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Cerebrovascular Disease

Cerebrovascular Disease. Daniel Costello CUH. Cerebral Vasculature. Arterial system. Venous system. Arterial (high flow) Embolic occlusion In situ occlusion Rupture Dissection Inflammation Spasm. Venous (low flow) Embolic occlusion In situ occlusion Rupture Dissection

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Cerebrovascular Disease

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  1. Cerebrovascular Disease Daniel Costello CUH

  2. Cerebral Vasculature Arterial system Venous system

  3. Arterial (high flow) Embolic occlusion In situ occlusion Rupture Dissection Inflammation Spasm Venous (low flow) Embolic occlusion In situ occlusion Rupture Dissection Inflammation Spasm Mechanisms of Vascular Disease

  4. Hypertension Heart disease Atrial fibrillation Hypercholesterolemia Diabetes mellitus Carotid stenosis Prior stroke or TIA PFO Elevated homocysteine, Lp(a) Prothrombotic conditions Migraine Sleep Apnea Smoking Sedentary lifestyle Obesity Alcohol abuse Risk Factors - Modifiable Medical conditions Behaviors

  5. Risk factor Relative Risk Prevalence Hypertension 3.0-5.0 25-40% Smoking 1.5-2.5 20-40% Diabetes 1.0-3.0 4-20% Hyperlipidemia 1.0-2.0 6-40% Physical Inactivity 2.7 20-40% Heavy alcohol use 1.0-3.0 5-30% Hyperhomocyst(e)inemia 2.0-3.0 10-15% Atrial Fibrillation 4.0-18.0 1-2% Major Modifiable Stroke Risk Factors

  6. Stroke Epidemiology in Ireland • Approximately 10,000 Stroke per annum in Ireland • Stroke:TIA ratio 4:1 • 3rd commonest cause of death in Western World • Short & long term consequences

  7. Stroke Epidemiology in Ireland

  8. Acute Ischaemic Stroke

  9. Cerebrovascular Disease: Stroke Types Ischemic Stroke (80%) Hemorrhagic Stroke (20%) Atherothrombotic Cerebrovascular Disease (20%) Intracerebral Hemorrhage (70%) Cryptogenic (30%) ? Lacunar (25%) (small vessel disease) Cardioembolic (20%) Subarachnoid Hemorrhage (30%) Albers GW et al. Chest. 1998;119:683S-698S. Rosamond WD et al. Stroke. 1999;30:736-743.

  10. TIA: old vs new definitions

  11. “Penumbra”= Tissue at risk

  12. Making a diagnosis • Sudden onset neurological deficits • Loss of consciousness uncommon • Involuntary movements uncommon • Headache common • Investigations determine: - effect of stroke i.e. ‘brain damage’ - cause of this stroke - risk of future strokes

  13. Vascular territories (Anterior)

  14. Vascular territories (Posterior)

  15. Vascular territories- MCA

  16. Vascular territories- MCA

  17. Vascular territories- MCA

  18. Vascular territories- ACA & PCA

  19. Vascular territories- Posterior

  20. Vascular territories- vertebrobasilar

  21. Brain imaging CT Brain MRI Brain ‘Stroke protocol’ with diffusion sequences Vessel imaging CTA MRA Ultrasound carotids Investigations • Cardiac- telemetry, Echocardiography • Clotting • Aorta- trans-oesophageal echocardiography

  22. Head CT Brain Stroke ‘window’

  23. T1-weighted Images Normal SI: CSF < GM < WM • Anatomic delineation • Only a few things are bright: • Fat • Protein (colloid cysts, melanin, methemoglobin) • Gadolinium Interpretation:

  24. T2-weighted Images Normal SI: WM < GM < CSF Interpretation: • Signal intensity generally follows water content. • Vasogenic edema looks bright. • Many pathologic processes result in increased water content.

  25. FLAIR Images “Fluid Attenuated Inversion Recovery” Normal SI: CSF < WM < GM • T2-weighted image in which signal from CSF has been suppressed. • Distinguishes CSF spaces from T2-bright lesions. • Increased conspicuity of T2-bright lesions next to CSF. • CSF signal will not suppress if: • SAH • Protein (as in infection/inflammation) • Hyperoxygenation • Propofol • Prior gadolinium Interpretation:

  26. “Susceptibility” images Gradient Echo images Normal SI: WM < GM < CSF Interpretation: • T2 weighted image. • Substances that exhibit susceptibility effect will look dark and “bloom:” • Deoxyhemoglobin • Intracellular methemoglobin • Hemosiderin • Calcium (sometimes) • Air • Metal (aneurysm clips, earrings, braces, etc).

  27. Diffusion-Weighted Images (DWI) Normal SI: CSF < WM < GM Interpretation: Normal SI: • T2-weighted image, in which substances look brighter if water diffusion is restricted. • In acute stroke, water diffusion is restricted, so tissue looks bright.

  28. Vessel imaging • Ultrasound • CT angiography • MR angiography • Conventional catheter angiography

  29. Magnetic Resonance Angiography (MRA) Interpretation: • Moving blood looks bright. • All other substances dark. • No contrast necessary (but we use gadolinium for better neck MRA images). • Less spatial resolution than CTA, more motion-sensitive.

