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Postprocedural Hypotension after Carotid Artery Stent Placement: Predictors and Short- and Long-term Clinical Outcomes¹

¹ From the Division of Cardiology and the Departments of Neuroradiology and Neurology, Washington Hospital Center, Washington, DC. Received April 7, 1999; revision requested June 1; final revision received August 17; accepted August 26. Supported in part by an educational grant from the Cardiovascular Research Foundation, New York, NY. Address correspondence to M.B.L., Cardiovascular Research Foundation, 55 E 59th St, 6th Floor, New York, NY 10022 (e-mail: mbleonmd@compuserve.com).

	Abstract

TOP Abstract Introduction MATERIALS AND METHODS RESULTS DISCUSSION References

 
PURPOSE: To describe the predictors of persistent hypotension after carotid artery stent (CAS) placement and define the clinical outcome of patients with this hemodynamic disturbance.

MATERIALS AND METHODS: One hundred forty CAS procedures were performed in 133 consecutive patients. Post-CAS hypotension—defined as a greater than 40 mm Hg decrease in arterial pressure without evidence of hypovolemia, with a systolic pressure lower than 90 mm Hg at the end of CAS and lasting at least 1 hour—was observed in 25 patients (group 1); 108 patients did not have hypotension (group 2).

RESULTS: Post-CAS hypotension developed in 33.9% of cases after balloon-expandable stent placement versus in 13.6% of cases after self-expanding stent placement (P = .04). In-hospital minor ipsilateral strokes occurred in 16% of cases in group 1 versus in 3% of cases in group 2 (P = .03). There was one (0.9%) major stroke (transient) and three (2.6%) transient ischemic attacks, all of which occurred in group 2 (not significant vs group 1 for both conditions). At 10 months ± 4 (SD) of follow-up, there was greater total mortality in group 1 than in group 2 (20% vs 4%, P = .02), whereas neurologic events did not differ significantly between the groups.

CONCLUSION: Hypotension due to carotid sinus stimulation is frequent after CAS with balloon-expandable stents. This phenomenon correlates with increased in-hospital complications and long-term risk of death.

Index terms: Arteries, transluminal angioplasty, 172.1286, 908.1286 • Carotid arteries, angiography, 172.1248, 908.122 • Carotid arteries, flow dynamics, 172.76, 908.76 • Carotid arteries, interventional procedures, 172.1286, 908.1286 • Carotid arteries, US, 171.1298, 172.1298, 908.1298

	Introduction

TOP Abstract Introduction MATERIALS AND METHODS RESULTS DISCUSSION References

 
Carotid artery stent (CAS) placement is an investigational technique for carotid arterial revascularization, and initial reports suggest that this procedure has promising short- and intermediate-term results (1–4).

A clinical syndrome of prolonged and persistent postprocedural hypotension has been described in association with carotid endarterectomy and surgical manipulation or compression of the carotid bulb (5–7). Persistent hypotension that is not related to hypovolemia also may occur after endovascular CAS (8). The cause of post-CAS hypotension has been attributed to the stretching of the carotid sinus (5–7); however, to our knowledge, a systematic evaluation of the predictors and sequelae associated with this phenomenon has not been conducted.

The purpose of our study was to define the clinical, angiographic, and procedural predictors of post-CAS hypotension and the short- and long-term clinical outcomes of patients who develop this hemodynamic disturbance.

	MATERIALS AND METHODS

TOP Abstract Introduction MATERIALS AND METHODS RESULTS DISCUSSION References

 
A total of 140 consecutive CAS procedures were performed in 133 patients at the Washington Hospital Center during an 18-month period. An interdisciplinary team from the interventional cardiology, neurology, neuroradiology, and vascular surgery departments was involved in patient care. The institutional review board at Washington Hospital Center approved the study protocol, and all patients gave written informed consent for CAS. Independent neurologic evaluation was scheduled before and after the CAS procedure. Neurologic imaging with computed tomography (CT) or nuclear magnetic resonance (MR) was routinely performed before CAS in all patients and after the procedure if it was clinically indicated. Carotid arterial duplex ultrasonography (US) was performed before CAS and immediately before hospital discharge, and it was scheduled at 6 months.

Persistent postprocedural hypotension was defined as a greater than 40 mm Hg decrease in systolic blood pressure, with a systolic blood pressure lower than 90 mm Hg at the end of CAS that lasted at least 1 hour, without evidence of bleeding, hypovolemia, or heart failure. This syndrome was observed in 25 (18.8%) patients, who composed group 1; the remaining 108 (81.2%) patients who did not have hypotension composed group 2.

