Vertebral Artery Stenosis Studies

5 Major Studies on Treatment of VA Stenosis:

  1. CAVATAS (1997) = Carotid and Vertebral Artery Transluminal Angioplasty Study
  2. SAMMPRIS (2011) = Stenting and Aggressive Medical Management for the Prevention of Recurrent Stroke in Intracranial Stenosis
  3. VISSIT (2012) = Vitesse Intracranial Stent Study for Ischemic Therapy
  4. VAST (2013) = Vertebral Artery Stenting Trial
  5. VIST (2015) = Vertebral Artery Ischaemia Stenting Trial

*year = end of recruitment.

 

Key features of the trials comparing stenting with medical treatment which included vertebral stenosisCapture

 

Treatment:

  1. DAPT x 90d
  2. Statin
  3. BP reduction <140mm Hg
  4. Angio +/- stenting

 

Note:

  1. low perioperative complications with extracranial stenting
  2. higher risk of stroke with intracranial VA stenosis
  3. stenting = medical management for extracranial stenosis
  4. medical management better for intracranial stenosis

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Powerpoint File for figure above

Reference:

Drazyk, A. and Markus, H. (2017). Recent advances in the management of symptomatic vertebral artery stenosis. Current Opinion in Neurology, p.1.

Algorithm for Treatment of Cerebral Venous Thrombosis (CVT)

An algorithm for the diagnosis and management of CVT:

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CTV, CT venography; CVT, cerebral venous thrombosis; ICH, intracerebral
hemorrhage; LMWH, low molecular weight heparin; MRV, magnetic resonance venography; PRES, posterior reversible encephalopathy syndrome; UHF,
unfractionated heparin.

 

Table 1 Major risk factors and conditions associated with CVT
Infection

  • INFECTION:
    • Paranasal sinusitis
    • Intracranial infections: abscess, meningitis
    • Trauma Head trauma, neurosurgical operations
    • Internal jugular catheter
  • MEDICAL / SURGICAL CONDITIONS
    • Dehydration
    • Pregnancy and puerperium
    • Coagulation disorders: factor V Leiden, protein C / S deficiency, antithrombin III deficiency, hyperhomocysteinemia, APAS
    • Hematologic disorders: polycythemia, sickle cell disease, TTP, polycythemia, PNH
    • Malignancies, inflammatory bowel disease, nephrotic syndrome, liver cirrhosis, collagen vascular disease including SLE, Wegener’s granulomatosis and Behçet syndrome
    • Previous surgical procedures
  • MEDICATION
    • Oral contraceptives, hormone replacement therapy,  L-asparagenase, corticosteroid

 

Table 3 Clinical presentations of CVT:

  • Symptoms
    • Headache
    • Double or blurred vision
    • Altered consciousness
    • Seizure
    • Behavioral symptoms (delirium, amnesia, mutism)
  • Signs
    • Papilledema
    • Focal neurologic deficit
    • Cranial nerve palsy
    • Nystagmus

 

Society of Neurointerventional Surgery (SNIS) Recommendations:

Imaging
► A combination of MRI/MRV or CT/CTV studies should be performed in patients with suspected CVT (class I; level of evidence C).
► DSA as a diagnostic modality is indicated in cases of suspected CVT when the diagnosis of CVT cannot be reliabl established with non-invasive imaging alone (class IIa; level of evidence C).

Medical and surgical treatment
► Anticoagulation with unfractionated heparin or low molecular weight heparin is reasonable in patients with CVT (class IIa; level of evidence C).
► Decompressive craniectomy may be considered in patients with large parenchymal lesions causing herniation or intractable intracranial hypertension (class IIb; level of evidence C).

Endovascular therapy
► Endovascular therapy may be considered in patients with clinical deterioration despite anticoagulation, or with severe neurological deficits or coma (class IIb; level of evidence C). The duration of anticoagulation therapy before declaring it to be a ‘failure’ and proceeding with endovascular therapy is unknown.
► There is insufficient evidence to determine which endovascular approach and device provides the optimal restoration of venous outflow in CVT. In many cases, a variety of treatment approaches is required to establish sinus patency.

 

Radiologic Findings in CVT:

  1.  noncontrast CT – hyperdensity of occluded sinuses + cerebral edema +/- ICH
  2. contrast CT – empty delta sign, HU>70% highly specific for acute CVT
  3. MRI – T2 hypointensity in acute CVT, T1 and T2 hyperintensity in subacute CVT

 

 

References

Lee, S., Mokin, M., Hetts, S., Fifi, J., Bousser, M. and Fraser, J. (2018). Current endovascular strategies for cerebral venous thrombosis: report of the SNIS Standards and Guidelines Committee. Journal of NeuroInterventional Surgery, 10(8), pp.803-810.

