Vascular Diseases PART 1 - PAD AAA CAD Avgerinos 2024 (1) PDF

Surgery II MD 420 Coordinator: Dimitrios Ntourakis MD, PhD, FACS Vascular Diseases Peripheral Arterial Disease Aortic Aneurysm Carotid Disease Venous Insufficiency – Varicose Veins Venous Thromboembolic Disease Lymphedema Efthymios “Makis” Avgerinos, MD, FACS, FEBVS Professor of Surgery - University...

Surgery II MD 420 Coordinator: Dimitrios Ntourakis MD, PhD, FACS Vascular Diseases Peripheral Arterial Disease Aortic Aneurysm Carotid Disease Venous Insufficiency – Varicose Veins Venous Thromboembolic Disease Lymphedema Efthymios “Makis” Avgerinos, MD, FACS, FEBVS Professor of Surgery - University of Pittsburgh Vis. Professor University of Athens Co-Director Vascular and Endovascular Surgery Clinic Athens Medical Center, Greece Vascular Diseases – Part A Peripheral Arterial Disease Aortic Aneurysm Carotid Disease Venous Insufficiency – Varicose Veins Venous Thromboembolic Disease Lymphedema Efthymios “Makis” Avgerinos, MD, FACS, FEBVS Professor of Surgery - University of Pittsburgh Vis. Professor University of Athens Co-Director Vascular and Endovascular Surgery Clinic Athens Medical Center, Greece Blood Vessels Vascular Diseases Aortic Aneurysm Peripheral Arterial Disease Diabetic Foot Carotid Disease & Stroke Lymphedema – Swollen Leg Varicose Veins Deep Vein Thrombosis & PE Vascular Diseases Number 1 Cause of Death It involves all of us How Can We Diagnose? Can we prevent? How can we treat? Vascular Diseases: Occlusive or Aneurysmal Stenosed Artery Normal Artery Normal Artery Lipid lining Aneurysmal Degenaration vessels will either clot or dilate Vascular Surgery Operating Room Vascular Surgery Operating Room Vascular Diseases Peripheral Arterial Disease Aortic Aneurysm Carotid Disease Venous Insufficiency – Varicose Veins Venous Thromboembolic Disease Efthymios “Makis” Avgerinos, MD, FACS, FEBVS Professor of Surgery - University of Pittsburgh Vis. Professor University of Athens Co-Director Vascular and Endovascular Surgery Clinic Athens Medical Center, Greece Peripheral Arterial Disease The clinical manifestation of Atherosclerosis at the legs Cerebrovascular Disease Coronary Disease Renovascular Disease Visceral Arterial Disease Peripheral Arterial Disease PAD Risk Reduction Increase Smoking Diabetes Hypertension Hypercholesterolemia Alcohol Relative Risk 0.75 Newman AB et al. Circulation 1993; 88: 837-845. TASC Working Group. J Vasc Surg 2000; 31 (1, pt 2): S1-S288. Djousse PM et al. Circulation 2000; 102: 3092-3097. 1 2 3 4 5 6 Mortality Rates in PAD Survival (% patients) 100 Normal 75 Asymptomatic PAD† 50 Symptomatic PAD† Severe PAD† 25 0 0 2 4 6 8 10 12 Years Criqui MH et al. N Engl J Med 1992; 326: 381-386. 1 in 10 patients with PAD has typical symptoms of Intermittent Claudication Many px remain undiagnosed 1 in 5 >65 y.o. has PAD (ABI200m IIB. Moderate: < 200m IIC. Severe: < 50m Στάδιο III: Rest pain(night) Στάδιο IV: Tissue Loss (ulcer - gangrene) Critical Ischemia Critical Ischemia ✓Rest pain (> 2 weeks) or ✓Tissue loss (ulcer, gangrene) and ✓Ankle pressure < 50mmHg (non diabetics) ✓Toe pressure < 50mmHg (non diabetics) < 60-90mmHg (diabetics) Nomenclature Critical Limb Ischemia Chronic Limb Threatening Ischemia CLTI Classification Amputation Risk Global Guidelines 2019 PAD Diagnosis Symptom Evaluation intermittent claudication critical ischemia Risk factor evaluation smoking diabetes age: men >55 & women >65 hypertension hyperlipidemia hx of cardiovascular disease PAD Diagnosis Physical Exam Skin color Skin temperature Muscle atrophy Hair loss Hypertrophic nails Peripehral pulses Blood pressure Cardiac murmurs Arrythmia Palpable aortic aneurysm PAD Diagnosis