Post-carotid Endarterectomy Hypertension Research Articles

Perioperative baseline β-blockers: An independent protective factor for post-carotid endarterectomy hypertension.

Post-carotid endarterectomy hypertension is a well-recognized phenomenon closely related to surgical complications. This study aimed to determine whether different kinds of perioperative antihypertensive drugs had a protective effect on post-carotid endarterectomy hypertension and influence on intraoperative hemodynamics. We retrospectively investigated 102 carotid stenosis patients who underwent conventional endarterectomy with a perioperative baseline antihypertensive regimen. Post-carotid endarterectomy hypertension was defined as a postoperative peak systolic blood pressure ≥160 mmHg and/or a requirement for any additional antihypertensive therapies. We compared the clinical characteristics and types of baseline perioperative antihypertensive drugs between patients with and without post-carotid endarterectomy hypertension and then determined the significant independent effect of antihypertensive drugs on post-carotid endarterectomy hypertension through multivariate regression and detected their influence on intraoperative hypertension (induction-related systolic blood pressure and vasodilators consumption) and hemodynamic depression (intra-arterial systolic blood pressure ≤100 mmHg and/or heart rate ≤50beats/min). We also investigated adverse events such as stroke, death, myocardial infarction, and cerebral hyperperfusion syndrome during the postoperative hospitalization. A total of 52/102 (51.0%) patients were defined as having post-carotid endarterectomy hypertension during the first three days postoperative, including eight patients with a postoperative systolic blood pressure that exceeded 160 mmHg at least once, 31 patients requiring postoperative antihypertensive treatment in addition to their baseline regimen, and 13 patients with both. The incidence of stroke/death/myocardial infarction and cerebral hyperperfusion syndrome after conventional endarterectomy during hospitalization were both 1.9%. A significantly increased risk of composite postoperative complications (including cerebral hyperperfusion syndrome, hyperperfusion-related symptoms, transient ischemic attacks, stroke, death, and cardiac complications) was observed in patients with post-carotid endarterectomy hypertension than without (15.4% versus 2.0%, p = 0.032). Patients free of post-carotid endarterectomy hypertension had a higher incidence of perioperative baseline β-blocker use than patients who suffered from post-carotid endarterectomy hypertension (46.0% versus 21%, p = 0.008). In multivariate analysis, β-blocker use was a significant independent protective factor for post-carotid endarterectomy hypertension (OR = 0.356, 95% CI: 0.146-0.886, p = 0.028). Patients taking β-blockers had a lower postoperative peak systolic blood pressure than the β-blocker-naïve population (137.1 ± 12.1 mmHg versus 145.0 ± 11.2 mmHg, p = 0.008), but the postoperative mean systolic blood pressure showed no intergroup difference. However, the incidence of hemodynamic depression during conventional endarterectomy was higher in patients with perioperative β-blocker use than in those without (44.1% versus 25.0%, p = 0.050). The difference in intraoperative hemodynamic depression became more prominent between the β-blocker and non-β-blocker groups (81.8% versus 33.3%, p = 0.014) for whose preoperative baseline heart rate was equal to or lower than 70beats/min. The perioperative use of β-blockers is a protective factor for post-carotid endarterectomy hypertension and contributes to stabilizing the postoperative peak systolic blood pressure three days after conventional endarterectomy. However, β-blockers might also lead to intraoperative hemodynamic depression, especially for patients with a low baseline heart rate.

