1000-2000 5 ьшò

to symptoms.

Teach patient to assume supine position if prodromal symptoms or presyncope occurs.

Explain diagnosis, provide reassurance, and explain risk of recurrence.

PROGNOSIS

The presence of CSH has not been demonstrated to confer an independent mortality risk.

Untreated CSS patients have a syncope recurrence rate as high as 62% within 4 years.

Patients with cardioinhibitory CSH who received a pacemaker had a significant reduction in their mean number of falls, from 9.3 to 4.1 falls in a 1- year follow-up period (3).

REFERENCES

1.Parry SW, Richardson DA, O’Shea D, et al. Diagnosis of carotid sinus hypersensitivity in older adults: carotid sinus massage in the upright position is essential. Heart. 2000;83(1):22–23.

2.Tan MP, Chadwick TJ, Kerr SR, et al. Symptomatic presentation of carotid sinus hypersensitivity is associated with impaired cerebral autoregulation. J Am Heart Assoc. 2014;3(3):e000514.

3.Seifer C. Carotid sinus syndrome. Cardiol Clin. 2013;31(1):111–121.

4.Moya A, Sutton R, Ammirati F, et al; for Task Force for the Diagnosis and Management of Syncope of the European Society of Cardiology (ESC). Guidelines for the diagnosis and management of syncope (version 2009). Eur Heart J. 2009;30(21):2631–2671.

5.Kapoor JR. Carotid sinus hypersensitivity: a diagnostic pearl. J Am Coll Cardiol. 2009;54(17):1633.

6.Epstein AE, DiMarco JP, Ellenbogen KA, et al. 2012 ACCF/AHA/HRS focused update incorporated into the ACCF/AHA/HRS 2008 guidelines for device-based therapy of cardiac rhythm abnormalities: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol. 2013;61(3):e6–e75.

ADDITIONALREADING

Moore A, Watts M, Sheehy T, et al. Treatment of vasodepressor carotid sinus

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syndrome with midodrine: a randomized, controlled pilot study. J Am Geriatr

Soc. 2005;53(1):114–118.

SEE ALSO

Syncope

CODES

ICD10

G90.01 Carotid sinus syncope

CLINICALPEARLS

Consider CSH as a potential cause for syncope, dizziness, or unexplained falls, especially in the elderly.

Diagnose CSH via CSM (using firm pressure for 5 to 10 seconds), producing asystole of at least 3 seconds and/or a drop in systolic BPof at least 50 mm Hg. (See contraindications discussed earlier before undertaking CSM as a diagnostic maneuver.)

Remember to auscultate for carotid artery bruit prior to considering CSM.

Consider dual-chamber pacemaker in patients with recurrent syncope and cardioinhibitory or mixed CSH subtypes.

The finding of CSH does not exclude other causes of syncope.

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CAROTID STENOSIS

Naureen Rafiq, MBBS Austin C. Saavedra, MD

BASICS

Carotid stenosis may be caused by atherosclerosis, intimal fibroplasia, vasculitis, adventitial cysts, or vascular tumors; atherosclerosis is the most common etiology.

DESCRIPTION

Narrowing of the carotid artery lumen is typically due to atherosclerotic changes in the vessel wall. Atherosclerotic plaques are responsible for 90% of extracranial carotid lesions and up to 30% of all ischemic strokes.

A“hemodynamically significant” carotid stenosis produces a drop in pressure or a reduction in flow. It corresponds approximately to a 60–99% diameterreducing stenosis.