Ankle Brachial Index ABI = Systolic ankle pressure Systolic brachial pressure ABI Interpretation > 0,90 Normal 0,71 – 0,90 Mild PAD 0,41 – 0,70 Moderate PAD ≤ 0,40 Severe PAD CAUTION: DIABETICS, Dialysis patients, ABI >1,1 (non compressible arteries) Toe pressure more reliable PAD Diagnosis Imaging PAD Anatomic Location Sites 1. Femoro-Popliteal arteries: 80-90% of Sx patients 2. Distal-tibial arteries: 40-50% of Sx patients 3. Aorta and iliac arteries: 30% of Sx patients PAD Anatomic Location Sites Normal Aortoiliac PAD Anatomic Location Sites Normal Femoropopliteal PAD Anatomic Location Sites PAD Anatomic Location Sites Normal Pedal Arteries University of Pittsburgh Medical Center PAD Treatment Risk Factor Control Smoking Hyperlipidemia Hypertension Diabetes Weight loss Antiplatelets Clopidogrel, Aspirin Treatment of Symptoms Exercise Medical Cilostazol, Pentoxifilline Revascularization Selectively! Advanced Intermittent Claudication CLTI Revascularization: Open Surgery or Endovascular ▪ Technique selection depends on: ▪ Stage of ischemia ▪ Extend of arterial lesions ▪ Ulcer size ▪ Presence of Infection University of Pittsburgh Medical Center Revascularization: Open Surgery or Endovascular ▪ In low surgical risk patients (good life expectancy) and extensive disease and a good quality saphenous vein conduit, open surgery is likely better… University of Pittsburgh Medical Center Revascularization: Open Surgery or Endovascular ▪ Few patients fulfill these criteria… ▪ Low risk ▪ Good life expectancy ▪ Good quality saphenous vein ▪ Endovascular techniques keep improving TIGRIS 6x60mm University of Pittsburgh Medical Center Open Surgery Open Surgery: Conduit Selection Autologous venous conduit “of good quality” is far superior (in terms of patency rates) than prosthetic grafts University of Pittsburgh Medical Center Pop Occlusion SFA Occlusion SFA Occlusion 60 y.o Female Left DFU – Hx Fem-Pop PTFE, Fem-Per GSV Factor V leiden - Right AKA Single Vessel Peroneal Peroneal anastomosis Posterior tibial artery Popliteal artery occlusion University of Pittsburgh Medical Center Proximal anastomosis Ankle PT anastomosis University of Pittsburgh Medical Center Medial plantar anastomosis University of Pittsburgh Medical Center Endovascular Techniques are Preferable ▪ ▪ ▪ ▪ ▪ Increasing rates (>70%) Small ulcers Shorter lesions High risk patients Poor venous conduit (20-30% of patients) PTA BMS Covered Stents Drug Elution Novel Stent Technologies University of Pittsburgh Medical Center Endovascular Techniques are Preferable “Good response to Angioplasty (PTA)” Pop I “Poor response to Angioplasty (PTA)” “Traditional Self Expanding Bare Metal Stents” Appropriate for very short lesions / spot stenting Long lesions after failed drug coated balloon University of Pittsburgh Medical Center “Covered Self Expanding Stents” “Drug Eluting Stents” Highest patency Long complex lesions High restenosis risk lesions (e.g. DM, CRF) Appropriate for long lesions / concern for thrombotic material University of Pittsburgh Medical Center “Novel Flexible Stents” SUPERA - ABBOTT Mimetic Implants Mimic the arterial anatomy No Fractures TIGRIS - GORE Highest patency Best available choice for distal SFA / POP University of Pittsburgh Medical Center We’ve become better… We’ve become better… University of Pittsburgh Medical Center Long SFA CTO (>40cm) Pop II SFA Stump FemPop Bypass? mid SFA distal SFA Long SFA CTO (>40cm) Pop II SFA Stump mid SFA Enrolled in BEST CLI distal SFA VIABAHN 5mm Re-entry Subintimal Recanalization VIABAHN 6mm 74 y.o. male Extensive Heel Ulcer Poor pedal outflow Ant Tibial runoff Dorsalis Pedis Recanalization University of Pittsburgh Medical Center Retrograde