Medications in Stroke Rehabilitation THE GOALS OF PRESENTATION STROKE STATISTICS 9/9/2014

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Lizbeth Bertha Strickland
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1 Medications in Stroke Rehabilitation THE GOALS OF PRESENTATION IDENTIFY POTENTIAL AREAS FOR PHARMACOLOGIC INTERVENTIONS IN THE STROKE REHAB PATIENT IDENTIFY AGENTS USED WITH GENERAL MECHANISM OF ACTION STROKE STATISTICS 150,000 stroke deaths annually 17%-34% mortality in first 30 days Third leading cause of death 600,000 strokes yearly in us 1

WITH GENERAL MECHANISM OF ACTION STROKE STATISTICS 150,000 stroke deaths annually

2 % of patients Mean rankings 9/9/2014 MORE STATISTICS LEADING CAUSE OF ADULT DISABILITY 4.4 M STROKE SURVIVORS WITH DISABILITIES 25%-50% PARTIALLY/TOTALLY DEPENDENT IN ADL COSTS $45.3 BILLION/YEAR IN CARE AND LOST EARNINGS Stroke Is the Primary Cause of Long-Term Disability in the United States Disabilities in patients 6 months after acute ischemic stroke 50% 40 35% 30 30% 26% 26% 20 19% 10 Hemiparesis Depressive symptoms Unable to walk without assistance Dependent in daily living activities Institutionalized in a nursing home Aphasia Rosamond et al. Circulation. 2007;115:e69-e171. Patients Perceive Severe Stroke Outcomes as Similar to or Worse Than Death Lower preference Mild deficit Moderate deficit Severe deficit Higher preference 0 Language deficits Cognitive deficits Motor deficits Death Solomon et al. Stroke (9);

26% 26% 20 19% 10 Hemiparesis Depressive symptoms Unable to walk without assistance Dependent in daily living activities Institutionalized in a nursing home Aphasia Rosamond et al. Circulation.

Mechanisms of Action of Oral Antiplatelet Therapies clopidogrel bisulfate dipyridamole ticlopidine HCl phosphodiesterase GP IIb/IIIa (fibrinogen receptor) COX camp Activation collagen thrombin TXA 2

Rehabilitation C o n t i n u o u s Q u a l i t y I m p r o v e m e n t Stroke Rehab Goals Optimize stroke recovery (integrate patient back into their environment with residual neurological deficits)

3 Mechanisms of Action of Oral Antiplatelet Therapies clopidogrel bisulfate dipyridamole ticlopidine HCl phosphodiesterase GP IIb/IIIa (fibrinogen receptor) COX camp Activation collagen thrombin TXA 2 aspirin TXA 2 1. Prevention Stroke System of Care 2. EMS Notification & Response Continuum of Care 3. Acute Treatment 4. Sub-Acute Care & Secondary Prevention 5. Rehabilitation C o n t i n u o u s Q u a l i t y I m p r o v e m e n t Stroke Rehab Goals Optimize stroke recovery (integrate patient back into their environment with residual neurological deficits) Treat every patient like it s you/your family!!! Optimize adaptive resources/techniques over time Prevent post-stroke related complications Optimize secondary stroke prevention Closely observe for any recurrent TIA/stroke events Optimal stroke-related education for the patient and family Provide stability and support from transition from inpatient to outpatient settings Cutting-edge research Evidence/guidelines-based treatment approach 3

MEDICATIONS IN ACCOMPLISHING THESE GOALS Antihypertensives Lipid lowering agent Diabetic GI prophylaxis Nicotine replacement therapy = Nimodipine in SAH Dihydropyridine calcium antagonist that blocks

Alternate putative mechanisms include vascular effects, such as decreased small vessel resistance with pial collateral augmentation, as well as neuroprotection via reduction of calcium-mediated

4 MEDICATIONS IN ACCOMPLISHING THESE GOALS Antihypertensives Lipid lowering agent Diabetic GI prophylaxis Nicotine replacement therapy = Nimodipine in SAH Dihydropyridine calcium antagonist that blocks calcium influx through L-type calcium channels and possesses regional selectivity for vascular smooth muscle. It does not significantly reverse angiographic vasospasm. Alternate putative mechanisms include vascular effects, such as decreased small vessel resistance with pial collateral augmentation, as well as neuroprotection via reduction of calcium-mediated excitotoxicity. Largest randomized study, the British Aneurysm Nimodipine Trial, demonstrated a 34% reduction in cerebral infarction and a 40% reduction in poor outcome at 3 months in the oral Nimodipine group when compared to the placebo cohort. Recent meta-analysis that evaluated 8 prospective randomized trials, including 1514 patients. In comparison to placebo, Nimodipine significantly reduced the incidence of delayed neurological deficits by 38% (OR 0.62, 95% CI ) and cerebral infarcts by 48% (OR 0.52, 95% CI ). Calcium antagonists for aneurysmal subarachnoid hemorrhage. Cochrane Database Syst Rev. 2007;(3):CD British Medical Journal, vol. 298, no. 6674, pp , CNS and Neurological Disorders, vol. 10, no. 7, pp ,

