et al found that bilateral CEA is associated with a higher incidence of refractory hypotension while those patients undergoing unilateral CEA were found to only have transient hypotension.10 It is important to note a fundamental anatomic difference between the procedures their patient underwent compared to bilateral CEA or CAS. Their patient did not undergo a carotid endarterectomy, and he did not have a carotid stent placed. Both of those surgical interventions could directly damage and physically alter the carotid
4
HOBIKA AND PORHOMAYON
baroreceptors. Instead, the carotid baroreceptors were responding only to increased blood flow once the proximal arterial stenosis at the common brachiocephalic trunk was bypassed. Furthermore, it is possible that his aortic arch baroreceptors were damaged during the operative dissection or ligation of his common brachiocephalic trunk, leading to their dysfunction and contributing to his prolonged postoperative hypotension. Arguing against the authors’ theory of baroreceptor hyperactivity is that the patient never had significant or even relative bradycardia. Given the severity and duration of their patient’s hypotension, they wondered if he could have had any other predisposing factors to indicate hypotension. Park et al retrospectively reviewed more than 1,500 patients undergoing CEA or CAS, and after examining numerous variables found that only preoperative nitrate use or tobacco use significantly correlated
with an increased risk of postoperative hypotension.11 While the authors’ patient was not on nitrates, he did have a history of significant tobacco use. Whether or not that played a role in the development or duration of his postoperative hypotension was difficult to determine. In regard to vasopressor therapy, Gupta et al evaluated 461 patients undergoing CAS; only one patient required vasopressor infusion for 96 hours although the mean time was 15.9 hours.12 Lastly, even though the authors’ patient’s anatomy was unusual, a retrospective review of 94 patients undergoing innominate artery intervention found that 5 (5.32 %) patients had a common brachiocephalic trunk.13 A small trial comparing intravenous dopamine with oral midodrine in patients undergoing CAS showed promising results in clinical outcomes and costs associated with these admissions.14
REFERENCES 1. Fadel PJ, Stromstad M, Hansen J, et al: Arterial baroreflex control of sympathetic nerve activity during acute hypotension: Effect of fitness. Am J Physiol Heart Circ Physiol 280:H2524-H2532. 2. Chevalier-Cholat AM, Friggi A: Carotid sinus, aortic, and subclavian baroreceptor activities during cardiopulmonary bypass in rabbits. J Physiol (Paris) 72:971-986, 1976 3. Kunze DL: Reflex discharge patterns of cardiac vagal efferent fibres. J Physiol 222:1-15, 1972 4. Barrett CJ, Bolter CP: The influence of heart rate on baroreceptor fibre activity in the carotid sinus and aortic depressor nerves of the rabbit. Exp Physiol 91:845-852, 2006 5. Harrop JS, Sharan AD, Benitez RP, et al: Prevention of carotid angioplasty-induced bradycardia and hypotension with temporary venous pacemakers. Neurosurgery 49:814-820, 2001 6. Fukuda S, Warner DS: Cerebral protection. Br J Anaesth 99: 10-17, 2007 7. McKevitt FM, Sivaguru A, Venables GS, et al: 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, 2003 8. Tan TW, Eslami MH, Kalish JA, et al: The need for treatment of hemodynamic instability following carotid endarterectomy is associated
with increased perioperative and 1-year morbidity and mortality. J Vasc Surg 59:16-24. e11-e12, 2014 9. Dangas G, Laird JR Jr, Satler LF, et al: Postprocedural hypotension after carotid artery stent placement: Predictors and short- and long-term clinical outcomes. Radiology 215:677-683, 2000 10. Govindarajan R, Kodali N, Aronsohn J, et al: Hemodynamic instability following bilateral carotid endarterectomy. Crit Care 9: P275, 2005 11. Park BD, Divinagracia T, Madej O, et al: Predictors of clinically significant postprocedural hypotension after carotid endarterectomy and carotid angioplasty with stenting. J Vasc Surg 50: 526-533, 2009 12. Gupta R, Abou-Chebl A, Bajzer CT, et al: Rate, predictors, and consequences of hemodynamic depression after carotid artery stenting. J Am Coll Cardiol 47:1538-1543, 2006 13. Azakie A, McElhinney DB, Higashima R, et al: Innominate artery reconstruction: Over 3 decades of experience. Ann Surg 228: 402-410, 1998 14. Sharma S, Lardizabal JA, Bhambi B: Oral midodrine is effective for the treatment of hypotension associated with carotid artery stenting. J Cardiovasc Pharmacol Ther 13:94-97, 2008
Prolonged Hypotension Following Innominate and Left Common Carotid Artery Bypass Geoffrey Hobika, MD, and Jahan Porhomayon, MD, FCCP
T