CAS Procedure
CAS was routinely performed by using the transfemoral approach through a 9-F arterial sheath. A temporary pacemaker was inserted routinely, and patients were pretreated with 1 mg of atropine intravenously. The common carotid artery was engaged with a 6-F guiding catheter, and then an angled, 0.035-inch hydrophilic guide wire (Terumo, Piscataway, NJ) was advanced in the external carotid artery with fluoroscopic guidance. The 6-F catheter was advanced over the guide wire into the external carotid artery, and then the hydrophilic guide wire was exchanged for a stiff-shaft, 0.035-inch guide wire (Amplatz SuperStiff; Boston Scientific/Vascular [formerly Medi-tech], Natick, Mass). Subsequently, the 6-F guiding catheter over the stiff wire was exchanged for a 9-F guiding catheter that was placed in the common carotid artery.

Baseline angiography was performed, and a floppy-tip, 0.014-inch coronary guide wire (MailMan; Boston Scientific/Vascular) was then manipulated across the lesion site and into the distal internal carotid artery and was used to track all subsequent devices as required. Pre-CAS dilation with a 4.0-mm, noncompliant coronary balloon was routinely performed, followed by implantation of one of three stent types: Palmaz stent (Cordis, Warren, NJ) in 73 (52%) procedures, Wallstent (Schneider, Minneapolis, Minn) in 64 (46%), and Integra (Boston Scientific/Vascular) in three (2%). Stent selection was at the discretion of the operator, but self-expanding stents were used in more than 90% of the cases in this study after they became available in the United States.

Balloon-expandable stents were initially used with a balloon sized to the distal internal carotid artery, and they appropriately covered the lesion site. The self-expanding stents were sized (1:1) to the common carotid arterial reference segment. Post-CAS dilation of the stents was performed with a balloon matched to the size of the distal internal carotid arterial reference segment. Owing to the substantial difference between the common carotid arterial and internal carotid arterial diameters, post-CAS dilation of the proximal part of the stent with a final balloon oversized relative to the internal carotid reference segment was required in selected cases. The self-expanding stents were placed in a way that both the distal common and the proximal internal carotid arteries were covered; however, the common carotid stent segment never underwent post-CAS dilation. The post-CAS dilation balloons were sized to the distal reference segment.

The patients were routinely treated with 250 mg of ticlopidine twice daily for 4 weeks and with 325 mg of aspirin daily for an indefinite period. Antiplatelet therapy with ticlopidine was typically initiated within 24 hours before the CAS procedure, with an initial 500-mg dose. Heparin was typically administered as a single bolus of 5,000 U immediately after sheath insertion, the target-activated clotting time was longer than 200 seconds, and no heparin was given after the procedure. All of the patients had previously undergone diagnostic angiography.

Angiography and Intravascular US
Qualitative analysis was performed at an independent core angiographic laboratory by using standard methods (three-reader consensus) and quantitative analysis with digital calipers (9). Measurements and calculations of the percentage of diameter stenosis were performed by using North American Symptomatic Carotid Endarterectomy Trial criteria (10,11). Angiographic success was a final diameter stenosis of less than 30%, and procedural success was the establishment of angiographic success in the absence of major procedural complications.

Intravascular US scans were obtained before the interventional procedure in selected cases and routinely after stent placement. The scans were obtained by using a commercially available intravascular US system (Endosonics, Sacramento, Calif) with a 25-MHz transducer that was withdrawn manually. Onscreen intravascular US scan interpretation and quantitative measurements were performed to assist in sizing the postdilation balloon and to verify the appropriate stent position and expansion. Onscreen quantitative carotid angiography was not routinely used for sizing the postdilation balloon. Qualitative and quantitative intravascular US analyses also were performed by means of two-reader consensus at an independent core laboratory. Quantitative intravascular US measurements included those of the luminal cross-sectional area and the vessel cross-sectional area (within the external elastic membrane) at the distal reference and lesion sites. The percentage of cross-sectional narrowing was calculated as the plaque plus media cross-sectional area (ie, total luminal cross-sectional area) divided by the total vessel cross-sectional area.