Clinical outcomes of postcarotid endarterectomy hypertension

ObjectiveThe objective of this study was to determine the clinical relevance of postcarotid endarterectomy hypertension (PEH) by investigating the effect of PEH on hospital length of stay (LOS) and by investigating short-term and long-term complications of PEH. In addition, risk factors for PEH were determined. MethodsA single-center retrospective cohort study was performed. Demographic, preoperative, intraoperative, and postoperative outcomes of 192 patients undergoing carotid endarterectomy were evaluated. Outcomes were compared between patients with PEH and patients without PEH. PEH was defined as an acute systolic blood pressure (SBP) rise >170 mm Hg or persistent SBP >150 mm Hg on the ward and leading to the consultation of an internist. The overall survival and event-free survival were compared using a Kaplan-Meier analysis and a Cox regression analysis. A multivariate logistic regression analysis was performed to determine risk factors for PEH. ResultsPEH developed in 44 of 192 patients (25%). Preoperative hypertension (SBP >150 mm Hg) was determined to be a risk factor for PEH (odds ratio, 3.3; 95% confidence interval [CI], 1.6-6.9). Hospital LOS was prolonged in patients with PEH compared with patients without PEH (median LOS of 5 days vs 3 days, respectively; P < .001). No difference in the occurrence of ischemic neurologic events or rebleeding during hospitalization was observed (P = .58 and P = .72, respectively). Cardiovascular and ischemic neurologic events during follow-up did not occur more often in patients with PEH than in patients without PEH (P = .46). There was no difference in mortality between the PEH and non-PEH groups (hazard ratio, 1.6; 95% CI, 0.6-4.3). The same applies to the event-free survival (hazard ratio, 0.77; 95% CI, 0.4-1.7). Combined event-free survival for stroke and myocardial infarction was 92% (95% CI, 87%-97%) at 2 years for patients without PEH and 86% (95% CI, 74%-98%) at 2 years for patients with PEH (P = .25). Event-free survival for mortality was 90% (95% CI, 85%-96%) at 2 years for patients without PEH and 94% (95% CI, 86%-100%) at 2 years for patients with PEH (P = .36). ConclusionsPatients with PEH had a significant increase in hospital LOS. However, adverse short-term and long-term events did not occur more often in patients with PEH. High preoperative SBP was identified as a risk factor for PEH; no other demographic and clinical variables were associated with PEH.

Post-Carotid Endarterectomy Hypertension. Part 1: Association with Pre-operative Clinical, Imaging, and Physiological Parameters

Post-endarterectomy hypertension (PEH) is a well recognised, but poorly understood, phenomenon after carotid endarterectomy (CEA) that is associated with post-operative intracranial haemorrhage, hyperperfusion syndrome, and cardiac complications. The aim of the current study was to identify pre-operative clinical, imaging, and physiological parameters associated with PEH. In total, 106 CEA patients undergoing CEA under general anaesthesia underwent pre-operative evaluation of 24 hour ambulatory arterial blood pressure (BP), baroreceptor sensitivity, cerebral autoregulation, and transcranial Doppler measurement of cerebral blood flow velocity (CBFv) and pulsatility index. Patients who met pre-existing criteria for treating PEH after CEA (systolic BP [SBP] > 170 mmHg without symptoms or SBP > 160 mmHg with headache/seizure/neurological deficit) were treated according to a previously established protocol. In total, 40/106 patients (38%) required treatment for PEH at some stage following CEA (26 in theatre recovery [25%], 27 while on the vascular surgical ward [25%]), while seven (7%) had SBP surges > 200 mmHg back on the ward. Patients requiring treatment for PEH had a significantly higher pre-operative SBP (144 ± 11 mmHg vs 135 ± 13 mmHg; P < .001) and evidence of pre-existing impairment of baroreceptor sensitivity (3.4 ± 1.7 ms/mmHg vs 5.3 ± 2.8 ms/mmHg; P = .02). However, PEH was not associated with any other pre-operative clinical features, CBFv, or impaired cerebral haemodynamics. Paradoxically, autoregulation was better preserved in patients with PEH. All four cases of hyperperfusion associated symptoms were preceded by PEH. Length of hospital stay was significantly increased in patients with PEH (P < .001). In this study, where all patients underwent CEA under general anaesthesia, PEH was associated with poorly controlled pre-operative BP and impaired baroreceptor sensitivity, but not with other peripheral or central haemodynamic parameters, including impaired cerebral autoregulation.

Post-carotid Endarterectomy Hypertension. Part 2: Association with Peri-operative Clinical, Anaesthetic, and Transcranial Doppler Derived Parameters

The first paper in this series observed that pre-operative baroreceptor dysfunction and poorly controlled hypertension were independently predictive for identifying patients who went on to require treatment for post-endarterectomy hypertension (PEH). The second paper examines the influence of intra-operative patient, transcranial Doppler (TCD) ultrasound, and anaesthetic variables on the incidence of PEH. In total, 106 patients underwent carotid endarterectomy (CEA) under general anaesthesia. Systolic blood pressure (SBP) changes, anaesthetic and vasoactive agents, analgesia, and post-operative pain scores, as well as TCD derived changes in middle cerebral artery (MCA) velocity during surgery were recorded. Patients who met pre-existing unit criteria for treating PEH after CEA (SBP>170mmHg without symptoms or SBP>160mmHg with headache/seizure/neurological deficit) were treated according to an established and validated protocol. In total, 40/106 patients (38%) required treatment for PEH following CEA (26 in theatre recovery [25%], 27 back on the vascular surgery ward [25%]), whereas seven (7%) had SBP surges>200mmHg on the ward. Patients requiring treatment for PEH had significantly higher pre-induction SBP (174±21mmHg vs. 153±21mmHg; p<.001), the greatest decreases in SBP after induction of anaesthesia (median decrease 100±32mmHg vs. 83±24mmHg; p=.01) and were significantly more likely to experience moderate/severe pain scores post-operatively (p=.003). Logistic regression analysis of the pre- and intra-operative data revealed that higher pre-induction mean SBP and lower pre-operative (impaired) BRS were the only independent predictors of PEH. This analysis of intra-operative variables has demonstrated that patients with poorly controlled and/or labile hypertension at induction of general anaesthesia were those at greatest risk of requiring treatment for PEH in the post-operative period after CEA. No other variables, including use of vasopressors, treatment of hypotension, anaesthetic agents, or changes in MCA velocity after clamp release and restoration of flow were able to predict who might go on to require treatment for PEH. Identification of at-risk individuals and aggressive blood pressure control in the post-operative period remains the mainstay of treatment.