PT recanalization University of Pittsburgh Medical Center Revascularize: Hybrid Procedures University of Pittsburgh Medical Center 71 y.o. male WS Prior iliac stenting Left toe Gangrene Ext Iliac Iliac Disease SFA Occlusion CFA Occlusion Peroneal Runoff AVF Distal SFA Reconstitution Post VIABAHN 7x100 External Iliac Artery Predilatation 6mm Fem Endarterectomy Antegrade access Reentry AVF Ligated Pop II lesion Subintimal recanalization PTA + DCB 5mm Dissection EverFlex 6x40mm Non Responding Pop lesion TIGRIS 5x40mm Sometimes Revascularization Doesn’t make Sense ▪ ▪ ▪ ▪ ▪ Bedbound patients Infection - Sepsis Extensive ulcer/gangrene Multiple previous failed procedures Very frail patients University of Pittsburgh Medical Center Take Away Messages for PAD ▪ ▪ ▪ ▪ It’s a manifestation of atherosclerosis It can be Asymptomatic – Intermittent Claudication – CLTI Look at the leg - Check pulses – Use ABI Treat Risk Factors ▪ Smoking, hypertension, hyperlipidemia, diabetes ▪ Recommend intervention in debilitating claudication or in CLTI ▪ Endarterectomy, Bypass Surgery, Baloon Angioplasty, Stenting Acute Limb Ischemia Acute limb ischaemia is defined as the sudden decrease in limb perfusion that threatens the viability of the limb. Acute Limb Ischemia Etiology Embolism Thrombosis Bypass graft occlusion Native artery occlusion Acute Limb Ischemia Etiology Embolism Cardiogenic: 80% Afib 50% MI 25% Other 5%- (prosthetic valves, infectious endocarditis, myxomas) Noncardiac: 10% Aneurysmal 6% Proximal artery 3% Paradoxical emboli 1% Acute Limb Ischemia Etiology Sites of peripheral embolization Lodge at arterial bifurcations Legs > Arms Aortic bifurcation 20% Iliac bifurcation 15% Femoral bifurcation 35% Popliteal 15% Upper extremities 10% Cerebral 10-15% Mesenteric/visceral 7% Acute Limb Ischemia Etiology Native Arterial Thrombosis Outnumbers embolic occlusion ~ 6:1 Final stage in progression of atherosclerosis Underlying vessel lesion Occurs at predictable locations Adductor canal Acute Limb Ischemia Clinical Manifestations Dependent on Level and severity of obstruction Adequacy of collateral circulation Acute Limb Ischemia Classification (Rutherford) Acute Limb Ischemia Diagnosis Acute Limb Ischemia Treatment Anticoagulation Surgical modalities Primary operative revascularization Endovascular modalities Thrombolytic therapy Percutaneous mechanical thrombectomy Acute Limb Ischemia Surgical Treatment Balloon catheter thromboembolectomy Fogarty #2, 3: Popliteal, profunda, tibial Fogarty #3,4: SFA, CFA Fogarty #4, 5: Aortoiliac system Acute Limb Ischemia Endovascular Treatment Take Away Messages for ALI ▪ It’s a manifestation of atherosclerosis and embolism (e.g. A.fib.) ▪ 5Ps ▪ Pulselessness, Paleness, Paralysis, Palor, Perishingly cold ▪ Time is tissue ▪ Anticoagulate, remove or bypass the thrombus Vascular Diseases Peripheral Arterial Disease Aortic Aneurysm Carotid Disease Venous Insufficiency – Varicose Veins Venous Thromboembolic Disease Efthymios “Makis” Avgerinos, MD, FACS, FEBVS Professor of Surgery - University of Pittsburgh Vis. Professor University of Athens Co-Director Vascular and Endovascular Surgery Clinic Athens Medical Center, Greece Vascular Diseases: Occlusive or Aneurysmal Stenosed Artery Normal Artery Normal Artery Lipid lining Aneurysmal Degenaration Aneurysmal Disease Abdominal Aortic Aneurysm Definition Infrarenal aortic diameter >1.5x of the aortic diameter at the level of the renal arteries Practically: AAA = Aortic Diameter >3cm Epidemiology USA: 3rd leading cause of sudden death Autopsies: 1.8-6.6% Males 3-8:1 6x in 1st degree relatives Age (years) Males Females 45-54 1.3% 0% 75-84 12.5% 5.2% 2.9 - 4.9 cm ΑΑΑ Risk Factors