Clinical Evaluation and Follow-up
Clinical follow-up information was obtained at an independent data-coordinating center by means of clinic visits or telephone calls to patients and referring physicians; no patient was lost to follow-up. All records relevant to clinical events were obtained and evaluated by a dedicated adjudication committee (an interventional neuroradiologist [L.H.M.], a cardiologist [R.M.], two research nurses, and a neurologist [R.L.] concurred in the adjudication) that made the final decision on the characterization of the event. Independent neurologic evaluations were performed before CAS in all patients and after CAS in the clinically indicated cases, and they were scheduled for 30 days, 6 and 12 months, and yearly thereafter. Patients were considered to be symptomatic at the time of CAS if they had had an ipsilateral neurologic event within the previous 4 months. Transient ischemic attack was defined as a cerebral vascular event that resolved completely within 24 hours. A minor stroke was defined as a new neurologic deficit that increased the National Institutes of Health stroke scale score to 4 or lower. A major stroke was defined as a new neurologic deficit that increased the National Institutes of Health stroke scale score to higher than 4. Strokes that reversed completely within 30 days (score of 0 on modified Rankin scale, of 100 on modified Barthel scale, or of 5 on Glasgow outcome scale) were classified as transient, whereas all other events were classified as permanent. Ocular embolization and optical neuropathy were considered to be neurologic events and were incorporated into the above criteria.

Statistical Analyses
Results were reported as the mean ± 1 SD or as the number and percentage. Categorical variables were compared with the Fisher exact test, and continuous variables were compared with the Student t test. Statistical significance was defined at the P less than .05 level. A P value of greater than .1 was reported as not significant.

	RESULTS

TOP Abstract Introduction MATERIALS AND METHODS RESULTS DISCUSSION References

 
Post-CAS hypotension occurred in 25 (18.8%) patients (group 1). In 12 (48%) of these patients, the hypotension lasted longer than 2 hours. Eleven (44%) of the 25 patients had intraprocedural hypotension, and two (8%) had intraprocedural bradycardia. The mean duration of hypotension (± SD) was 19.7 hours ± 25.8 (range, 1.0–96.0 hours). In 11 (44%) patients, treatment with intravenous vasopressor agents (dopamine or norepinephrine, dose titrated to systolic blood pressure >80 mm Hg) was required for 41.2 hours ± 24.6 (range, 13.5–96.0 hours) in addition to atropine and volume expansion.

The baseline demographics and characteristics of the patients in groups 1 and 2 are shown in Table 1. Unstable angina was more frequent in the group 1 patients: It occurred in five (20%) of 25 procedures in group 1 versus in six (5.2%) of 115 procedures in group 2 (P = .01). No significant between-group differences existed with respect to the medications (including antihypertensive agents) taken or to the baseline heart rates and arterial pressures. Although the two groups did not differ significantly with regard to history of any stroke, the patients in group 1 had had more previous major ipsilateral strokes than had those in group 2: five (20%) cases in group 1 versus seven (6.1%) cases in group 2 (P = .04). No patients in group 2 had a substantial intraprocedural change in arterial pressure.

View larger version (89K): [in this window] [in a new window] [Download PPT slide]   Figure 1. Angiograms obtained in the 30° left anterior oblique projection in a 68-year-old man demonstrate treatment of a carotid arterial lesion with a balloon-expandable stent. As evident in panel 3 (left), final post-CAS dilation with a large balloon, relative to the size of the internal carotid artery, was required to achieve appropriate stent position and expansion at the proximal part of the stent. This patient developed hypotension.

In-Hospital Events
Although there were no significant differences in deaths or Q-wave myocardial infarctions between the groups, the patients in group 1 had more in-hospital complications compared with group 2 patients (Table 3). In the patients who had both post-CAS hypotension and a neurologic event (n = 5), the latter was diagnosed during or after the hypotension in 60% (three of five) of the cases and before the hypotension in 40% (two of five) of the cases. The patients in group 1 needed longer treatment in the intensive care unit (2.7 days ± 0.9 [SD]) and had a longer hospital stay (7.5 days ± 9.2) after CAS compared with the patients in group 2 (0.2 days ± 0.4 and 2.0 days ± 1.3, respectively; P < .01). There was no evidence, either clinically or at CT, of bleeding at the puncture site or into the retroperitoneum in any patients. (All patients with hypotension were screened with CT of the abdomen and pelvis.) All patients had patent carotid arteries at predischarge duplex US.