HE AUTONOMIC NERVOUS system and carotid sinus baroreceptor activities play an important role in the regulation of arterial blood pressure and cardiovascular homeostasis. When these peripheral baroreceptors are exposed to a low-or high-pressure state, the changes in carotid sinus tension wall lead to reduced or increased baroreceptor discharge and, subsequently, to altered sympathetic and vagal tone.1–4 In clinical practice, this reflex is manipulated in the form of carotid massage for the treatment of supraventricular tachycardia. After carotid endarterectomy (CEA) or carotid artery stenting (CAS), carotid baroreceptors may be exposed to a relative increase in blood flow or wall tension, which can result in postoperative systemic hypotension (baroreceptor hyperactivity).5 The authors present a case of prolonged postoperative hypotension after innominate and left common carotid artery bypass for severe common brachiocephalic trunk stenosis in a patient with an aortic arch anomaly. They postulated that his prolonged postoperative hypotension was due to bilateral carotid baroreceptor dysfunction. CASE REPORT
A 55-year-old man with a past medical history of hyperlipidemia and a 46-pack-year smoking history sought medical attention with symptoms of right arm claudication and amaurosis fugax involving his right eye. In his initial evaluation, the right arm pain during exertion raised concern for angina, and coronary ischemia was evaluated with a normal treadmill stress test, and echocardiography revealed normal left ventricular systolic function, wall motion, and no valvular issues. Then after an episode of amaurosis fugax, his vascular anatomy was studied, revealing an aortic arch variant in which both the innominate artery and the left common carotid artery had a common origin from the aorta (also referred to as a “common brachiocephalic trunk”) (Fig 1). The patient had a significant flow-limiting proximal stenosis involving the common brachiocephalic trunk, in effect causing significant reduction of blood flow to his left and right common carotid arteries as well as his right subclavian artery. His carotid arteries were without other flow-limiting atherosclerotic lesions. His left subclavian artery takeoff from the aorta was in a normal location and without significant atherosclerotic disease. Physical examination revealed a diminished right radial pulse and a significant discrepancy in his upper extremity blood pressure recordings (left: 121/83 mmHg, right: 61/37 mmHg). Home medication included clopidogrel, simvastatin, and loratadine. He came for elective bypass, and preoperatively, largebore peripheral intravenous access was secured and a left radial
arterial catheter was placed. The patient then was brought to the operating room and general anesthesia was induced; invasive arterial pressure monitors, including a pulmonary artery catheter and a right radial arterial catheter, were placed. Bilateral radial artery catheters were placed to assess the success of revascularization of the innominate artery. Through a median sternotomy, the patient underwent an ascending aorta-to-innominate artery and left common carotid artery bypass. This was accomplished with a bifurcated Dacron graft anastomosed in an end-to-side manner from the ascending aorta to his right innominate and left common carotid arteries, which were each anastomosed each in an end-to-end manner (Fig 2). After the completion of the bypass, the bilateral upper extremity blood pressures were equivalent to within 10 mmHg. Immediately, the post-bypass patient required multiple intravenous boluses of phenylephrine to maintain mean arterial pressure (MAP) above 65 mmHg (Fig 3). A strategy of lowdose inhalation anesthesia as well as infusion of low-dose propofol plus maintenance of baseline hemodynamics provided the necessary mechanisms for brain protection against cerebral ischemia.6 Additionally, healthy young individuals can tolerate temporary partial occlusion of the innominate artery because of sufficient collateral flow from the contralateral carotid and vertebral arteries. Upon arrival to the intensive care unit, the patient was intubated and became hemodynamically unstable, with systolic blood pressure decreasing to the 70 mmHg-to-80 mmHg range. Oxygenation, filling pressures, and cardiac output remained within normal parameters; however, systemic vascular resistance was reduced. Bleeding from the 2 mediastinal tubes that were placed intraoperatively was minimal. Hypotension was refractory to crystalloid boluses, and vasopressor therapy was initiated. Norepinephrine was started at 4 μg/min and titrated up to 16 μg/min. A vasopressin infusion was started at 0.04 U/min to maintain MAP above 65 mmHg. Vasopressin was discontinued on postoperative day (POD) 1. Electrocardiogram showed
From the Department of Anesthesiology, VA Western New York Healthcare System, State University of New York at Buffalo School of Medicine and Biomedical Sciences, Buffalo, NY. Address reprint requests to Jahan Porhomayon, MD, FCCP, VA Medical Center, Room 203C, 3495 Bailey Avenue, Buffalo, NY 14215. E-mail: [email protected] © 2014 Elsevier Inc. All rights reserved. 1053-0770/2602-0033$36.00/0 http://dx.doi.org/10.1053/j.jvca.2014.12.002 Key words: innominate artery, carotid sinus/body, bypass, hypotension, carotid artery, baroreceptors
Journal of Cardiothoracic and Vascular Anesthesia, Vol ], No ] (Month), 2014: pp ]]]–]]]
1
2
HOBIKA AND PORHOMAYON
IA LSCA
Le carod artery
Fig. 1. Variant anatomy. There is a common origin of the left common carotid artery and innominate artery (bovine arch). IA, innominate artery; LSCA, left subclavian artery.