 

Criteria for Thrombectomy / Endovascular Treatment of Stroke

Patients eligible for intravenous alteplase should receive intravenous alteplase even if endovascular treatments are being considered

Patients should receive endovascular therapy with a stent retriever if they meet all the following criteria:

  1. prestroke mRS score 0–1,
  2. acute ischemic stroke receiving intravenous alteplase within 4.5 h of onset
  3. causative occlusion of the internal carotid artery or proximal MCA (M1),
  4. age >18 years, (note: there is no upper age limit),
  5. NIHSS score of C6,
  6. ASPECTS of C6
  7. treatment can be initiated (groin puncture) within 6 h of symptom onset

As with intravenous alteplase, reduced time from symptom onset to reperfusion with endovascular therapies is highly associated with better clinical outcomes

When treatment is initiated beyond 6 h from symptom onset, the effectiveness of endovascular therapy is uncertain for patients with acute ischemic stroke who havecausative occlusion of the internal carotid artery or proximal MCA (M1)

In carefully selected patients with anterior circulation occlusion who have contraindications to intravenous alteplase, endovascular therapy with stent retrievers completed within 6 h of stroke onset is reasonable

Although the benefits are uncertain, use of endovascular therapy with stent retrievers may be reasonable for carefully selected patients with acute ischemic stroke in whom treatment can be initiated (groin puncture) within 6 h of symptom onset and who have causative occlusion of the M2 or M3 portion of the MCAs, anterior cerebral arteries, vertebral arteries, basilar artery, or posterior cerebral arteries

Endovascular therapy with stent retrievers may be reasonable for some patients <18 years of age with acute ischemic stroke who have demonstrated large vessel occlusion in whom treatment can be initiated (groin puncture) within 6 h of symptom onset, but the benefits are not established in this age group

Observing patients after intravenous alteplase to assess for clinical response before pursuing endovascular therapy is not required to achieve beneficial outcomes and is not recommended

Endovascular therapy with stent retrievers is recommended over intra-arterial fibrinolysis as first-line therapy

It might be reasonable to favor conscious sedation over general anesthesia during endovascular therapy for acute ischemic stroke. However, the ultimate selection of anesthetic technique during endovascular therapy for acute ischemic stroke should be individualized based on patient risk factors, tolerance of the procedure, and other clinical characteristics

Reference:

Gross, H. and Grose, N. (2017). Emergency Neurological Life Support: Acute Ischemic Stroke. Neurocritical Care, 27(S1), pp.102-115.

Heads up Maneuver

Clinical scenario:  Patient with stroke comes in with large vessel occlusion and neuro deficits; he was placed supine for CT scan and NIHSS improved.  Vascular imaging still shows clot, but deficits are now nondisabling and NIHSS is low.  Should you proceed with thrombectomy?

Small study from UCLA used the Heads Up maneuver to select patients who should proceed to thrombectomy.

 

Patients included:

  1. stroke within 7.5h onset
  2. disabling neuro deficit on presentation
  3. improved while on CT to nondisabling deficit
  4. evidence (in MRA) of persisting large vessel occlusion

 

Heads up Maneuver: (performed in angio suite)

  1. position 90 degrees upright x 30 minutes, monitor BP/HR q5-10mins
  2. if worsened –> lower to supine, proceed with angio
  3. if remained stable –> lower to supine or 30 deg HOB; transfer to stroke unit

 

Pathophysiology of Delayed Collateral Failure:

STROKE –> increased CO / SVR –> improved flow to peri-infarct regions –> MI / CHF / dysrhythmias / sepsis / dysautonomia / drugs –> reduced CPP –> delayed collateral failure –> expansion of core infarct

 

Heads Up:

Head position influences collateral flow by increasing flow velocity in affected MCA. Impaired autoregulation allows perfusion to collateral channels to become passive-pressure dependent.  Head flat position increases CPP by 20%, improves neurologic function in 15% of patients.  Risk of aspiration PNA with head flat position is <5%.

 

Outcome:

The study found that heads up maneuver can be used to stress collateral systems and identify those patients who are vulnerable to hemodynamic failure.

  1. Only 5 patients included in the series – all had high NIHSS on arrival, improved during MRI scanning.
  2. Two patients tolerated 30 minutes, no thrombectomy performed, had excellent outcome with just medical therapy.
    1. *Spontaneous recanalization occurred within 72h (assumed that vigorous collaterals promoted recanalization).
  3. Three patients worsened with manuever and had successful recanalization and excellent outcomes as well.

