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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3876_Библиотеки_им_академика_М_И_Перельмана
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1.2 Results
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Table 1.2 Outcome after Transcervical Carotid Artery Revascularization (TCAR) (according to
Sagris etal. [23]). Meta-analysis based on 45 studies with 14,588 patients
Parameter Studies included (n) Events/patients total, n (%)
30-day mortality 44 75/14,427 (0.5)
30-day stroke (total) 41 179/13,744 (1.3)
– Symptomatic patients only 10 61/3830 (1.6)
30-day TIA (total) 30 97/12,667 (0.8)
– Symptomatic patients only 5 15/1953 (0.8)
30-day myocardial infarction (total) 34 65/14,173 (0.6)
– Symptomatic patients only 9 10/3674 (0.3)
Technical success 30 1195/1223 (99.0)
Access site complications 30 288/9305 (2.0)
Cranial nerve injury 21 33/8994 (0.36)
Haemodynamic instability 6 1306/5183 (21.0)
Bleeding 20 278/8726 (2.0)
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based on 45 studies with 14,588 patients, published by May 2020 (Table1.2). The
technical success rate was 99%. Cranial nerve injuries were very rare (33in 8994
patients), bleeding complications were reported at 2%. The overall periprocedural
all-cause mortality and stroke rate was 0.5% and 1.3%, respectively, and the TIA
rate was 0.8%. In-stent restenosis was observed in 4 of 260 patients (1.5%; 7 studies), and early (30-day) reocclusion or acute thrombosis of the target lesion occurred
in 12 of 1243 patients (∼1%; 11 studies). The results provided signicant evidence
that TCAR is a very promising and safe carotid revascularization approach with
favorable technical success rates associated with low periprocedural stroke and CN
injury rates. However, the data did not allow a direct comparison with CAS and
CEA; these were predominantly single-arm studies.
Another meta-analysis [24] included 18 studies, published up to September
2020, with 4852 patients. The authors reported a pooled 30-day mortality rate of
0.7%, a 30-day stroke rate of 1.4% and a stroke/TIA rate of 2%. The pooled technical success rate was 97.6%. Cranial nerve injuries (10 studies) were observed in
1.2% and the early myocardial infarction rate was 0.4%. The rate of haematoma/
bleeding was 3.4% (one third of these cases required drainage or intervention).
Within a follow-up of 3–40months, the restenosis rate was 4% (9 studies) and the
stroke/death rate was 4.5% (5 studies). The authors reported a higher risk of early
stroke/TIA for symptomatic patients than for asymptomatic patients (2.5%
vs. 1.2%).
Both meta-analyses describe TCAR as a promising procedure with low rates of
early death, stroke and other complications. Long-term results remain to be seen.
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1.2.4.2 TCAR-Study Results
Columbo etal. [25] tested the hypothesis that TCAR may be particularly valuable
in patients with challenging anatomy, such as a high carotid artery bifurcation or a
carotid lesion close to the skull base, that would make traditional carotid endarterectomy (CEA) technically difcult. For these patients, TCAR provides a therapeutic alternative that may be associated with a lower risk prole than CEA.Patients
captured by the Vascular Quality Initiative (VQI) database who underwent TCAR or
CEA from January 2015 were analyzed. 7664 patients (8.9%) underwent TCAR
and 78,363 patients (91.1%) underwent CEA.The use of TCAR out of the total
carotid revascularization procedures increased from 90 of 12,276 procedures (0.7%)
in 2015 to 2718 of 15,956 procedures (17.0%) in 2019, a 24-fold increase over
5 years. Overall, the crude rate of MACE (Major Adverse Cardiovascular
Events = composite stroke, myocardial infarction, death) was similar for TCAR
(2.3%) and CEA (2.4%). However, over time, the rate of MACE decreased for CEA
(from 2.5% to 1.9%); this was also the case with TCAR, but not signicantly (from
3.1% to 2.2%). Centres that included TCAR in their treatment spectrum showed a
10% decrease in the likelihood of MACE at 12months after TCAR adoption compared to centres that continued to perform CEA only. The study demonstrated that
availability of TCAR at a hospital was associated with a decrease in the likelihood
of perioperative MACE after carotid revascularization.