Smoking Genetics Aging Atherosclerosis Male Hypertension Hyperlipidemia COPD Odds Ratio 5.17 1.9 1.7 1.6 Lederle et al. Arch Intern Med 2000 ACC/AHA Guidelines on PAD. Circulation 2006 AAA Manifestations Natural History Gradual dilatation, thining, angulation Mural thrombus Complications Rupture Thromboembolic events Compression of adjacent organs Natural History Natural history n=52 32.5% n=85 10.2% 9.4% JAMA 2002; 287:2968 n=61 Natural History 5-year Rupture Risk (%) 80 70 60 50 40 30 20 10 0 75% 25% 5-5.9cm 35% 6-6.9cm ≥7cm Diameter Simplifed estimates based on various studies Tan W Abdominal Aortic Aneurysm Rupture www.emedicine.com Ruptured AAA Mortality ~80% >1/3 die before making it to the hospital 1. Adam. J Vasc Surg 1999;30:922-8. 2. Thomas. Br J Surg Aug 1988 Clinical Signs and Symptoms Stable AAA Asymptomatic – incidental finding(70-75%) Pulsatile abdominal Chronic abdominal/back pain Embolism Hydronephrosis Ruptured AAA(20-25%) Pain Sudden onset Abdominal or back May radiate to the buttocks, groins, scrotum or leg Continuous or colick Shock - Syncope Pulsatile abdominal mass Diagnosis Clinical Exam Duplex US SCREENING CT Scan MRI Angiography Preoperative Workup AAA Management Conservative – Medical Smoking cessation, blood pressure and lipidemic control Open repair Endovascular Repair Hybrid procedures When should the AAA be treated invasively? Ruptured AAA Symptomatic AAA Asymptomatic AAA >5-5.5cm When should the AAA be treated invasively? Comparative Studies Observation VS Surgery for AAA 4-5.5cm ADAM trial UK SAT Dubost & Economos 1950: 1η Successful Open AAA Repair Mortality: 1960: 12-15%, 1980: 3-5%, 2000: < 3% Open Repair: Advantages Well studied with high clinical success for over 50 years Enduring procedure Open Repair: Disadvantages Wide laparotomy 30–90 minutes clamping Long open procedure / anesthesia Perioperative complications Postoperative complications 1–2 days in ICU 7–10 postoperative stay 4–6 weeks recovery Postop Hernias? Incidence of incisional hernias in patients operated for AAA or occlusive disease. Liapis et al. Am Surg 2004 Endovascular Repair ▪ First reported by Volodos in 1988 ▪ First published by Parodi in 1991 EVAR ▪ Originally, only tube grafts could be placed in the aorta ▪ Later, a tube down to the iliac artery followed by a femoral – femoral bypass ▪ Now, modular grafts can be deployed in a sequential fashion Preop CTA Postop CTA Preop CTA Postop CTA Preoperative CTA Postoperative CTA Currently using 4th Generation Devices Zenith Fenestrated Cook Medical Preop CTA Postop CTA EVAR Advantages No laparotomy – Minimally invasive No clamping Short procedure / mild anesthesia No major perioperative complications No ICU 1-2 days postoperative stay Minimal need for recovery EVAR Advantages No laparotomy – Minimally invasive No clamping Short procedure / mild anesthesia No major perioperative complications No ICU 1-2 days postoperative stay Minimal need for recovery EVAR Disadvantages ▪ EVAR-1 Study indicated higher aneurysm Aneurysm is not removed related mortality for EVAR (>8 years) Need for long term surveillance ▪ EVAR-1 Study indicated higher malignancy Need for reinterventions - conversion rates for EVAR Long term complications Endoleak Migration Thrombosis Rupture ▪ DREAM and OVER Studies did not find differences ▪ All studies indicated higher secondary intervention rates for EVAR Endoleak (20-30%) Endoleak (20-30%) Almost non existing neck Multiple cuffs Conversion Second Bif Excl for AI conversion Large Type I Endoleak Occluded limb / Ischemic leg Migration Migration Open vs EVAR: Individualize Treatment Take Away Messages AAA if not diagnosed early can be lethal Population screening is very