Carotid lesions are classified by the following:

–Symptom status

Asymptomatic: tend to be homogenous and stable

Symptomatic: tend to be heterogeneous and unstable; present with stroke or transient cerebral ischemic attack

–Degree of stenosis

High grade: 80–99% stenosis

Moderate grade: 50–79% stenosis

Low grade: <50% stenosis

EPIDEMIOLOGY

More common in men and with increasing age (see “Risk Factors”)

Incidence

Unclear (asymptomatic patients often go undiagnosed)

Prevalence

Moderate stenosis

–Age <50 years: men 0.2%, women 0%

–Age >80 years: men 7.5%, women 5%

Severe stenosis

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–Age <50 years: men 0.1%, women 0%

–Age >80 years: men 3.1%, women 0.9%

ETIOLOGYAND PATHOPHYSIOLOGY

Atherosclerosis begins during adolescence, consistently at the carotid bifurcation. The carotid bulb has unique blood flow dynamics. Hemodynamic disturbances cause endothelial injury and dysfunction. Plaque formation in vessel wall results and stenosis then ensues.

Initial cause is not well understood, but certain risk factors are frequently present (see “Risk Factors”). Tensile stress on the vessel wall, turbulence, and arterial wall shear stress seem to be involved.

Genetics

Increased incidence among family members Genetically linked factors

–Diabetes mellitus (DM), race, hypertension (HTN), family history, obesity

–In a recent single nucleotide polymorphism study, the following genes were strongly associated with worse carotid plaque: TNFSF4, PPARA, TLR4,

ITGA2, and HABP2.

RISK FACTORS

Nonmodifiable factors: advanced age (>65 years old), male sex, family history, cardiac disease, congenital arteriopathies

Modifiable factors: smoking, diet, dyslipidemia, physical inactivity, obesity, HTN, DM

GENERALPREVENTION

Antihypertensive treatment to maintain BP<140/90 mm Hg (systolic BPof 150 mm Hg is target in elderly)

Smoking cessation to reduce the risk of atherosclerosis progression and stroke

Lipid control: regression of carotid atherosclerotic lesions seen with statin therapy

COMMONLYASSOCIATED CONDITIONS

Transient ischemic attack (TIA)/stroke

Coronary artery disease (CAD)/myocardial infarction (MI)

Peripheral vascular disease (PVD) HTN

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DM

Hyperlipidemia

DIAGNOSIS

Screening for carotid stenosis is not recommended. However, in the setting of symptoms suggestive of stroke or TIA, workup for this condition may be indicated.

HISTORY

Identification of modifiable and nonmodifiable comorbidities (see “Risk Factors”)

History of cerebral ischemic event

Stroke, TIA, amaurosis fugax (monocular blindness), aphasia

CAD/MI

Peripheral arterial disease

Review of systems, with focus on risk factors for

–Cardiovascular disease

–Stroke (HTN and arrhythmias)

PHYSICALEXAM

Lateralizing neurologic deficits: contralateral motor and/or sensory deficit

Amaurosis fugax: ipsilateral transient visual obscuration from retinal ischemia

Visual field defect

Dysarthria, aphasia (in the case of dominant hemisphere involvement, usually left)

Carotid bruit (low sensitivity and specificity)

DIFFERENTIALDIAGNOSIS

Aortic valve stenosis

Aortic arch atherosclerosis

Arrhythmia with cardiogenic embolization

Migraine

Brain tumor

Metabolic disturbances

Functional/psychological deficit Seizure

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DIAGNOSTIC TESTS & INTERPRETATION

Initial Tests (lab, imaging)

Workup for suspected TIA/stroke may include the following:

CBC with differential

Basic metabolic panel

ESR (if temporal arteritis a consideration)

Glucose/hemoglobin A1c

Fasting lipid profile

Duplex ultrasonography is the recommended initial diagnostic test in asymptomatic patients with known or suspected carotid stenosis.

Duplex ultrasound (US) identifies ≥50% stenosis, with 98% sensitivity and 88% specificity.

Follow-Up Tests & Special Considerations

Proceed to imaging if there is suggestion of stenosis from history or physical exam.