In a retrospective analysis of VQI data, Mehta etal. [26] investigated whether
80-year-old patients would benet from TCAR.Among 33,115 patients who underwent either CEA, TFCAS or TCAR for carotid artery stenosis, 21% were at least
80years old. Across all, 80-year-old patients had higher death/stroke rates compared to younger patients. Among octogenarians, the adjusted hazards of TCARs
relative to CEAs was similar for both 30-day stroke/death (hazard ratio [HR], 1.12;
95% condence interval [CI], 0.59–2.13) and 1-year stroke/death (HR, 1.28; 95%
CI, 0.85–1.94), whereas transfemoral carotid artery stenting had higher hazards of
both 30-day stroke/death (HR, 1.78; 95% CI, 1.10–2.89) and 1-year stroke/death
(HR, 1.85; 95% CI, 1.35–2.54). The authors concluded that TCARs may serve as a
promising less invasive treatment for carotid disease in older patients who are
deemed high anatomic, surgical, or clinical risk for CEAs.
1 Extracranial Carotid Stenosis
1.3 Conclusions forClinical Practice
1. CEA is the method of choice for the treatment of asymptomatic and symptom-
atic carotid stenosis. Nevertheless, the postprocedural outcomes after CEA and
CAS suggest that improvements in the periprocedural safety of CAS may provide similar outcomes of both procedures in the future.
1.4 Perioperative Management
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2. All patients should take acetylsalicylic acid (ASA, 100 mg) before and after
CEA, continuous treatment with ASA should not be interrupted. All patients
should take a statin before and after CEA, continuous therapy with statins should
not be interrupted. Dual antiplatelet therapy with ASA (100mg) and clopidogrel
(75mg) should precede CAS.Dual antiplatelet therapy should be maintained for
at least 1 month.
3. CEA should be performed as early as possible (within 3–14 days) after the
index event.
4. The choice of surgical procedure (eversion CEA, conventional CEA with patch-
plasty) should be made depending on the personal experience of the operating
surgeon and the lesion’s anatomy.
5. Patchplasty should always be used for conventional CEA.There is insufcient
evidence for the routine (obligatory) insertion of a shunt during surgical carotid
reconstruction. Intraoperative neuromonitoring should be considered for CEA
under general anaesthesia.
6. Transcarotid arterial revascularisation (TCAR) is a promising procedure with
low rates of early death, stroke and other complications. Long-term results
remain to be seen. However, the data do not yet allow a direct comparison with
CAS and CEA; the reports are predominantly single-arm studies.
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1.4 Perioperative Management
1.4.1 Imaging Strategies inCarotid Artery Disease
1.4.1.1 European Society forVascular Surgery (ESVS) [1]
Recommendation 1: For patients undergoing evaluation of the extent and severity of
extracranial carotid stenoses, duplex ultrasound, computed tomographic angiography and/or magnetic resonance angiography are recommended. (Class I; Level B).
Recommendation 2: For patients where carotid endarterectomy is being considered, it is recommended that duplex ultrasound stenosis estimation be corroborated
by computed tomographic angiography or magnetic resonance angiography, or by a
repeat duplex ultrasound performed by a second operator. (Class I; Level B).
Recommendation 3: For a patient where carotid artery stenting is being considered, it is recommended that any duplex ultrasound study be followed by computed
tomographic angiography or magnetic resonance angiography, which will provide
additional information on the aortic arch, as well as the extra- and intracranial circulation. (Class I; Level B).
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1 Extracranial Carotid Stenosis
1.4.2 Anaesthesia
1.4.2.1 European Society forVascular Surgery (ESVS) [1]
Recommendation 65: In patients undergoing carotid endarterectomy, decisions
regarding choice of anaesthesia (locoregional, general) should be considered at the
discretion of the surgeon/anaesthetist performing the procedure, taking account of
local experience, patient preference, and preferred antiplatelet strategy. (Class IIA/
Level B).