Post-Carotid Endarterectomy Hypertension. Part 1: Association with Pre-operative Clinical, Imaging, and Physiological Parameters

Post-endarterectomy hypertension (PEH) is a well recognised, but poorly understood, phenomenon after carotid endarterectomy (CEA) that is associated with post-operative intracranial haemorrhage, hyperperfusion syndrome, and cardiac complications. The aim of the current study was to identify pre-operative clinical, imaging, and physiological parameters associated with PEH. In total, 106 CEA patients undergoing CEA under general anaesthesia underwent pre-operative evaluation of 24 hour ambulatory arterial blood pressure (BP), baroreceptor sensitivity, cerebral autoregulation, and transcranial Doppler measurement of cerebral blood flow velocity (CBFv) and pulsatility index. Patients who met pre-existing criteria for treating PEH after CEA (systolic BP [SBP]>170mmHg without symptoms or SBP>160mmHg with headache/seizure/neurological deficit) were treated according to a previously established protocol. In total, 40/106 patients (38%) required treatment for PEH at some stage following CEA (26 in theatre recovery [25%], 27 while on the vascular surgical ward [25%]), while seven (7%) had SBP surges>200mmHg back on the ward. Patients requiring treatment for PEH had a significantly higher pre-operative SBP (144±11mmHg vs. 135±13mmHg; p<.001) and evidence of pre-existing impairment of baroreceptor sensitivity (3.4±1.7 ms/mmHg vs. 5.3±2.8 ms/mmHg; p=.02). However, PEH was not associated with any other pre-operative clinical features, CBFv, or impaired cerebral haemodynamics. Paradoxically, autoregulation was better preserved in patients with PEH. All four cases of hyperperfusion associated symptoms were preceded by PEH. Length of hospital stay was significantly increased in patients with PEH (p<.001). In this study, where all patients underwent CEA under general anaesthesia, PEH was associated with poorly controlled pre-operative BP and impaired baroreceptor sensitivity, but not with other peripheral or central haemodynamic parameters, including impaired cerebral autoregulation.

The effect of eversion and conventional-patch technique in carotid surgery on postoperative hypertension

Postcarotid endarterectomy hypertension (HTN) is associated with neurological and cardiac complications. The purpose of this study was to assess the influence of eversion carotid endarterectomy (E-CEA) and conventional carotid endarterectomy (C-CEA) on postoperative blood pressure in the first 4 days after surgery. Two hundred seventy-six consecutive CEAs that were performed between February 2008 and September 2009 were reviewed retrospectively with a computerized registry. After exclusion of patients with severe stroke (modified Rankin Scale of 3-5), prior contralateral and ipsilateral carotid surgery and more than 70% stenosis of the contralateral carotid artery, 201 cases remained (E-CEA group: n = 100 vs C-CEA group: n = 101) for analysis. Results in terms of systolic blood pressure, use of intravenous and oral vasodilators, alterations of the existing antihypertensive medications, and perioperative complications (neck hematoma, myocardial infarction, stroke, and death) were compared. Groups were similar with regard to age, sex, and cardiovascular risk factors except for a higher incidence of nicotine use (59% vs 43%; P = .02) in the C-CEA group. Patients in the C-CEA group had a significantly higher percentage of symptomatic carotid artery stenosis (54% vs 23%, respectively; P < .0001). Despite a lower preoperative (baseline) mean systolic blood pressure (130 mm Hg vs 135 mm Hg; P = .02) patients in the E-CEA group had a significantly higher mean systolic blood pressure in the postoperative course up to the day 4 after surgery (134 mm Hg vs 126 mm Hg; P < .0001) and required more frequent intravenous (28% vs 9.9%; P = .001) and oral vasodilators (54% vs 27.7%; P = .0002) compared to those in the C-CEA group. Two-thirds (14 of 21 = 66%) of patients in the E-CEA group with preoperative high blood pressure (systolic blood pressure ≥140 mm Hg and diastolic pressure ≥90 mm Hg) required vasodilators and only one-third (11 of 33 = 33%) in the C-CEA group (P = .03). Atropine use due to bradycardia was necessary after 8 cases (8%) in the C-CEA group and only after 1 case (1%) in the E-CEA group (P = .03). Furthermore, the dosage of existing antihypertensive medications was increased and/or additional medications were prescribed twofold more in the E-CEA group (33% vs 17%; P = .009). No statistically significant difference was noted in the perioperative complication rate. It is concluded that E-CEA is associated with significantly higher postoperative blood pressure that persists for at least 4 days after surgery. Patients with inadequate preoperative high blood pressure control are particularly at risk after E-CEA.