important AAA medical management: aspirin, statin, blood pressure reduction, smoking cessation AAA should be managed operatively when symptomatic or when >5cm EVAR vs Open repair: EVAR first policy makes sense in high risk older population – Individualize! Vascular Diseases Peripheral Arterial Disease Aortic Aneurysm Carotid Disease Venous Insufficiency – Varicose Veins Venous Thromboembolic Disease Efthymios “Makis” Avgerinos, MD, FACS, FEBVS Professor of Surgery - University of Pittsburgh Vis. Professor University of Athens Co-Director Vascular and Endovascular Surgery Clinic Athens Medical Center, Greece CAROTID = “ΚΑΡΩΤΙΣ” = PUT SOMEBODY TO SLEEP Case Scenario 67 year old male ER with acute weakness of his right arm and leg. Symptoms started 12 hours ago. h/o of HTN and dyslipidemia PE: 97 pulses/min, 170/100 mmHg He has a 4/5 right sided weakness Cardiovascular Exam Sinus rhythm No chest pain Left Carotid bruit MRI: Acute Infarct of the Left Middle Cerebral Artery Territory MRA: Critical Stenosis of the Left ICA Case Scenario Patient is admitted to the Stroke Unit Blood pressure management Initiation of aspirin, statin and heparin Patient gradually recovers (72h) 80% of his functionality What is your suggestion? Patient is improving, so continue medical management Carotid Endarterectomy of Left ICA Carotid Stenting of Left ICA University of Pittsburgh Medical Center Cerebrovascular Disease ▪ ▪ ▪ ▪ ▪ 5th cause of death in western world 2nd cause of cardiovascular death U.S. Prevalence 2.7% → 3.9% in 2030 Neurologic disability High socioeconomic impact “Every 3 minutes and 45 seconds, someone in U.S. has a stroke, and every 4 minutes, someone dies of a stroke” University of Pittsburgh Medical Center Mozaffarian Circulation 2015 Cerebrovascular Event Classification ▪ Transient Ischemic Attack (no infarct) ▪ Stroke (infarct = cell death) University of Pittsburgh Medical Center Transient Ischemic Attack (time-based definition) “Sudden, focal neurologic deficit lasting less than 24 hours, confined to an area of the brain or eye perfused by a specific artery.” Transient Ischemic Attack (tissue-based definition) “Brief episode of neurologic dysfunction caused by focal brain or retinal ischemia, with clinical symptoms typically lasting less than one hour, and without evidence of acute infarction.” Most TIAs last seconds to 10 minutes, with symptoms lasting greater than 1 hour in only 25% of patients University of Pittsburgh Medical Center Transient Ischemic Attack Facts 10-20% of TIAs will be followed by a stroke within 3 months, half of them within 48 hours. Among those who present with a stroke the prevalence of prior TIA is reported 7-40% – Northern Manhattan Study – Harvard Stroke Registry – National Institute of Neurologic Disorders – Stroke Data Bank – Oxford Vascular Study University of Pittsburgh Medical Center Stroke Infarction of the central nervous system tissue related to hypoperfusion, embolization, thrombosis, or intracranial hemorrhage Ischemic 85% Hemorrhagic 15% University of Pittsburgh Medical Center Extracranial atherosclerosis ◦ Carotid / Vertebral / Aortic Arch Intracranial atherosclerosis - Lacunar (small vessel) Cardioembolic Miscellaneous (e.g. hypercoagulability) Cryptogenic University of Pittsburgh Medical Center Extracranial Atherosclerosis The common sites include (1) the points of takeoff for the branches of the aortic arch (2) the origins of the vertebral artery (3) the bifurcation of the common carotid artery (carotid bulb) (4) the carotid siphon (5) the origins of the anterior and middle cerebral arteries. Carotid Artery Disease Atherosclerosis 90% Remaining 10%: Fibromuscular dysplasia Arterial kinking Extrinsic