Chapter 89 - Cerebrovascular disease medical therapy Flashcards
Best medical therapy on stroke and CV events
1) Antiplatelet (1 or 2) - reduce stroke and MACE 2) Anti-HTN to reduce 10/5 mmHg or to 140/90 (130/90 if lacunarin HTN pt) - reduce stroke 3) DM: A1c <7 - reduce stroke 4) smk cessation - reduce stroke and MACE 5) statin reduce LDL by 50% or < 70 mg/dl 6) alcohol - avoid excessive use
HTN control around stroke
within first 24 hr should not aggressively lower BP but after 24 yes
ACCORD trial on diabetes control for stroke
251 patient randomized to tight vs routine control No benefit of tight control ( a1c <6) in fact higher mortality in tighet control recommend A1C < 7 is sufficient
ADVANCE trial
randomized 11140 patient for targets of < 6.5 and < 7 A1c no difference
Stroke prevention by aggressive reduction in cholesterol level trial (SPARCL)
1) atorvastatin 80 mg on reducing subsequent stroke in pt with CVA without CAD and moderate LDL (100-190) 2) 5 year reduced stroke and CV risk in statin group 3) increase risk of hemorrhagic stroke in statin group 4) biggest pt in people with biggest LDL reduction
Alcohol on stroke
Mild consuption < 2 drinks/day associated wtih reduced risk of stroke
Define metabolic syndrome
1) increased waist circumference (>102 cm male; > 88cm female) 2) TG > 150 mg/dl 3) HDL < 50 male or 40 female 4) BP > 135/85 5) fasting glucose > 100 mg/dl 3/5 = diagnostic
European stroke prevention study ESPS-1
325 ASA + 75 dipyridamole better than placebo at stroke prevention
ESPS-2
ASA and dipyridamole reduced stroke combination therapy even better but SE = headache, GI symptoms same observation in PROFESS study: combination not better than plavix alone
Ticlopidine in stroke prevention
250 mg po BID lower bleeding risk than ASA side effect: neutropenia, TTP
Clopidogrel vs aspirin in patients at risk of ischemic events (CAPRIE) trial
1) 19000 patients 2) plavix 5.32 vs asa 5.83 CV event rate minimal but significant improvement
MATCH trial
1) recent stroke patients or TIA 2) plavix vs DAPT 3) no benefit of adding ASA but increase bleeding 1.3% absolute risk
CHARISMA trial
1) ASA vs DAPT 2) no difference in effect
DAPT in stroke
1) reduce stroke rate HR 0.61 2) increase bleeding HR 1.71 after CEA
Biggest predictor of future stroke
Stroke/tia within 6 months after 6 months plaque has stabilized
Key carotid trials and lesions that show significant benefit from NASCET ECST ACAS ACST CEA vs BMT with rate of stroke
TABLE 89.2
ACSRS on controlateral stroke history in now asymptomatic ipsilater risk
still higher than total asymptomatic assumes that plaque morphology on both sides are similar
Contralateral carotid occlusion with ipsilateral stenosis
1) ACAS showed decrease stroke at 5 years (weird) 2) ACST and AbuRahma showed increased risk of stroke with contralateral occlusion likely has to do with with amount of collateral intracranial circulation
Clinical silent emboli detection
1) evidence on CT or MRI 2) embolic material in ipsilatera MCA using TCD
Asymptomatic patients that have had a silent cortical infarction on CT
20%
Asymptomatic patients degree of stenosis relationship to stroke risk
ACAS and ACST did not identify this 1) underpowered 2) duplex rather than angiographic determination of stenosis 3) uneven distribution of degree of stenosis 4) not enough strokes (hits) natural history study suggest a correlation NASCET contralateral disease suggest a relationship
Plaque characteristics associated with increased stroke risk
1) diameter stenosis 2) ulceration 3) plaque progression 4) echolucent plaque 5) plaque area 6) disrupted fibrous cap 7) discrete white areas within plaque 8) active inflammation on MRI
Patient factors associated with increased stroke risk
1) ipsilateral CVA 2) history of contralateral stroke 3) contralateral carotid occlusion 4) renal insufficiency 5) smoking 6) clinically silent emboli on TCD or MRI/CT
Life expectancy on decision to treat symptomatic and asymptomatic
Symptomatic benefits quite evident therefore treat always Asymptomatic needs survival at least 3-5 years
Higher risk of stroke in carotid stenting after this age
64
NASCET stroke risk perioperative in patients with and without contralateral carotid occlusion
14% vs 5.8% metaanalysis shows slight increase in risk not as drastic
Factors associated with stroke risk for CEA vs that for CAS
CEA 1) CAD/CHF 2) lesion above C2 or below clavicle 3) scarring 4) recurrent stenosis 5) neck stoma CAS 1) symptomatic lesion (especially in first week) 2) age > 70 3) vessel/arch tortuosity 4) adverse lesion characteristics
Adverlesion characteristics bad for CAS
1) length > 15 mm 2) echolucent, irregular 3) tandem lesions 4) pre-occlusive lesions 5) circumferential calcification
SPARCL trial
demonstrate improved risk reduction with improved medical therapy for stroke does not differentiate stroke caused by carotid vs all stroke carotid is only 20%
Abbott meta analysis on asymptomatic carotid stenosis 50%
1) 11 trials 2) 3724 patients 3) 1985-2007 4) risk of stroke declined in medical group now similar to surgical cohort in ACAS FLAW 1) heterogenous including complete asymptomatic ACAS and contralateral asymptomatic from NASCET and ECST 2) included stnosis from 50-100% (including total occlusion) 3) ACST was excluded for no apparent reason
SMART study
1) 2684 neurologically asymptomatic with arterial disease or diabetes 2) 8% had carotid disease > 50% 3) stroke risk trended towards higher risk with higher lesion
REACH registry
2x increase stroke in asymptomatic > 70% most pt were on statins
SAMMPRIS trial
1) BMT vs intracranial angioplasty for patients with symptomatic intracranial carotid stenosis 2) BMT alone just as good and negated benefit of endo intervention
CREST
1) 2500 normal risk patient (1182 asymptomatic) to CAS or CEA 2) DAPT and protection devices for CAS 3) no difference in composite MACE 4) stroke less in CEA, MI less in CAS 5) age > 64 worse for CAS 6) stroke and death benefit favor CEA in symptomatic disease
CREST 10 year
1) late stroke and death favor CEA driven by perioperative events 2) restenosis the same
ACT1 trial
1) 1453 patients - stopped early because of slow enrollment 2) no difference between CAS and CEA for MACE or perioperative stroke/death 3) freedom from ipsilateral stroke > 97% at 3 years and 94% at 5 years
Societal guidelines on treating carotid disease
TABLE 89.6
Treatment for symptomatic < 50% stenosis
BMT
Treatment for asymptomatic < 50% stenosis
if no other manifestation of CV disease then not even BMT
Treatment of asymptomatic with carotid stenosis 70-99%
operate if life expectancy 3-5 years CAS not done over age 70
Role of urgent or expedited Carotid intervention
unstable neurologic syndromes 1) Crescendo TIA 2) stroke in evolution (waxing and waning neurologic events)
Rate of restenosis after CEA and CAS
8-12%
Significance on the timing of restenosis
< 24 months likely intimal hyperplasia = relatively benign > 36 months may be new atherosclerotic disease = might need intervention
Radiation induced stenosis treated with CEA or CAS
1) stroke risk same 3.5-3.9% 2) CEA higher CN injury 3) CAS higher restenosis
