Posterior Cerebral Artery Stroke Medication

Updated: Jul 30, 2018
  • Author: Erek K Helseth, MD; Chief Editor: Helmi L Lutsep, MD  more...
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Medication

Medication Summary

As previously mentioned, long-term anticoagulation to prevent recurrent strokes is indicated in several settings, including the following:

  • Atrial fibrillation

  • Selected cases with significant global or regional cardiac hypokinesis (ejection fraction < 35%)

  • Patent foramen ovale with documented hypercoagulable condition

  • Arterial hypercoagulable state

When no cause for recurrent strokes can be found, antiplatelet therapy—eg, with aspirin, ticlopidine, clopidogrel, or aspirin plus extended-release dipyridamole (Aggrenox)—is generally recommended instead of anticoagulation therapy.

As a result, patients entering the rehabilitation phase of their hospital course may be prescribed an anticoagulant, clopidogrel, or aspirin. The selection of these agents is dependent on the etiology of the posterior cerebral artery (PCA) stroke, associated complications, comorbidities, and prior medical history. These medications are used to prevent further cerebral vascular ischemic events.

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Antiplatelet Agents

Class Summary

These agents inhibit the cyclooxygenase system, decreasing the level of thromboxane A2, a potent platelet activator.

Clopidogrel (Plavix)

Clopidogrel selectively inhibits adenosine diphosphate (ADP) from binding to the platelet receptor and the subsequent ADP-mediated activation of glycoprotein GPIIb/IIIa complex, thereby inhibiting platelet aggregation.

Aspirin (Bayer Aspirin, Ascriptin Maximum Strength, Ecotrin, Bufferin)

Aspirin treats mild to moderate pain and headache. It inhibits prostaglandin synthesis, which prevents the formation of platelet-aggregating thromboxane A2.

Ticlopidine

Ticlopidine is second-line antiplatelet therapy for patients in whom aspirin is not tolerated or is ineffective.

Dipyridamole 200 mg/aspirin 25 mg (Aggrenox)

Dipyridamole-aspirin is a combination antiplatelet agent that takes advantage of the additive antiplatelet effects of the 2 drugs. Dipyridamole acts via the adenosine-platelet A2-receptor system, whereas aspirin inhibits platelet aggregation by causing irreversible inhibition of cyclooxygenase system, thereby reducing generation of thromboxane A2, a powerful enhancer of platelet aggregation and vasoconstriction.

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Anticoagulants

Class Summary

Anticoagulants prevent recurrent embolism and the extension of the thrombosis.

Warfarin (Coumadin, Jantoven)

Warfarin interferes with the hepatic synthesis of vitamin K-dependent coagulation factors. It is used for the prophylaxis and treatment of venous thrombosis, pulmonary embolism, and thromboembolic disorders. Tailor the dose to maintain an INR in the range of 2-3. Patients with prosthetic cardiac valves may require higher INR levels.

Dabigatran (Pradaxa)

Competitive, direct thrombin inhibitor. Thrombin enables fibrinogen conversion to fibrin during the coagulation cascade, thereby preventing thrombus development. Inhibits both free and clot-bound thrombin and thrombin-induced platelet aggregation. Indicated for prevention of stroke and thromboembolism associated with nonvalvular atrial fibrillation.

Rivaroxaban (Xarelto)

Factor Xa inhibitor indicated to reduce risk of stroke and systemic embolism with nonvalvular atrial fibrillation. Dose is adjusted according to estimated creatinine clearance.

Apixaban (Eliquis)

Inhibits platelet activation and fibrin clot formation via direct, selective, and reversible inhibition of free and clot-bound factor Xa. Factor Xa, as part of the prothrombinase complex, catalyzes the conversion of prothrombin to thrombin. Thrombin both activates platelets and catalyzes the conversion of fibrinogen to fibrin.

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HMG-CoA Reductase Inhibitors

Class Summary

In patients with elevated cholesterol, sustained reduction in cholesterol levels may also reduce the chances of stroke. These agents lower LDL-C levels by reducing the production of mevalonic acid from HMG-CoA and by stimulating LDL catabolism. They also lower triglyceride levels and raise serum HDL-C levels, and they have a low incidence of adverse effects, the most common being hepatotoxicity and myopathy.

Lovastatin (Altoprev, Mevacor)

Competitively inhibits HMG-CoA, which catalyzes rate-limiting step in cholesterol synthesis. Adjunct to dietary therapy in reducing serum cholesterol. Before initiating therapy, place patients on cholesterol-lowering diet for 3-6 mo, and continue diet indefinitely.

Simvastatin (Zocor)

Competitively inhibits HMG-CoA, which catalyzes rate-limiting step in cholesterol synthesis. In addition, agents in this class possess pleitropic properties including improved endothelial function and reduced inflammation at the site of the coronary plaque. Before initiating therapy, place patients on cholesterol-lowering diet for 3-6 mo, and continue diet indefinitely.

Pravastatin (Pravachol)

Competitively inhibits HMG-CoA, which catalyzes rate-limiting step in cholesterol synthesis. Agents in this class also inhibit platelet aggregation and have anticoagulant effects. Before initiating therapy, place patients on cholesterol-lowering diet for 3-6 mo, and continue diet indefinitely.

Atorvastatin (Lipitor)

Competitively inhibits HMG-CoA, which catalyzes rate-limiting step in cholesterol synthesis. Agents in this class also decrease levels of high-sensitivity C-reactive protein, which is a protein associated with inflammatory responses. Before initiating therapy, place patients on cholesterol-lowering diet for 3-6 mo, and continue diet indefinitely.

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