VA AM Report 4.12.17-Neuro report, stroke prevention

Summary of Recommendations and References Re: Secondary Prevention of Stroke:
Anti platelet therapy:
1) Does the dose of ASA matter?
 ASA 81 is not inferior to ASA 325 mg 
 We load with ASA 325 mg daily in acute stroke, then will decrease to 81 mg daily the next day
(J Stroke Cerebrovasc Disease 2016.
 People used to give even high doses of ASA 650mg in patients with carotid stenosis, but this was shown NOT to be beneficial 
2) What if the patient has a stroke on ASA?
–  If they were not compliant on ASA, we will restart ASA
  Plavix is slightly better at preventing stroke, but not much better. If a patient has a stroke with good compliance on ASA, we will change them to Plavix 75 mg daily monotherapy as long as it is not financially prohibitive
(CAPRIE 1996
3) What about dual antiplatelet therapy?
 Chronic dual antiplatelet therapy (ASA+Plavix) increases risk of bleeding without changing outcomes compared to antiplatelet monotherapy
 Short term dual antiplatelet therapy for 90 days has been shown to be beneficial in small stroke or TIA in one Chinese study. This study is being repeated the US, and we are actively enrolling patients at UCSF in the POINT trial.
 Some providers use 90 days of ASA and Plavix for patients with bad intracranial atherosclerosis or if patient opts to medically treat for carotid stenosis. Data for this is not based on RCT data, but comes from “optimal medical treatment arm” outlined in SAMMPRIS trial. 
4) What about Aggrenox (ASA-dipyridamole)?
 It reduces stroke risk, but 40% of patients developed headache. It is not prescribed regularly at UCSF, due to this side effect of headache and it causes more GI upset compared to ASA or plavix alone. 
Cardiac Monitoring (To help decide to transition from anti platelet to anticoagulation):
1) How long do we need to monitor patients for after a stroke, after they have been on telemetry in an in-patient setting?
 One month of monitoring for Afib has been shown to increase chance of finding Afib in patients with cryptogenic stroke. At UCSF, we recommend at least 1 month of monitoring with Ziopatch, life watch, or consider implantable loop recorder if high suspicion for Afib  
2) What is a cryptogenic stroke?
 A stroke that occurred and we don’t have an exact etiology or mechanism
1) How do I decide if my patient needs to be anticoagulated?
 Use CHADS2VASC to risk stratify. Pretty much, we recommend everyone with Afib and stroke should be anticoagulated if there are no contraindications
2) What if my patient has a stroke and only Aflutter is found on monitoring?
 Afib and Aflutter carry similar risk for stroke, and for the purpose of stroke prevention, you can use CHADS2Vasc in the decision to start anticoagulation
(AHA/ASA Guidelines for prevention of Stroke in Patients with Stroke and TIA 2014) 
3) What if the patient has Afib is ablated or only has paroxysmal atrial fibrillation?
 We would still recommend using CHADS2Vasc and recommend anticoagulation in a patient who suffered a stroke and  there are no contraindications to anticoagulation
(AHA/ASA Guidelines for prevention of Stroke in Patients with Stroke and TIA 2014)
4) When can I safely start anticoagulation?
 This is provider dependent with limited data. Generally, earlier is better, as early recurrence of ischemic stroke related to AF may be as high as 8% in 14 days (HAEST, Lancet 2000)
 One prospective observational study concluded sometime between 4 to 14 days is best
(RAF. Stroke 2015
5) Do we need to bridge with anticoagulation if the patient has Afib and an acute stroke, or if we hold the anticoagulation?
 After acute stroke, we bridge with ASA until INR>2, we do not acutely bridge with Lovenox or other anticoagulation while waiting for warfarin to become therapeutic
 If the patient has to stop anticoagulation for a short period of days, we generally recommended against bridging for Afib 
TTE: At minimum, check TTE
1)Should I anticoagulate my patient with severely reduced EF in sinus rhythm?