Eversion technique increases the risk for post–carotid endarterectomy hypertension

Objective: The incidence of postoperative hypertension (HTN) after eversion carotid endarterectomy (e-CEA) was compared with that after standard carotid endarterectomy (s-CEA). Methods: In a retrospective analysis from January 1998 to January 2000, 217 patients underwent 219 CEAs for symptomatic (68) or asymptomatic (151) high-grade (>80%) carotid artery stenosis by either standard (137) or eversion (82) techniques. The eversion technique involves an oblique transection of the internal carotid artery at the carotid bulb and a subsequent endarterectomy by everting the internal carotid artery over the atheromatous plaque. All procedures were done under general anesthesia, and somatosensory-evoked potentials were used for cerebral monitoring. Patients with s-CEA were compared with those with e-CEA for postoperative hemodynamic instability, carotid sinus nerve block, requirement for intravenous vasodilators or vasopressors, stroke, and death. Results: Patients who underwent e-CEA had a significantly (P <.005) increased postoperative blood pressure and required more frequent intravenous antihypertensive medication (24%), compared with patients having an s-CEA (6%). Furthermore, postoperative vasopressors were required after 10% of s-CEAs, but after none of the e-CEAs. No statistically significant difference was noted in the morbidity or mortality of patients after s-CEA and e-CEA. Conclusion: e-CEA is a substantial risk factor for HTN in the immediate postoperative period, when compared with the s-CEA. This difference would be even more remarkable in the absence of antihypertensive medications in the e-CEA group and vasopressors in the s-CEA group. Therefore, particular attention should be focused on diagnosing and controlling postoperative HTN in patients after e-CEA. (J Vasc Surg 2001;34:839-45.)

Preoperative Hypertension does Predict Post-Carotid Endarterectomy Hypertension

Preoperative Hypertension does Predict Post-Carotid Endarterectomy Hypertension

Post-carotid endarterectomy hypertension: Association with elevated cranial norepinephrine

The cause and mechanism of post-carotid endarterectomy hypertension remains unknown. To determine the influence of the sympathetic and renin-angiotensin system, we measured cranial and peripheral plasma levels of catecholamine and renin in patients undergoing carotid endarterectomy. Baseline samples were drawn just before carotid clamping (sample I) and compared with study samples drawn immediately after clamp release (sample II), 2 to 6 hours after surgery (sample III), and then 18 to 24 hours after surgery (sample IV). The patients with post-carotid endarterectomy hypertension had an associated increase of cranial and peripheral norepinephrine levels in the postoperative hypertensive period whereas the patients without post-carotid endarterectomy hypertension did not. This association was most pronounced and statistically significant in cranial samples II (p = 0.032) and III (p = 0.005). Epinephrine and dopamine values did not correlate with post-carotid endarterectomy hypertension. Renin values were higher in cranial than in peripheral samples at time period 2 (p = 0.011), sugestive of a central nervous system Goldblatt phenomenon. However, the renin values did not correlate with post-carotid endarterectomy hypertension. We conclude that post-carotid endarterectomy hypertension is associated with elevated cranial norepinephrine levels, suggestive of a central nervous system sympathomimetic mechanism. Optimal prevention and treatment of this brief but frequently occurring hypertension should include a central-acting sympatholytic agent.

Post-carotid endarterectomy hypertension: association with elevated cranial norepinephrine.