  30. Treatment of Acute Ischaemic Stroke • Rapid assessment- NIHSS • Consider tPA (IV or IA) • Anti-coagulation • Anti-platelet agent • Blood pressure, glucose monitoring, fever control • Surgery • Early evaluation- fasting glucose & lipids, brain & vessel imaging, screen for Atrial Fibrillation, TTE +- TOE • Rehabilitation- SALT, PT, OT

  31. ECASS III: tPA 3-4.5 hrs

  32. ECASS III Outcomes • 821- 418 to alteplase group and 403 to placebo. • Median NIHSS lower in tPA group (9 vs 10, p=.03) and fewer patients with prior stroke (7.7% vs. 14.1%; p= 0.03) • The median OTT time was 3 hours 59 minutes. • More patients had a favorable outcome with alteplase (52.4% vs. 45.2%; odds ratio, 1.34; 95% CI 1.02 to 1.76; P = 0.04). • In the global endpoint, the outcome was also improved with alteplase (odds ratio, 1.28; 95% CI, 1.00 to 1.65; P<0.05). • An adjusted analysis accounting for predictors of poor outcome showed a more favorable (odds ratio, 1.42; 95% CI, 1.02 to 1.98; P = 0.04)

  33. ECASS III Safety • The incidence of intracranial hemorrhage was higher with alteplase than with placebo for any ICH, (27.0% vs. 17.6%; P = 0.001) or for symptomatic ICH (2.4% vs. 0.2%; P = 0.008). Mortality did not differ (7.7% and 8.4%; P = 0.68). • There was no significant difference in the rate of other serious adverse events.

  34. Meta-Analysis of the major IV tPA trials shows clear benefit up to 3 hrs and beyond NINDS 12% ECASS3 7% Lancet 2004; 363: 768–74

  35. Comparison of Efficacy TrialsPts Rx To Prevent CEA (NASCET) 6 1 major stroke Pro-UK 7 1 major stroke tPA NINDS 8 1 major stroke tPA ECASS3 14 1 major stroke Stroke Unit^ 18 1 major stroke/death CEA (ACAS) 15-20 1 stroke OAT AFIB 20 1 stroke /yr tPA AMI* 26 1 death from MI NASCET (n=659), NINDS (n=624) ^ BMJ 1997; 314:1151-9. *Lancet 1994;343:311-22

  36. Courtesy Dr. Huang-Hellinger

  37. Carotid and Vertebral Artery Dissection • 2% of all ischemic strokes • 25% of stroke in young • Incidence 2.6 per 100,000 (carotid) and 1.0 per 100,000 (vertebral) • Peaks in the 5th decade • Intracranial dissections are rare, occur at younger ages Intimal tear  sub intimal or sub adventitial hematoma (arterial occlusion, ‘pseudo’ aneurysm) From Schievink WI, NEJM 2001

  38. Dissection: management Management is controversial, no RCT • Medical • Short term anticoagulation with heparin / warfarin followed by long term anti-platelet agents • CTA, MRA, Carotid duplex useful for follow-up • Endovascular • Balloon occlusion or stenting considered if recurrent symptoms occur despite medical treatment • Coiling of a ‘pseudo’aneurysm • Surgical • Bypass, Surgery for pseudoaneurysm

  39. Secondary Preventionof Ischemic Stroke • Carotid endarterectomy: >50% stenosis • Anticoagulation therapy: Cardioembolic stroke • Antiplatelet therapy: Most common therapy

  40. Antiplatelet Agentsfor Stroke Prevention • Aspirin • Ticlopidine • Clopidogrel • Dipyridamole

  41. Efficacy of Antiplatelet Agentsfor Prevention of Stroke, MI,or Vascular Death Risk Reductions Patient Relative Risk Odds Population Therapy Reduction (%) Reduction (%) All Vascular All antiplatelet 22 27Diseases regimens Stroke/TIA All antiplatelet 17 22 regimens Stroke/TIA Aspirin 13 16 Source: Antiplatelet Trialists’ Collaboration, 1994: Algra and Van Gijn 1996.

  42. Efficacy of Antiplatelet Agents vs Placebo for Prevention of Stroke, MI, or Vascular Death in Stroke/TIA Patients Relative Risk Antiplatelet Agent No. of Studies Reduction (%) Aspirin (all doses) 10 13 Ticlopidine 1 23 Dipyridamole + ASA 4 30 All Antiplatelet Agents 18 17 Source: Algra and Van Gijn 1996; Gent et al.1989; Tijssen, 1998; Antiplatelet Trialists’ Collaboration, 1994.

  43. Stroke Subtypes in WARSS Aspirin Warfarin N (%) N(%) Cryptogenic embolic 281(25.5) 295 (26.7) Large Artery 144 (13.1) 115 (10.4) Lacunar 612 (55.5) 625 (56.7) Other 66 (6.0) 68 (6.2)

  44. Carotid Endarterectomy Trials • NASCET I (70-99%) • Medical 26% • Surgical 9% (5.8% risk of stroke or death within 30 days) • NASCET II (50-69%) • Medical 22.2% • Surgical 15.7% ( 6.7% risk of stroke or death within 30 days) • ACAS (>60%) • Medical 11% • Sugical 5.1% (2.3%risk of stroke or death within 30 days)

  45. WASID Wafarin v.s. Aspirin for Symptomatic Intracranial Arterial Stenosis • Randomized, double-blind, placebo-controlled, multicenter trial • 569 patients with TIA or stroke attributable to 50-99% stenosis of MCA, ICA or V-B system • Randomized to • Warfarin with target INR 2.0-3.0 • ASA 650 mg bid • Primary endpoint: IS, ICH, death from vascular cause Chimowitz et al. N Engl J Med. 2005;352:1305-16.

  46. Potential Stroke Risk Reduction for Individuals -- AHA Guidelines Factor Potential Benefit with Treatment Hypertension 30% - 40% Smoking 50% within 1 year, baseline after 5 years Diabetes 44% reduction in hypertensive diabetics with tight blood pressure control Hyperlipidemia 20-30% with statins in patients with known coronary heart disease Atrial fibrillation 68% (warfarin) 21% (aspirin) Adapted from Goldstein, et al. Circulation 2001;103:163-182.

  47. CVST

  48. CVST

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