Long-term Follow-up
Six-month follow-up data were complete in all the cases, with a mean follow-up duration of 10 months ± 4 (Table 4); 1-year follow-up was completed in 91 (65%) of the cases. There was evidence of greater total mortality in the group 1 patients than in the group 2 patients—five (20%) cases in group 1 versus five (4.3%) cases in group 2 (P = .02). All deaths were judged to be nonneurologic and were not associated with evidence of ipsilateral cerebral infarction. One patient in group 2 underwent ipsilateral carotid endarterectomy because of asymptomatic stent restenosis that was diagnosed at routine follow-up vascular duplex US and subsequent angiography.

	DISCUSSION

TOP Abstract Introduction MATERIALS AND METHODS RESULTS DISCUSSION References

 
Postprocedural hypotension after carotid endarterectomy or surgical manipulation of the carotid bulb that is not related to systemic hypovolemia, bleeding, or cardiac failure has been extensively described in the literature (5–8). Baroreflex stimulation has been recognized as the probable cause of this syndrome. Fluctuation in blood pressure after carotid endarterectomy has been considered to be a risk factor for neurologic complications after carotid endarterectomy (12–14). Increased baroreflex sensitivity has been associated with decreased carotid arterial distensibility in healthy individuals (15). In patients with atherosclerotic disease, baroreflex sensitivity has been attributed to the distortion and stretching of the carotid sinus (5–7). Mendelsohn et al (8) initially reported a 37% (seven of 19 cases) prevalence of post-CAS hypotension in a small patient sample treated with self-expanding stents and aggressive post-CAS dilation.

We systematically studied the development of persistent hypotension after percutaneous endovascular CAS that was not related to hypovolemia, bleeding, or heart failure. With respect to baseline characteristics, the patients who developed this phenomenon had a higher prevalence of unstable angina at index admission and of previous major ipsilateral strokes. Despite the otherwise similar demographics, the above differences may reflect a higher atherosclerotic severity or burden in the affected patients.

Procedural Considerations
During CAS, the atherosclerotic plaque is compressed, and the procedure can cause the arterial wall and the carotid sinus to be stretched. The present study results indicate that there is an important association between post-CAS hypotension and procedural factors that might lead to more aggressive carotid sinus stretching. The endovascular deployment of balloon-expandable stents with larger final balloons rather than self-expanding stents was associated with the development of post-CAS hypotension. Similarly, there was a trend toward a larger final lumen and greater stent dimensions at intravascular US in the patients with hypotension. Vessel dimensions may not be the only factors in the development of post-CAS hypotension. Adopting the proper contour of the tapering carotid artery by using the more flexible self-expanding stents may be important for avoiding post-CAS hypotension (Fig 2).

View larger version (92K): [in this window] [in a new window] [Download PPT slide]   Figure 2a. (a) Angiograms obtained in the 70° anterior oblique projection in a 66-year-old man demonstrate treatment of a carotid arterial lesion with a self-expanding stent. The stent, which is substantially longer than the stenotic lesion, adapts to the proximal and distal vessel contour by itself, without balloon dilation. (b) Transverse intravascular US images obtained in the same patient before CAS. In the center of each image is the cross section of the intravascular US imaging catheter (left panel), which is withdrawn from the distal (left panel) to the proximal (right panel) regions and thus facilitates the acquisition of sequential, vertical transverse images of the vessel wall. The luminal area also is seen on the left panel. On the middle panel, the plaque almost encompasses the intravascular US catheter and nearly eliminates the luminal area. Post-CAS dilation was not applied at the proximal or distal part of the stent. (c) Transverse intravascular US scans obtained at the distal (left), middle (middle), and proximal (right) parts of the stent in the same patient verify the appropriate final stent position and expansion. The narrowest stent lumen (middle panel) is at the lesion site. Because complete positioning and expansion were verified at US, no further dilation was applied. This patient did not develop hypotension.

View larger version (60K): [in this window] [in a new window] [Download PPT slide]   Figure 2b. (a) Angiograms obtained in the 70° anterior oblique projection in a 66-year-old man demonstrate treatment of a carotid arterial lesion with a self-expanding stent. The stent, which is substantially longer than the stenotic lesion, adapts to the proximal and distal vessel contour by itself, without balloon dilation. (b) Transverse intravascular US images obtained in the same patient before CAS. In the center of each image is the cross section of the intravascular US imaging catheter (left panel), which is withdrawn from the distal (left panel) to the proximal (right panel) regions and thus facilitates the acquisition of sequential, vertical transverse images of the vessel wall. The luminal area also is seen on the left panel. On the middle panel, the plaque almost encompasses the intravascular US catheter and nearly eliminates the luminal area. Post-CAS dilation was not applied at the proximal or distal part of the stent. (c) Transverse intravascular US scans obtained at the distal (left), middle (middle), and proximal (right) parts of the stent in the same patient verify the appropriate final stent position and expansion. The narrowest stent lumen (middle panel) is at the lesion site. Because complete positioning and expansion were verified at US, no further dilation was applied. This patient did not develop hypotension.