1.4.2.2 Studies
Harky et al. [27] published a meta-analysis comparing general (GA) and local
anaesthesia (LA) for CEA. 31 studies (including 6 randomised controlled trials
(RCT)) with a total of 152,376 patients were analysed. LA was associated with
shorter operative time (mean difference − 9.15 min; p = 0.005), less strokes
(OR=0.76; 95% CI =0.59–0.92; p=0.006), cardiac complications (OR=0.59;
95% CI=0.47–0.73; p<0.00001) and lower in-hospital mortality (OR=0.72; 95%
CI = 0.59–0.9; p = 0.003). Transient neurological decits occurred with similar
frequency in both groups. In a subgroup analysis, only the randomised controlled
trials were assessed. The number of patients included there was relatively small
(total n=3956). There was no signicant difference between LA and general anaesthesia for CEA.In summary, this meta-analysis showed a slight superiority of LA
over general anaesthesia when evaluating the non-randomised (larger) data set,
while the randomised trials did not show any differences. Anaesthetic choice in
CEA therefore depends on the experience of the anaesthetist and surgeon and on the
patient’s preferences.
1.4.3 Perioperative Antibiotic Prophylaxis
1.4.3.1 Guidelines American Society ofHealth-System Pharmacists
(ASHP) [28]
• Patients undergoing brachiocephalic procedures (e.g., CEA, brachial artery
repair) without implantation of prosthetic graft material do not appear to benet
from routine antimicrobial prophylaxis.
1.4 Perioperative Management
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1.4.3.2 The Steering Committee oftheFrench Society ofAnaesthesia
andResuscitation [29]
• Arterial endoprosthesis, Carotid surgery with patch: perioperative antibiotic pro-
phylaxis with 2g cefazolin or cefamandole or cefuroxime 1.5g slow i.v.; Single
dose (if duration >2h, reinject 0.75g).
• Carotid procedures without patch: No antibiotic prophylaxis.
• Angiography, Angioplasty: No antibiotic prophylaxis.
• Stent (excluding intra-coronary): Cefazolin 2g i.v. slow; Single dose (if duration
>4h, reinject 1g).
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1.4.4 Beta-Blocker Perioperative
1.4.4.1 European Society ofCardiology (ESC) andtheEuropean Society
ofAnaesthesiology (ESA)- Guideline [30]
In this guideline, CEA and CAS are designated as low perioperative risk procedures
in patients with asymptomatic carotid stenosis; in patients with symptomatic carotid
stenosis, CEA and CAS are assigned to the moderate perioperative risk category.
For these categories, the following recommendations apply with regard to the management of perioperative medication with beta-blockers:
• Perioperative continuation of beta-blockers is recommended in patients currently
receiving this medication.
• Preoperative initiation of beta-blockers may be considered in patients scheduled
for high-risk surgery and who have ≥2 clinical risk factors or ASA status ≥3 [this
does not include CAS and CEA].
• Preoperative initiation of beta-blockers may be considered in patients who have
known ischaemic heart disease or myocardial ischaemia.
• Preoperative initiation of treatment with beta-blockers is not recommended in
patients scheduled for low-risk surgery [this would generally be CEA and CAS
in asymptomatic carotid stenosis].
1.4.5 Blood Pressure Management After Carotid Intervention
1.4.5.1 ESVS-Guideline [1]
• Recommendation 38: For patients presenting with a transient ischaemic attack or
minor ischaemic stroke with hypertension, antihypertensive treatment is recom-
mended. (Recommendation class I, evidence level A).
• Recommendation 39: For symptomatic carotid stenosis patients awaiting endar-
terectomy or stenting, caution should be considered when rapidly lowering blood
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1 Extracranial Carotid Stenosis
pressure in the early time period after onset of symptoms, but uncontrolled
hypertension (>180/90mmHg) should be treated. (Recommendation class IIa,
evidence level C).