5 PREVENTING DVT Heparin-low molecular weight or low dose unfractionated Other measures-walking Intermittent pneumatic compression Elastic stockings STOP! Stroke Prevention (ischemic) Antiplatelet therapy Aspirin (low-dose) Clopidogrel (Plavix)? Low-dose aspirin + Clopidogrel combination therapy Extended-release Dipyridamole + low-dose aspirin (Aggrenox) Cilastazol (Pletal) Anticoagulation (full-dose) Cardioembolic source, hypercoaguable state, arterial dissection (short-term), and venous sinus thrombosis (+/- ICH) Timing with recent large radiographic strokes and hemorrhagic transformation/ich Mechanisms of Action of Oral Antiplatelet Therapies clopidogrel bisulfate dipyridamole ticlopidine HCl phosphodiesterase GP IIb/IIIa (fibrinogen receptor) COX camp Activation collagen thrombin TXA 2 aspirin TXA 2 5

Low-dose aspirin + Clopidogrel combination therapy Extended-release Dipyridamole + low-dose aspirin (Aggrenox) Cilastazol (Pletal) Anticoagulation (full-dose) Cardioembolic source, hypercoaguable

6 ANTIPLATELET AGENTS Aspirin Plavix Aggrenox Dipyridamole Antithrombotic Actions Dipyridamole inhibits adenosine uptake in red blood cells, thereby inhibiting platelet aggregation. Dipyridamole inhibits the breakdown of cgmp and camp, potentiating the antithrombic effects of nitric oxide and prostacyclin (PGI 2 ) on platelets. Dipyridamole has been shown to stimulate endothelial PGI 2 production and release, a potent inhibitor of platelet aggregation. Eisert WG. In: Michelson AD, ed. Platelets. Academic Press; 2002: Additional Dipyridamole Actions Dipyridamole enhances the anti-thrombotic effects of endothelial cells, possibly through PGI 2 and/or NO release. Dipyridamole decreases the levels of the inflammatory cytokines and chemokines MCP-1, MMP-9 and IL-8 from activated platelet /monocyte aggregates. 6

Dipyridamole has been shown to stimulate endothelial PGI 2 production and release, a potent inhibitor of platelet aggregation. Eisert WG. In: Michelson AD, ed. Platelets. Academic Press; 2002:803-815.

7 Plavix vs. Aggrenox Plavix (75 mg daily) Acute ischemic stroke or TIA with stuttering/fluctuating neurological deficits. Acute symptomatic carotid artery disease/stenosis Large vessel disease Aspirin intolerance/allergy Inability to swallow capsule Comorbid symptomatic CAD or PAD. Plavix metabolism and drug-drug interactions (PPIs, Prilosec) Aggrenox (one capsule bid) Primary cerebrovascular disease Small vessel/lacunar disease Prior non-cardioembolic TIA/stroke (high risk individuals) Antiplatelet Therapy Avoid aspirin and Plavix combination therapy for long-term stroke prevention, due to lack of efficacy and increased bleeding risk. Possible short-term (<90 days) benefit to combination therapy, with ongoing clinical research trials. ANTICOAGULANTS Coumadin Xarelto Eliquis 7

Plavix metabolism and drug-drug interactions (PPIs, Prilosec) Aggrenox (one capsule bid) Primary cerebrovascular disease Small vessel/lacunar disease Prior non-cardioembolic TIA/stroke (high risk

8 BOWEL MEDICATIONS Miralax Senna Colace Dulcolax Lactulose BLADDER MEDICATIONS Ditropan Detrol Urecholine Flomax Proscar PAIN NSAIDs NEURONTIN LYRICA LIDODERM PATCH TRAZODONE 8

9 Spasticity Zanaflex Baclofen Valium Dantrium Botox Treating Depression Mild Depression attention/encouragement, therapeutic activities simple environmental changes More Severe Depression antidepressant medication Psychotherapy Fluoxetine (Prozac) Fluoxetine for motor recovery after acute ischemic stroke (FLAME): a randomized placebo-controlled trial. 9 stroke centers in France Patients had an acute ischemic stroke and hemiplegia or hemiparesis, had Fugl-Meyer motor scale (FMMS) scores of 55 or less, and were between ages 18 years and 85 years. Patients were randomly assigned to either fluoxetine (20 mg once per day) or placebo for 3 months, starting 5-10 days after the onset of stroke. 118 patients were randomly assigned to fluoxetine (n=59) or placebo (n=59), and 113 were included in the analysis (57 in the fluoxetine group and 56 in the placebo group). FMMS improvement at day 90 was significantly greater in the Fluoxetine group (adjusted mean 34.0 points [95% CI ]) than in the placebo group (24.3 points [ ]; p=0.003). The Lancet Neurology, Volume 10, Issue 2, Pages , February

9 stroke centers in France Patients had an acute ischemic stroke and hemiplegia or hemiparesis, had Fugl-Meyer motor scale (FMMS) scores of 55 or less, and were between ages 18 years and 85 years.

10 Medications to Enhance Stroke Recovery Ritalin Symmetrel Modafinil Dopaminergic Meds Antidepressant Meds Cholingeric Meds CONCLUSION Multiple meds are available to enhance stroke outcome and help with prevention of recurrent stroke and complications 10

Meds CONCLUSION Multiple meds are available to enhance stroke

Antiplatelet and anticoagulation treatment of patients undergoing carotid and peripheral artery angioplasty

Round Table: Antithrombotic therapy beyond ACS Antiplatelet and anticoagulation treatment of patients undergoing carotid and peripheral artery angioplasty M. Matsagkas, MD, PhD, EBSQ-Vasc Associate Professor