Other noninvasive imaging techniques can add detail to duplex results:

–CT angiography

88% sensitivity and 100% specificity

Requires IV contrast with risk for subsequent renal morbidity

–MR angiography

95% sensitivity and 90% specificity

Evaluates cerebral circulation (extracranial and intracranial) as well as aortic arch and common carotid artery

The presence of unstable plaque can be determined if the following characteristics are seen:

■Presence of thin/ruptured fibrous cap

■Presence of lipid-rich necrotic core

■Tends to overestimate degree of stenosis

Diagnostic Procedures/Other

Cerebral angiography is the traditional gold standard for diagnosis:

Delineates the anatomy pertaining to aortic arch and proximal vessels The procedure is invasive and has multiple risks:

–Contrast-induced renal dysfunction (1–5% complication rate)

–Thromboembolic-related complications (1–2.6% complication rate) and neurologic complications

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– Should be used only when other tests are not conclusive

Test Interpretation

Stenosis consistently occurs at the carotid bifurcation, with plaque formation most often at the level of the proximal internal carotid artery:

–Plaque is thickest at the carotid bifurcation.

–Plaque occupies the intima and inner media and avoids outer media and adventitia.

Plaque histology

–Homogenous (stable) plaques seldom hemorrhage or ulcerate: Fatty streak and fibrous tissue deposition

Diffuse intimal thickening

–Heterogenous (unstable) plaques may hemorrhage or ulcerate:

Presence of lipid-laden macrophages, necrotic debris, cholesterol crystals

Ulcerated plaques

–Soft and gelatinous clots with platelets, fibrin, and red and white blood cells

TREATMENT

Smoking cessation, BPcontrol, blood glucose control, antiplatelet medication, and statin medication are the primary treatments for both asymptomatic and symptomatic carotid stenosis.

GENERALMEASURES

Lifestyle modifications: dietary control and weight loss, exercise of 30 min/day at least 5 days/week

Patients should be advised to quit smoking and offered smoking cessation intervention to reduce the risk of atherosclerotic progression and stroke.

Control of HTN with antihypertensive agents to maintain BP<140/90 mm Hg; <150/90 mm Hg in the elderly. In carefully selected individuals, tighter blood pressure control might reduce cerebrovascular events, but this remains uncertain.

MEDICATION

Antihypertensive treatment (<140/90 mm Hg), <150/90 mm Hg in the elderly

Diet, smoking cessation, and exercise are useful adjuncts to therapy. Statin initiation is recommended; choose moderateto high-intensity statin therapy for anti-inflammatory benefit.

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Acomprehensive program that includes tight control of HTN with ACEI or

ARB treatment reduces the risk in individuals with diabetes. Aspirin: 75 to 325 mg/day

If patient has sustained TIAor ischemic stroke, antiplatelet therapy with

–Aspirin alone (75 to 325 mg/day) or

–Clopidogrel alone (75 mg/day), or

–Aspirin plus extended-release dipyridamole (25 and 200 mg BID, respectively)

–Acombination of clopidogrel plus aspirin is NOT recommended within 3 months post-TIAor CVA.

ISSUES FOR REFERRAL

For acute symptomatic stroke, order imaging and contact neurology.

For known carotid stenosis, some suggest duplex imaging every 6 months if stenosis is >50% and patient is a surgical candidate.

SURGERY/OTHER PROCEDURES

Symptomatic carotid stenosis (history of ischemia ipsilateral to stenosis)

–Carotid endarterectomy (CEA) is of some benefit in 50–69% symptomatic stenosis, highly beneficial for those with 70–99% stenosis without near occlusion and has no benefit in people with carotid near-occlusion (1)[A].

–CEAis recommended for patients with a life expectancy of at least 5 years. The anticipated rate of perioperative stroke or mortality must be <6% (2) [B].

–Treatment with aspirin (81 to 325 mg/day) is recommended for all patients who are having CEA. Aspirin should be started prior to surgery and continued for at least 3 months postsurgery but may be continued indefinitely (2)[B].

–Carotid artery stenting (CAS) provides similar long-term outcomes as CEA (3)[A]. Age should be considered when planning a carotid intervention.