 

Reference:

Ali, L., Weng, J., Starkman, S., Saver, J., Kim, D., Ovbiagele, B., Buck, B., Sanossian, N., Vespa, P., Bang, O., Jahan, R., Duckwiler, G., Viñuela, F. and Liebeskind, D. (2016). Heads Up! A Novel Provocative Maneuver to Guide Acute Ischemic Stroke Management. Interventional Neurology, 6(1-2), pp.8-15.

Posterior Cerebral Artery Branches

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4 anatomic segments of the PCA:

  1. P1 segment: from tip of basilar to origin of PComm
  2. P2 segment: from Pcomm to dorsal midbrain
    1. P2A – anterior segment
    2. P2P – posterior segment
  3. P3 segment: from lateral quad cistern at origin of post temporal artery to ant limit of calcarine fissure
  4. P4 segment:  terminal cortical branches of PCA after takeoff of parieto-occipital and calcarine arteries

 

REFERENCE:

AJNR Am J Neuroradiol. 2001 Jan;22(1):27-34. “Aneurysms of the posterior cerebral artery: classification and endovascular treatment.”   Ciceri EF1, Klucznik RP, Grossman RG, Rose JE, Mawad ME.

Carotid Stenosis Algorithm

NASCET (North American Symptomatic CEA Trial) – CEA vs medical reduced risk of stroke (17%) and death (7%) at 2 years for stenosis >70%.

ACAS (Asymptomatic Carotid Artery Stenosis Trial) – CEA vs medical reduced risk of stroke or death (6%) at 5 years for stenosis >60%.

CREST (Carotid Revascularization Endarterectomy vs Stenting Trial) – CEA vs CAS in both symptomatic and asymptomatic – comparable rates of primary outcome measures (death, stroke, MI, stroke at 4 years).  Periop stroke more in stenting, periop MI more in CEA.  **NB Periopr stroke more disabling (based on 1 year in QOL assessment).

 

ICA Stenosis Algorithm

 

References:

Experiences with carotid endarterectomy at Sree Chitra Tirunal Institute.  Unnikrishnan M, Siddappa S, Anto R, Babu V, Paul B, Kapilamoorthy TR, Sivasankaran S, Sandhyamani S, Sreedhar R, Radhakrishnan K – Ann Indian Acad Neurol (2008)

 

Lee, Kiwon. The Neuroicu Book. 1st ed. Print.

Heparin Drip for DCI prevention in Aneurysmal SAH?

Interesting article from Journal of Neurointerventional Surgery looking at use of heparin after endovascular treatment of cerebral aneurysms.  The study was retrospective, included ~400 patients (~200 given heparin post-coiling and ~200 matched controls), and collected data on incidence of vasospasm, DCI, and functional outcome.

Results of the study is shown in the graph below:

neurintsurg-2016-012925-F1.large.jpg

Rate of severe vasospasm was shown to be significantly reduced in the heparin group (14.2 vs 25.4% p=0.005).  The study concluded that patients who received continuous heparin after endovascular coiling of cerebral aneurysms have a reduced rate of severe vasospasm.

 

Mechanism of Action

How does heparin prevent DCI? (theoretically)  The article explains that heparin prevents secondary injury in SAH through its anti-inflammatory effects.  Heparin is the highest negatively charged biological molecule existing.  Due to the negative charges, it can bind to positively charged proteins and surfaces, including growth factors, cytokines and chemokines – thereby reducing inflammation.  It can also bind oxyhemoglobin and block free radical activity.  It can also antagonize endothelin, reducing endothelin-related vasoconstriction.

 

Limitations

The study has several limitations – including the retrospective and single-center nature of the study design, and the potential for selection bias – even with case matching.  This study adds more evidence (albeit weak) to the argument that heparin infusions may help prevent secondary brain injury in patients with aneurysmal SAH who undergo endovascular coiling.

 

Heparin would be a potential “4th H,” adding to the 3 H’s historically used in the vasospasm prevention – i.e. hypervolemia, hemodilution, hypertension.  As with the previous H’s, randomized controlled studies will need to be performed to prove this theory.  The first 3 Hs have largely been debunked, and instead, the current standard of care is to keep patients with subarachnoid hemorrhage euvolemic, and induce hypertension only in the setting of vasospasm and/or delayed cerebral ischemia.  Therefore, as with the first 3 Hs, until more evidence surfaces, the use of continuous heparin cannot be recommended in this setting.

 

 

Reference:

Bruder, Markus et al. “Effect Of Heparin On Secondary Brain Injury In Patients With Subarachnoid Hemorrhage: An Additional ‘H’ Therapy In Vasospasm Treatment”. Journal of NeuroInterventional Surgery (2017): neurintsurg-2016-012925.