normal sinus rhythm with no ischemic changes or current of injury, and transthoracic echocardiogram did not reveal any new wall motion abnormality, cardiac tamponade, significant valvular abnormality, or reduced left ventricular end-diastolic/end-systolic volume. Dexamethasone, 4 mg, was given intravenously without improvement in MAP, suggesting adrenal insufficiency was not the etiology. Sepsis was ruled out after all culture results were negative. He was extubated on POD 1. The patient failed attempts to be weaned completely from vasopressor therapy, and he was maintained on norepinephrine infusion until POD 2, at which point he was transitioned to oral midodrine (an
Fig 2.
α1-adrenergic agonist). He was discharged to home on POD 6 with a 10-day taper of midodrine (10 mg BID for 5 days followed by 5 mg BID for 5 days), and he was without neurologic deficits. The patient was seen in follow-up on POD 20, which was 2 days after completion of his midodrine taper, and his blood pressure remained low at 83/62 mmHg. DISCUSSION
This case highlights the role of baroreceptors in cardiovascular homeostasis and the way in which their function may
Schematic diagram of aortic arch bifurcated graft.
PROLONGED HYPOTENSION FOLLOWING BYPASS
3
Fig 3. Time graph represents a trend for mean arterial pressure (MAP) and heart rate (HR). Intraoperative time events are in minutes recorded in different time interval by an assigned number, and postoperative time events are in hours assigned also by a number (covering a total of 3 days). PE, phenylephrine.
be altered by disease processes and surgery. Hypotension and hypertension are known complications that can occur after either CEA or CAS for carotid artery stenosis.7 It has been speculated widely that this is secondary to baroreceptor dysfunction. While these hemodynamic alterations may not be preventable, it is important to be aware that they can occur after these procedures, and are associated with increased morbidity and mortality. In a database review of more than 7,500 patients undergoing CEA, the use of intravenous vasoactive medications for postoperative hypotension was associated with increased myocardial infarction, stroke, congestive heart failure, perioperative mortality, and 1-year death or stroke.8 Similarly, patients who developed persistent hypotension after CAS were at increased risk of both in-hospital complications as well as long-term risk of death.9 The authors’ case is interesting specifically because of the patient’s aortic arch anomaly and the duration of his postoperative hypotension requiring vasopressor therapy. They hypothesized that because the patient had severe stenosis of a common brachiocephalic trunk, which gave rise to the innominate and left common carotid arteries, the left and right
carotid baroreceptors were exposed chronically to low pressures. After the bypass, however, both carotid baroreceptors were exposed to higher pressures than they had been acclimated to preoperatively. The resulting feedback from these conditioned baroreceptors likely affected an increased vagal tone and decreased sympathetic tone, which would explain this patient’s postoperative hypotension. Since both carotid baroreceptors were involved, there was the absence of the attenuating influence of the unaffected, contralateral baroreceptor that normally is present after a standard unilateral CEA or CAS. In that sense, the surgery the authors’ patient underwent is similar to bilateral CEA or CAS. Using a small sample size, Govindarajan et al found that bilateral CEA is associated with a higher incidence of refractory hypotension while those patients undergoing unilateral CEA were found to only have transient hypotension.10 It is important to note a fundamental anatomic difference between the procedures their patient underwent compared to bilateral CEA or CAS. Their patient did not undergo a carotid endarterectomy, and he did not have a carotid stent placed. Both of those surgical interventions could directly damage and physically alter the carotid
4
HOBIKA AND PORHOMAYON