compression Traumatic occlusion Intimal dissection Inflammatory angiopathies Migraine Radiation-induced arteriosclerotic Fibrinoid necrosis Amyloidosis Polyarteritis Allergic angiitis Wegener’s granulomatosis Granulomatous angiitis Giant cell arteritis Amphetamine-associated arteritis Infectious arteritis Moyamoya disease University of Pittsburgh Medical Center Risk Factors… Carotid Anatomy Superficial Temporal Internal Maxillary Ascending Pharyngeal Post Auricular Occipital Facial Lingual Superior Thyroid Internal Carotid Carotid Bulb External Carotid Common Carotid Carotid Anatomy – Internal Carotid AP VIEW LATERAL VIEW University of Pittsburgh Medical Center Posterior Circulation Circle of Willis Only 20% of individuals actually have the symmetrical circle of Willis Hypoplasia, or absence of one or both Pcom As : 25% to 30% isolating the anterior and posterior circulations Anomalies of the Acom A: 10% (hypoplasia, absence, duplication) University of Pittsburgh Medical Center University of Pittsburgh Medical Center Carotid Artery Disease Degree / Progression of atherosclerotic stenosis Plaque Quality (stable vs unstable) PLAQUE DEBRIS EMBOLIZATION HYPOPERFUSION TIA / STROKE University of Pittsburgh Medical Center Carotid Artery Disease - Embolization The primary mechanism responsible for episodes of TIA/STROKE is cerebral emboli originating from the plaque surface : Atheromatous debris Platelet aggregates Thrombus University of Pittsburgh Medical Center The Vulnerable Carotid Plaque Stable plaques are unlikely to result in TIA or stroke Unstable Plaques are mainly associated with these events Identifying the vulnerable carotid plaque Clinical information, family history, genetics Imaging Biological Markers University of Pittsburgh Medical Center Carotid Artery Disease – Hypoperfusion High grade stenosis prevents adequate brain supply particularly in pts with multivessel disease Autoregulatory mechanism may fail during episodes of hypotension => syncope or near syncope Carotid Artery Disease – Presentation Symptomatic CAD (TIA/Stroke) Asymptomatic Symptomatic Carotid Artery Disease ICA Territory Opthalmic Artery Anterior Cerebral Artery (ACA) Middle Cerebral Artery (MCA) Posterior Cerebral Artery (PCA) Amaurosis Fugax BMT for Carotid Disease – Stabilizing the Carotid plaque Treatment of hypertension Treatment of diabetes Treatment of lipids Moderate or high intensity statin Smoking cessation Physical Activity Antiplatelets The Rational for Intervention Eliminate the embolic focus – Prevent a major stroke Increase perfusion to the ischemic penumbra surrounding the area of cerebral infarct Enhance arterial flow to augment clot dissolution therapies Improve access for intervention on the intracranial lesions Improve the patency of the prior intracranial intervention Carotid Interventions University of Pittsburgh Medical Center Carotid Endarterectomy University of Pittsburgh Medical Center Carotid Endarterectomy University of Pittsburgh Medical Center Carotid Endarterectomy – Monitoring & Shunting Consensus & Guidelines No evidence for the routine use of shunts [A] Little evidence to support the use of one form of monitoring over another for selective shunting Regional anesthesia Stump pressure Transcranial doppler Electroencephalogram (EEG) Somatosensory evoked potentials (SSEP) Dual EEG & SSEP University of Pittsburgh Medical Center Carotid Endarterectomy University of Pittsburgh Medical Center Carotid Endarterectomy Carotid Endarterectomy – Closure Techniques Primary Closure Patch Closure Eversion University of Pittsburgh Medical Center Carotid Stenting (Transfemoral) University of Pittsburgh Medical Center Carotid Stenting - Stents