• Recommendation 94: For patients with post-carotid hypotension, administration
of intravenous crystalloids and volume expanders should be considered as rst
line treatment. If this fails to improve blood pressure, titrated intravenous vaso-
pressors should be considered to maintain systolic blood pressure>90mmHg.
(Recommendation class IIa, evidence level C).
• Recommendation 95: For patients undergoing carotid interventions, regular
blood pressure monitoring is recommended for the rst 3–6h after carotid end-
arterectomy, as well as in carotid stent patients who develop haemodynamic
instability during the procedure. (Recommendation class I, evidence level C).
• Recommendation 96: For carotid stenting patients who develop haemodynamic
instability during the procedure, regular blood pressure monitoring is recom-
mended for the rst 24h after carotid revascularisation. (Recommendation class
I, evidence level C).
• Recommendation 97: In centres performing carotid interventions, it is recom-
mended that they have written criteria for treating post-procedural hypertension.
(Recommendation class I, evidence level C).
1.4.5.2 Studies
A review by Vanpeteghem etal. [31] is available on perioperative haemodynamic
management in carotid surgery. According to this, severe postoperative hypertension is dened by a systolic blood pressure of at least 180mmHg. In these cases,
invasive blood pressure monitoring is recommended with the aim of keeping the
systolic blood pressure below 160mmHg. The antihypertensive agents commonly
used in carotid surgery are listed in Table1.3.
Table 1.3 Commonly used antihypertensives agents in carotid artery surgery (according to
Vanpeteghem etal. [31])
Drug Mechanism of action Recommended intravenous dose
Esmolol Selective β1-antagonist – Loading dose 0.5–1mg/kg
– Continuous infusion:
25–300μg/kg/min
Labetolol Selective α1–antagonist,
non-selective β-antagonist
Nicardipine Calcium channel blocker – 2–4mg/min until desired effect
Clonidine α2-agonist – Loading dose 2–4μg/kg
Sodium-nitroprusside NO-release – Continuous infusion: 0.25–2
Nitroglycerine NO-release – Continuous infusion: 0.25–2
– Loading dose 20mg
– Continuous infusion:
0.5–2mg/min
– Maintenance 3–30mg/h
– Continuous. Infusion: 1–4μg/
kg/h
μg/kg/min
μg/kg/min
1.4 Perioperative Management
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The extent to which low-dose dexmedetomidine can contribute to hemodynamic
stability during the emergence and the recovery phases of general anesthesia in
patients undergoing carotid endarterectomy was evaluated by Tsujikawa and
Ikeshita [32] in a double-blind randomised placebo-controlled trial.
Dexmedetomidine is a highly selective α2-adrenoceptor agonist that is signicantly
more specic than clonidine. Dexmedetomidine decreases the release of noradrenaline. In this study, patients in the therapy group received dexmedetomidine intraoperatively and in the rst 3h after surgery, which resulted in signicantly less use of
nicardipine for blood pressure regulation compared to the control group. The use of
dexmedetomidine facilitates blood pressure management in the immediate postoperative period after CEA under general anaesthesia.
1.4.5.3 Hyperperfusion Syndrome
Cerebral hyperperfusion syndrome (CHS) is a preventable cause of perioperative
stroke after CEA [33]. It typically develops in the rst postoperative week, with a
peak on day 6 after CEA and after 12h in CAS.Cerebral hyperperfusion is dened
as an increase in blood ow velocity in the middle cerebral artery >100% compared
to the preoperative baseline [31]. Bouri etal. [33] proposed the following denition
for CHS:
1. Occurrence within 30days after CEA.
2. Evidence of hyperperfusion (on transcranial Doppler [TCD], single photon
emission computed tomography [SPECT] or CT/MR perfusion imaging), or systolic blood pressure>180mmHg.
3. Clinical features such as new headache, seizure, hemiparesis, Glasgow Coma
Scale (GCS)<15 or radiological features such as cerebral oedema or intracerebral haemorrhage: and
4. No evidence of new cerebral ischaemia, postoperative carotid occlusion and
metabolic or pharmacologic cause.