 Anticoagulation for low EF (<35%) in sinus rhythm was deemed to be a negative study. However, if you look at the outcomes, there was a significant decrease in ischemic stroke risk in warfarin group compared to ASA. The author concluded that the significant reduction in strokes was canceled out by the increased risk of GI bleeds 
2) We found a PFO, should we close it?
 There are multiple failed trials that show that PFO closure is not helpful in strokes
3) We found a thrombus, now what?
 Finding left atrial thrombus on TTE is unlikely, but should be treated with at least 3 months of Warfarin if you do find it
(RAF Neurology 2016, AHA 2014 stroke guidelines)
 Of note, LAE and LV enlargement are associated with higher risk of stroke
HTN: Check BP
 Lacunar or DM: consider SBP<130; this is not a hard rule that we follow (SAMMPRIS)
 Bad intracranial atherosclerosis: 120-150  (No evidence, best practice and this range is usually documented in neurology’s note if this blood pressure range is preferred)
HLD: Check LDL
 We start all patients with acute ischemic stroke on Atorvastatin 80 mg on admission
(SPARCL, Stroke 2009.
How do we decide to keep a patient on statin therapy after ischemic stroke?
 Many people in the neurology department still targets goal LDL levels. The current AHA guidelines state that all patients LDL >100 should be on intensive lipid lowering agent, and all patients LDL<100 with atherosclerotic cardiovascular disease should be on intensive statin therapy
(AHA/ASA 2014 stroke guidelines)
DM: Check HgA1c
1) Is there a goal HgA1C or glucose level?
 There is no data as to goal glucose level is optimal following stroke. However, here is an ongoing trial called SHINE that is currently enrolling patients to tight glycemic control (80-130) vs standard practice (glucose goal <180) and there is no recommended guideline from the stroke community regarding goal HgA1C.
 American Diabetes Guidelines 2016: Goal HgA1C: <6.5% if young, <7.0% for most patients, or <8% in elderly with short life expectancy. 
Carotid Disease: Image external carotid arteries
1) What is symptomatic and asymptomatic carotid stenosis?
 Stroke occurs ipsilateral or “down stream” to the carotid artery. Asymptomatic means the stenosis is contralateral to the stroke, or it was incidentally found.
2) Based on the imaging, I found symptomatic carotid stenosis, what do I do?
 For patients with a TIA or ischemic stroke within the past 6 months and ipsilateral severe (70%–99%), CEA is recommended if the perioperative morbidity and mortality risk is low (<6%) (VACS, NASCET, and ECST, AHA 2014 recommendations)
 Patients with a moderate (50%–69%) stenosis who are at reasonable surgical and anesthetic risk may benefit from intervention when performed by a surgeon with excellent operative skills (NASCET Stroke 1999
3) I incidentally found asymptomatic stenosis, what do I do?
 For patients with severe stenosis (the number varies based on guidelines, but generally, >70%), who have life expectancy of >5 years and the patient is a good surgical candidate, CEA should be considered
(VA trial, ACAS, and ACST) Of note, there is a lot of variability in recommendations regarding this one!
4) When is the best time to stent?
 Generally, the timing if you are going to do this is best within two weeks, but for ipsilateral and severe, it can be corrected even up to 6 months out (NASCET, ECST)
5) When do we stent in carotid stenosis?
–  The earliest studies of stenting in carotid stenosis after TIA or nondisabling stroke were negative, in part, because the optimal medical therapy arm did so well (defined as ASA 325 mg+Plavix 75 for 90 days, SBP<140 or in diabetic patient <130, LDL<70, weight loss).  However, for people who have symptomatic carotid stenosis that is significant (>70%), carotid artery stenting may be done. Most studies show stenting has higher risk of death and restenosis then CEA
Nice things to think about: Nutrition, OSA (think about screening your patients), weight loss, and stop smoking!



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