View larger version (58K): [in this window] [in a new window] [Download PPT slide]   Figure 2c. (a) Angiograms obtained in the 70° anterior oblique projection in a 66-year-old man demonstrate treatment of a carotid arterial lesion with a self-expanding stent. The stent, which is substantially longer than the stenotic lesion, adapts to the proximal and distal vessel contour by itself, without balloon dilation. (b) Transverse intravascular US images obtained in the same patient before CAS. In the center of each image is the cross section of the intravascular US imaging catheter (left panel), which is withdrawn from the distal (left panel) to the proximal (right panel) regions and thus facilitates the acquisition of sequential, vertical transverse images of the vessel wall. The luminal area also is seen on the left panel. On the middle panel, the plaque almost encompasses the intravascular US catheter and nearly eliminates the luminal area. Post-CAS dilation was not applied at the proximal or distal part of the stent. (c) Transverse intravascular US scans obtained at the distal (left), middle (middle), and proximal (right) parts of the stent in the same patient verify the appropriate final stent position and expansion. The narrowest stent lumen (middle panel) is at the lesion site. Because complete positioning and expansion were verified at US, no further dilation was applied. This patient did not develop hypotension.

Previous data from therapeutic interventions for post–carotid endarterectomy hypotension indicate that a local lidocaine injection has the potential to anesthetize the carotid sinus nerve and interrupt the afferent loop of the hypotension-inducing reflex with promising results (15,16). Although such precise administration would be difficult with CAS, it could be achieved with US guidance.

Clinical Outcomes
The short- and long-term clinical outcomes of the patients with post-CAS hypotension in our study were considerably worse than those of the patients in the control group. Particularly, in-hospital minor strokes were much more common in the patients who had post-CAS hypotension (Table 3). Although no cause-and-effect relationship was established with these data, the need for early recognition of and therapy for this hemodynamic disturbance appears to be warranted.

The documentation of increased long-term risk of death in the group 1 patients indicates that this phenomenon is a predictor of a poor long-term prognosis. Nervous system–mediated hypotension also has been identified as a predictor of poor long-term survival (17). This suggests that, in addition to procedure-related variables, patient-related susceptibility contributes to the development of post-CAS hypotension.

On the basis of the results of the present study, our current CAS protocol includes the use of self-expanding stents, the routine placement of a temporary pacemaker, and prompt aggressive treatment of intraprocedural hypotension.

Study Limitations
The purpose of this study was to describe the frequency, procedural correlations, and short- and long-term outcomes of post-CAS hypotension. The methodology followed was a post hoc analysis of a prospectively evaluated consecutive series of patients who underwent CAS; the follow-up was designed to determine the clinical outcomes following CAS. Post-CAS hypotension was a predefined variable, and the data coordination center and all the laboratories that controlled the data were independent of the principal investigator and the interventional team. However, to accurately evaluate this syndrome and establish a differential diagnosis and time course in relation to evolving post-CAS neurologic symptoms is an inherently difficult task. In addition, in this study we did not assess whether a specific preventive or therapeutic strategy affects the occurrence or sequelae of post-CAS hypotension, and there was no controlled angiographic follow-up in the cohort of patients.

In conclusion, in our study, postprocedural hypotension in relation to carotid sinus stimulation occurred in 19% of CAS cases (25 of 133 patients), and the patients who developed this syndrome had increased in-hospital complications and long-term risk of death.

	Acknowledgments

 
The authors thank Hong-sheng Wu, PhD, for statistical consultation.