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Therapy consists of lowering the blood pressure to systolic <140mmHg or higher
when symptoms disappear. Patients should be admitted to a monitoring unit.
Another consequence is that patients be not discharged with severe hypertension or
a systolic blood pressure that is rising.
1.4.6 Perioperative Management ofPatients
withAnticoagulants
1.4.6.1 European Society ofCardiology (ESC) andtheEuropean Society
ofAnaesthesiology (ESA)- Guideline [30]
Patients treated with oral anticoagulant therapy using vitamin K antagonists (VKAs)
are subject to an increased risk of peri-and post-procedural bleeding. If the international normalized ratio (INR) is ≤1.5, surgery can be performed safely; however, in
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1 Extracranial Carotid Stenosis
anticoagulated patients with a high risk of thrombo-embolism—for example,
patients with:
• Atrial brillation with a CHA2DS2-VASc [Cardiac failure, Hypertension,
Age≥75 (Doubled), Diabetes, Stroke (Doubled)—Vascular disease, Age 65–74
and Sex category (Female) score of ≥4] or
• mechanical prosthetic heart valves, newly inserted biological prosthetic heart
valves, or
• mitral valvular repair (within the past 3months) or
• recent venous thrombo-embolism (within 3months) or
• thrombophilia,
discontinuation of VKAs is hazardous and these patients will need bridging
therapy with unfractionated heparin (UFH) or therapeutic-dose LMWH.In general, there is better evidence for the efcacy and safety of LMWH compared to
UFH.LMWH is usually administered subcutaneously and weight-adjusted, once
or twice daily, without laboratory monitoring. Therapeutic doses (LMWH twice
daily) are recommended for patients at high risk of thromboembolism (TE), and
prophylactic once-daily doses in low-risk patients. The last dose of LMWH
should be administered no later than 12h before the procedure. Further dose
adjustment is necessary in patients with moderate- to-high kidney function
impairment. It is recommended that VKA treatment be stopped 3–5days before
surgery (depending on the type of VKA), with daily INR measurements, until
<1.5 is reached, and that LMWH or UFH be started 1 day after discontinuation
of VKA—or later, as soon as the INR is <2.0.
VKA treatment should be resumed on day 1 or 2 after surgery—depending on
adequate haemostasis—with the preoperative maintenance dose plus a boosting
dose of 50% for two consecutive days; the maintenance dose should be administrated thereafter. LMWH or UFH should be continued until the INR returns to
therapeutic levels.
• In patients treated with the direct oral anticoagulants (DOACs) dabigatran, rivaroxaban, apixaban or edoxaban, bridging is unnecessary in most cases due to
their short biological half-lives. An exception to this rule is the patient with high
thromboembolic risk, whose surgical intervention is delayed for several days.
The overall recommendation is to stop DOACs for 2–3 times their respective
biological half-lives prior to surgery in surgical interventions with ‘normal’
bleeding risk, and 4–5 times the biological half-lives before surgery in surgical
interventions with high bleeding risk.
Because of the fast ‘on’-effect of DOACs (in comparison with VKAs),
resumption of treatment after surgery should be delayed for 1–2 (in some cases
3–5) days, until post-surgical bleeding tendency is diminished.
1.4 Perioperative Management
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1.4.7 Intraoperative Heparin andReversal
Guideline recommendations on intraoperative anticoagulation are lacking, but in
the European Carotid Surgery Trial [34], the only surgical technique associated with
a signicant increase in stroke/death was that in which no intraoperative anticoagulation was given. Consequently, most surgeons routinely give intravenous unfractionated heparin before clamping the artery, but there is no consensus on dosage.
Some titrate the dosage based on the activated coagulation time (ACT), others use a
standard dose of 3000 to 5000 I.U.Evidence to favour either method is not available [35].
The question is whether heparin should be reversed with protamine at the end of
the procedure. The ESVS guidelines [1] recommend:
• Recommendation 69: For patients undergoing carotid endarterectomy, protamine
reversal of heparin should be considered. (Recommendation class IIa, evidence
level B).