baroreceptors. Instead, the carotid baroreceptors were responding only to increased blood flow once the proximal arterial stenosis at the common brachiocephalic trunk was bypassed. Furthermore, it is possible that his aortic arch baroreceptors were damaged during the operative dissection or ligation of his common brachiocephalic trunk, leading to their dysfunction and contributing to his prolonged postoperative hypotension. Arguing against the authors’ theory of baroreceptor hyperactivity is that the patient never had significant or even relative bradycardia. Given the severity and duration of their patient’s hypotension, they wondered if he could have had any other predisposing factors to indicate hypotension. Park et al retrospectively reviewed more than 1,500 patients undergoing CEA or CAS, and after examining numerous variables found that only preoperative nitrate use or tobacco use significantly correlated
with an increased risk of postoperative hypotension.11 While the authors’ patient was not on nitrates, he did have a history of significant tobacco use. Whether or not that played a role in the development or duration of his postoperative hypotension was difficult to determine. In regard to vasopressor therapy, Gupta et al evaluated 461 patients undergoing CAS; only one patient required vasopressor infusion for 96 hours although the mean time was 15.9 hours.12 Lastly, even though the authors’ patient’s anatomy was unusual, a retrospective review of 94 patients undergoing innominate artery intervention found that 5 (5.32 %) patients had a common brachiocephalic trunk.13 A small trial comparing intravenous dopamine with oral midodrine in patients undergoing CAS showed promising results in clinical outcomes and costs associated with these admissions.14
REFERENCES 1. Fadel PJ, Stromstad M, Hansen J, et al: Arterial baroreflex control of sympathetic nerve activity during acute hypotension: Effect of fitness. Am J Physiol Heart Circ Physiol 280:H2524-H2532. 2. Chevalier-Cholat AM, Friggi A: Carotid sinus, aortic, and subclavian baroreceptor activities during cardiopulmonary bypass in rabbits. J Physiol (Paris) 72:971-986, 1976 3. Kunze DL: Reflex discharge patterns of cardiac vagal efferent fibres. J Physiol 222:1-15, 1972 4. Barrett CJ, Bolter CP: The influence of heart rate on baroreceptor fibre activity in the carotid sinus and aortic depressor nerves of the rabbit. Exp Physiol 91:845-852, 2006 5. Harrop JS, Sharan AD, Benitez RP, et al: Prevention of carotid angioplasty-induced bradycardia and hypotension with temporary venous pacemakers. Neurosurgery 49:814-820, 2001 6. Fukuda S, Warner DS: Cerebral protection. Br J Anaesth 99: 10-17, 2007 7. McKevitt FM, Sivaguru A, Venables GS, et al: 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, 2003 8. Tan TW, Eslami MH, Kalish JA, et al: The need for treatment of hemodynamic instability following carotid endarterectomy is associated
with increased perioperative and 1-year morbidity and mortality. J Vasc Surg 59:16-24. e11-e12, 2014 9. Dangas G, Laird JR Jr, Satler LF, et al: Postprocedural hypotension after carotid artery stent placement: Predictors and short- and long-term clinical outcomes. Radiology 215:677-683, 2000 10. Govindarajan R, Kodali N, Aronsohn J, et al: Hemodynamic instability following bilateral carotid endarterectomy. Crit Care 9: P275, 2005 11. Park BD, Divinagracia T, Madej O, et al: Predictors of clinically significant postprocedural hypotension after carotid endarterectomy and carotid angioplasty with stenting. J Vasc Surg 50: 526-533, 2009 12. Gupta R, Abou-Chebl A, Bajzer CT, et al: Rate, predictors, and consequences of hemodynamic depression after carotid artery stenting. J Am Coll Cardiol 47:1538-1543, 2006 13. Azakie A, McElhinney DB, Higashima R, et al: Innominate artery reconstruction: Over 3 decades of experience. Ann Surg 228: 402-410, 1998 14. Sharma S, Lardizabal JA, Bhambi B: Oral midodrine is effective for the treatment of hypotension associated with carotid artery stenting. J Cardiovasc Pharmacol Ther 13:94-97, 2008