CAS has an increased risk of adverse cerebrovascular events in the elderly compared to the young but similar mortality risk. CEAis associated with similar neurologic outcomes in the elderly and young, at the expense of increased mortality (4)[A].

CAS is suggested in selected patients with neck anatomy unfavorable for arterial surgery and those with comorbid conditions that greatly increase the risk of anesthesia and surgery.

Dual antiplatelet therapy with aspirin (81 to 325 mg/day) plus clopidogrel

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(75 mg/day) is recommended for 30 days post-CAS.

Asymptomatic patients

–As compared with CAS, CEAis the preferred option for the management of asymptomatic carotid stenosis if a surgical option is chosen. CAS has the potential for increased risks of periprocedural stroke and periprocedural death (5)[A].

–The advantage of surgical compared with medical therapy has decreased with contemporary medical management. It is not possible to make an evidence-based recommendation for or against surgical therapy with current literature (6)[A].

ADMISSION, INPATIENT, AND NURSING CONSIDERATIONS

Any patient with presentation of acute symptomatic carotid stenosis should be hospitalized for further diagnostic workup and appropriate therapy.

Rapid evaluation for symptoms compatible with TIAshould be obtained in the emergency department (ED) or inpatient setting.

Discharge criteria: 24 to 48 hours post-CEA, if ambulating, taking adequate PO intake, and neurologically intact

ONGOING CARE

FOLLOW-UPRECOMMENDATIONS

Patient Monitoring

Duplex at 2 to 6 weeks postoperatively

Duplex every 6 to 12 months

Reoperative CEAor CAS is reasonable, if there is rapidly progressive restenosis.

Patients with any of the following: renal failure, heart failure, diabetes, and age >80 years have a high readmission rate following CEA; thus, intensive medical therapy and rigorous follow-up is recommended.

DIET

Low-fat, low-cholesterol, low-salt diet at discharge

PATIENT EDUCATION

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For patient education materials on this topic, consult the following:

American Heart Association: http://www.heart.org

Mayo Clinic Information: http://www.mayoclinic.org/diseases- conditions/carotid-artery-disease/basics/definition/con-20030206

COMPLICATIONS

Untreated: TIA/stroke (risk of ipsilateral stroke approximately 1.68% per year)

Postoperative (s/p CEA)

–Perioperative (within 30 days)

Stroke/death, cranial nerve injury, hemorrhage, hemodynamic instability, MI

–Late (>30 days postop)

Recurrent stenosis, false aneurysm at surgical site

REFERENCES

1.Orrapin S, Rerkasem K. Carotid endarterectomy for symptomatic carotid stenosis. Cochrane Database Syst Rev. 2017;(6):CD001081.

2.Chaturvedi S, Bruno A, Feasby T, et al. Carotid endarterectomy—an evidence-based review: report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Neurology. 2005;65(6):794–801.

3.Bonati LH, Lyrer P, Ederle J, et al. Percutaneous transluminal balloon angioplasty and stenting for carotid artery stenosis. Cochrane Database Syst Rev. 2012;(9):CD000515.

4.Antoniou GA, Georgiadis GS, Georgakarakos EI, et al. Meta-analysis and meta-regression analysis of outcomes of carotid endarterectomy and stenting in the elderly. JAMA Surg. 2013;148(12):1140–1152.

5.Moresoli P, Habib B, Reynier P, et al. Carotid stenting versus endarterectomy for asymptomatic carotid artery stenosis: a systematic review and metaanalysis. Stroke. 2017;48(8):2150–2157.

6.Meschia JF, Bushnell C, Boden-Albala B, et al; and American Heart Association Stroke Council, Council on Cardiovascular and Stroke Nursing, Council on Clinical Cardiology, Council on Functional Genomics and Translational Biology, Council on Hypertension. Guidelines for the primary prevention of stroke: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2014;45(12):3754–3832.

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