The reduced risk of bleeding after protamine administration must be considered against a possible increased rate of thrombotic complications. A meta-analysis of 12 observational studies with 10,621 patients is available [36]. According
to this analysis, surgeons should consider the use of protamine routinely in CEA
to reduce the risk of bleeding. Protamine did not lead to an increased rate of
thrombotic complications, including stroke, myocardial infarction or death.
The results of this meta-analysis were conrmed by a review of a prospective
national registry (Society for Vascular Surgery Vascular Quality Initiative) of
72,787 patients undergoing elective asymptomatic CEA by 1879 surgeons from
316 centres in the USA and Canada from 2012 to 2018 [37]. 69% of patients
received protamine, while 31% did not, with protamine administration increasing over time, to a nal 73% of patients. This study documented the safety and
efcacy of using protamine sulphate to reverse intra-operative heparin at the time
of carotid endarterectomy (CEA) using a large national analysis. The work demonstrated a 50% reduction in reoperation for bleeding events with no attendant
increased risk of stroke, myocardial infarction or death in patients who received
protamine. Furthermore, this analysis highlighted the precarious nature of operative re-exploration for bleeding in patients who did not receive protamine with
substantially increased rates of thrombotic complications. Based on this analysis,
surgeons should strongly consider using protamine at the time of CEA to optimise surgical outcomes. The authors identied heparin reversal with protamine
as a quality indicator in CEA.
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1.4.8 Prevention ofVenous Thromboembolism
There are no clear guideline recommendations on perioperative prevention of
venous thromboembolism with CEA, perhaps due to the rarity of the events. In an
analysis of the National Surgical Quality Improvement Program (NSQIP) database
(45,548 vascular procedures, including 20,785 CEA), the incidence of venous
thromboembolism (VTE) after CEA was the lowest of all vascular procedures at
0.2% [38]. The authors explained the low rate of VTE after CEA by the fact that
these patients are able to ambulate early after their operation, in contrast to other
vascular procedures, highlighting the importance of early ambulation for reduction
of VTE risk. Other factors that contribute to the low incidence of VTE after CEA
could be the relatively short duration of surgery and the aggressive antiplatelet strategies. Accordingly, the authors did not comment on the need for VTE prophylaxis
in CEA and referred to the recommendations of the American College of Chest
Physicians on VTE prophylaxis in non-orthopaedic surgical patients [39]. There,
the risk of VTE for CEA is also given as only 0.2% and it is stated:
• Among patients with a very low risk of symptomatic VTE (0.5%), there is
moderate- quality evidence that the harms of pharmacologic prophylaxis with
low-dose unfractionated heparin or low-molecular-weight heparin (LMWH) outweigh the benets. Compared with no prophylaxis, one can expect zero to three
fewer nonfatal VTE events and four to 10 more nonfatal major bleeding complications per 1000 patients treated with unfractionated heparin. Trade-offs are
similar for LMWH and no prophylaxis.
• For patients at very low risk for VTE (< 0.5%) we recommend that no specic
pharmacologic (Grade 1B) or mechanical (Grade 2C) prophylaxis be used other
than early ambulation.
Consequently, according to this guideline, prevention of VTE is not neces-
sary in CEA.
1.4.9 Antiplatelet Therapy withCEA/CAS
1.4.9.1 European Society forVascular Surgery (ESVS) [1]
• Recommendation 9: For patients with >50% asymptomatic carotid stenosis,
lower dose aspirin (75–325mg daily) should be considered, mainly for the prevention of late myocardial infarction and other cardiovascular events. (Class IIA;
Level C).
• Recommendation 10: For patients with >50% asymptomatic carotid stenosis
who are intolerant or allergic to aspirin, clopidogrel 75mg daily should be considered. If intolerant or allergic to both aspirin and clopidogrel, dipyridamole
monotherapy (200mg twice daily) should be considered. (Class IIA; Level C).
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