University of Pittsburgh Medical Center Carotid Stenting – Embolic Protection Filters University of Pittsburgh Medical Center University of Pittsburgh Medical Center University of Pittsburgh Medical Center Transcarotid Carotid Artery Revascularization (TCAR) University of Pittsburgh Medical Center CEA vs CAS CEA vs CAS – 30 day Stroke or Death in Sx Patients CEA is superior to CAS in the primary end-point of death or any stroke (8.9% vs. 5.8%; p = 0.0006). Age was the only variable that modified the effect: 120-day risk was higher in CAS (12%) vs. CEA (5.9%) in patients >70 years Meta-analysis SPACE – EVA3S – ICSS 3,433 patients But not In patients ≤70 years CAS 5.8% vs. CEA 5.7% CAS for Sx patients should be avoided in older, but might be as safe as CEA in younger patients. CSTC. Lancet 2010 CEA vs CAS CREST Trial – Too Many Minor Strokes for CAS in Sx Silver et al Stroke 2011 CEA vs CAS Too Many DW-MRI Hits Transfemoral vs Transcarotid CAS The transcarotid approach for CAS can minimize stroke risk by avoiding the tortuous atherosclerotic aortic arch Symptomatic Carotid Artery Disease Which Carotid Stenosis is considered Clinically Significant? Is the risk of intervention lower than the anticipated risks of the natural history? When to intervene (Carotid Endarterectomy or Carotid Stenting)? ECST NASCET Guidelines for Sx Patients Carotid Endarterectomy (CEA) is recommended in Sx patients within the preceding 6 months with CAD >50% CEA should be preferred over CAS for patients >70 y.o. CAS (Carotid Stenting) may be considered for patients 60%, CEA should be considered if life expectancy exceeds >5 years CAS may be an alternative CAS can be considered in “high risk” patients with Asx CAD >60%, CEA should be considered if life expectancy exceeds >5 years ESVS Carotid Guidelines 2018 University of Pittsburgh Medical Center Average annual risk of ipsilateral stroke in Asx >50% stenosis % 4 3.5 Johnson12 3 Norris14 Satiani13 2.5 VA15 ACAS1 Mansour17 2 NASCET19 ACSRS20-22 ECST16 1.5 ACBS18 1 ASED23 0.5 0 1980 SMART24 1985 1990 1995 2000 2005 AR Naylor Sem Vasc Surg 2008 2010 Benefit is questionable in the elderly 5-year risk (& se): AGE 75+ Carotid Territory Ischaemic STROKE (not perioperative) 100% Immediate 5.50%(1.57) 95% Deferred 8.79%(2.11) 90% Difference = 3.29% (CI -1.86-8.44), z = 1.25 z = 1.25, p = 0.21 (non sigt.) 85% Age 75+: 12 vs 18 CTI strokes 0 1 2 3 Years 4 5 University of Pittsburgh Medical Center Case Scenario 67 year old male ER with acute weakness of his right arm and leg. Symptoms started 12 hour ago. h/o of HTN and dyslipidemia PE: 97 pulses/min, 170/100 mmHg He had a 4/5 right sided weakness Cardiovascular Exam Sinus rhythm No chest pain Left Carotid bruit MRA: Critical Stenosis of the Left ICA Case Scenario Patient is admitted to the Stroke Unit Blood pressure management Initiation of aspirin, statin and heparin Patient gradually recovers (72h) 80% of his functionality What is your suggestion? Patient is improving, so continue medical management Carotid Endarterectomy of Left ICA Carotid Stenting of Left ICA Take Away Messages Am. Fugax, TIA or minor stroke are typically a warning sign of a major stroke in the setting of carotid stenosis ≥50% Imaging techniques and biomarkers CAN identify carotid plaque vulnerability Risk of stroke with BMT is declining (statins, antiplatelets, anti-hypertensives etc) Sx patients with >50% stenosis will benefit from an intervention to prevent a new stroke Asx patients with >70% stenosis will benefit from an intervention (to prevent a stroke) provided they have a good 3-5 year life expectancy Risk of perioperative stroke with intervention is also declining Interested in Vascular Surgery?