	Footnotes

 
Abbreviation: CAS = carotid artery stent

Author contributions: Guarantors of integrity of entire study, G.D., M.B.L., J.R.L., L.F.S.; study concepts, G.D., M.B.L., J.R.L., L.F.S., R.M., R.L., L.H.M.; study design, G.D., M.B.L., J.R.L., L.F.S., R.M., L.H.M.; definition of intellectual content, G.D., J.R.L., M.B.L., L.F.S., R.M., A.J.L., G.S.M.; literature research, G.D., E.M.P., G.L., A.J.L., L.G., G.S.M.; clinical studies, J.R.L., L.F.S., M.B.L., L.H.M., R.L.; experimental studies, A.J.L., G.L., G.S.M., L.G.; data acquisition, R.M., E.M.P., G.L., L.G.; data analysis, R.M., G.L.; statistical analysis, R.M.; manuscript preparation, G.D., G.L.; manuscript editing, G.D., J.R.L., L.F.S., M.B.L., R.L., G.S.M.; manuscript review, G.D., M.B.L., J.R.L., L.F.S., R.M., L.H.M., R.L., G.S.M.

	References

TOP Abstract Introduction MATERIALS AND METHODS RESULTS DISCUSSION References

 

1. Yadav JS, Roubin GS, Sriram I, et al. Elective stenting of the extracranial carotid arteries. Circulation 1997; 95:376-381.[Abstract/Free Full Text]
2. Yadav JS, Roubin GS, King P, Iyer S, Vitek J. Angioplasty and stenting for restenosis after carotid endarterectomy: initial experience. Stroke 1996; 27:2075-2079.[Abstract/Free Full Text]
3. Mathur A, Roubin GS, Gomez CR, et al. Elective carotid artery stenting in the presence of contralateral occlusion. Am J Cardiol 1998; 81:1315-1317.[Medline]
4. Wholey MH, Wholey M, Bergeron P, et al. Current global status of carotid artery stent placement. Cathet Cardiovasc Diagn 1998; 44:1-6.[Medline]
5. Tyden G, Samnegard H, Thulin L, Muhrbeck O. Effect of carotid endarterectomy on baroreflex sensitivity in man: intraoperative studies. Acta Chir Scand 1980; 500:67-69.
6. Landesberg G, Adam D, Berlatzky Y, Akselrod S. Step baroreflex response in awake patients undergoing carotid surgery: time- and frequency-domain analysis. Am J Physiol 1998; 274:H1590-H1597.[Abstract/Free Full Text]
7. Eskridge JM, Harris AB, Finch L, Alotis MA. Carotid sinus syndrome and embolization procedures. Am J Neuroradiol 1993; 14:818-820.[Abstract]
8. Mendelsohn FO, Weissman NJ, Lederman RJ, et al. Acute hemodynamic changes during carotid artery stenting. Am J Cardiol 1998; 82:1077-1081.[Medline]
9. Popma JJ, Bashore TD. Qualitative and quantitative angiography. In: Topol E, eds. Textbook of interventional cardiology. Philadelphia, Pa: Saunders, 1994; 1052-1068.
10. Barnett HM, Taylor DW, Eliasziw M, et al. Benefit of carotid endarterectomy in patients with symptomatic moderate or severe stenosis: North American Symptomatic Carotid Endarterectomy Trial Collaborators. N Engl J Med 1998; 339:1415-1425.[Abstract/Free Full Text]
11. Chassin MR. Appropriate use of carotid endarterectomy. N Engl J Med 1998; 339:1468-1471.[Free Full Text]
12. Tu JV, Hannan EL, Anderson GM, et al. The fall and rise of carotid endarterectomy in the United States and Canada. N Engl J Med 1998; 339:1441-1447.[Abstract/Free Full Text]
13. White JS, Sirinek KR, Root HD, Rodgers W. Morbidity and mortality of carotid endarterectomy. Arch Surg 1981; 116:409-412.[Abstract/Free Full Text]
14. Owens ML, Wilson SE. Prevention of neurologic complications of carotid endarterectomy. Arch Surg 1982; 117:551-555.[Abstract/Free Full Text]
15. Tyden G, Samnegard H, Thulin L. Rational treatment of hypotension after carotid endarterectomy by carotid sinus nerve blockade. Acta Chir Scand 1980; 500:61-64.
16. Pine R, Avellone JC, Hoffman M, Plecha FR, Swayngim DM, Urban J. Control of post-carotid endarterectomy hypotension with baroreceptor blockade. Am J Surg 1984; 147:763-765.[Medline]
17. Masaki KH, Schatz IJ, Burchfiel CM, et al. Orthostatic hypotension predicts mortality in elderly men: the Honolulu Heart Program. Circulation 1998; 98:2290-2295.[Abstract/Free Full Text]

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