The cause and mechanism of post-carotid endarterectomy hypertension remains unknown. To determine the influence of the sympathetic and renin-angiotensin system, we measured cranial and peripheral plasma levels of catecholamine and renin in patients undergoing carotid endarterectomy. Baseline samples were drawn just before carotid clamping (sample I) and compared with study samples drawn immediately after clamp release (sample II), 2 to 6 hours after surgery (sample III), and then 18 to 24 hours after surgery (sample IV). The patients with post-carotid endarterectomy hypertension had an associated increase of cranial and peripheral norepinephrine levels in the postoperative hypertensive period whereas the patients without post-carotid endarterectomy hypertension did not. This association was most pronounced and statistically significant in cranial samples II (p = 0.032) and III (p = 0.005). Epinephrine and dopamine values did not correlate with post-carotid endarterectomy hypertension. Renin values were higher in cranial than in peripheral samples at time period 2 (p = 0.011), suggestive of a central nervous system Goldblatt phenomenon. However, the renin values did not correlate with post-carotid endarterectomy hypertension. We conclude that post-carotid endarterectomy hypertension is associated with elevated cranial norepinephrine levels, suggestive of a central nervous system sympathomimetic mechanism. Optimal prevention and treatment of this brief but frequently occurring hypertension should include a central-acting sympatholytic agent.

The Relationship of Early Hypertension Following Carotid Endarterectomy to Intraoperative Cerebral Ischemia

The relationship between early hypertension following carotid endarterectomy, and intraoperative cerebral ischemia was investigated. Two measures of the adequacy of collateral cerebral circulation during carotid clamping were used: collateral cerebral perfusion pressure (delta P), and the ratio of collateral to ipsilateral cerebral vascular resistance (R/R). Change in blood pressure was measured by the ratio of mean early post to preendarterectomy pressure (P/P). Nitroprusside or nitroglycerin (NN) was used after endarterectomy to maintain systolic blood pressure less than 160 mmHg. The mean values for NN (n = 26) and no NN (n = 81) groups were: delta P = 30.0 and 40.2 mmHg (p less than 0.001); R/R = 1.93 and 1.24 (p less than 0.005); and P/P = 1.03 and 0.857 (p less than 0.001 p by unpaired t test). Linear regression analysis of the two measures of cerebral perfusion with the ratio of post-to preoperative blood pressure gave correlation coefficients between 0.629 and 0.841 with a probability that the slope of the regression line greater than 0 of less than 0.01. Low delta P and high R/R correlate with early postcarotid endarterectomy hypertension. These results support the hypothesis that one determinant of early post endarterectomy hypertension is inadequate collateral cerebral circulation during carotid clamping.

Incidence and mechanism of post-carotid endarterectomy hypertension.

Hypertension following carotid endarterectomy occurs frequently but is poorly understood. Its occurrence has been correlated with an increased incidence of neurologic complication. We identified those factors that correlate with an increased incidence of post-carotid endarterectomy hypertension. The records of 100 patients who underwent carotid endarterectomy at UCLA Medical Center from November 1981 to September 1983 were examined. One hundred fifty variables were surveyed to determine those factors associated with this problem. Fifty-eight percent of the study patients developed post-carotid endarterectomy hypertension (an increase in systolic blood pressure greater than 35 mm Hg over baseline, and/or blood pressure requiring treatment with sodium nitroprusside). Of patients who developed this problem, 93% had diabetes mellitus, 75% received isoflurane anesthesia, 71% had peripheral vascular occlusive disease, 71% underwent ipsilateral transient ischemic attacks, and 65% had high-grade ipsilateral carotid stenosis. These variables have in common the loss of or interference with cerebral autoregulation. Central dysautoregulation may set the stage for a positive feedback mechanism that results in increased blood pressure. Anesthetic agents that do not interfere with cerebral autoregulation may reduce the incidence of this complication, and an aggressive treatment program may prevent neurologic complications.

Avoidance of postcarotid endarterectomy hypertension.

To minimize extreme blood pressure changes after carotid endarterectomy, dissection methods were developed to preserve the intercarotid neural bundle supplying the carotid baroreceptors and applied to our last 90 consecutive carotid endarterectomies. Hypertension was defined as a rise in systolic blood pressure greater than 40 mmHg and hypotension as a drop of 40 mmHg in those with preoperative hypertension or a systolic blood pressure of less than 100 mmGh. There were 46 cases hypertensive before operation, and the remaining 44 were normotensive before operation. When the series was analyzed, half the patients undergoing nerve-sparing dissection became hypotensive, irrespective of pre-existing hypertension extent and bilaterality of stenoses, and preoperative neurologic deficits. Hypotension was a transient and benign process and easily controlled by catheter instillation of 2% xylocaine in the postoperative period. Hypertension, which occurred in ten patients, was equally benign; only five required treatment. There were no deaths or neurologic deficits. Nerve-sparing carotid dissection and catheter placement for block of the carotid sinus nerves are valuable methods to minimize extreme blood pressure changes after carotid endarterectomy.