MOA: reduces stress

this decreases SNS activity and decreases ischemia

MOA: enhances cardiac blood flow via coronary vasodilation

decreases ventricular preload (increase venous capacitance)

MOA: binds to fibrin and converts plasminogen to plasmin

(fibrinolytic)

MOA: binds to plasminogen, conformational change, exposure of active site on plasminogen which cleaves other free plasminogen to form plasmin

produced by beta hemolytic streptococci and has no intrinsice enzymatic activity

antibodies can develop

Recombinant depletion mutant form on t-PA lacking difference domains

longer t1/2

less expensive

less fibrin specific

mutant of t-PA with specific amino acid substitutions that decreases plasma clearance

increases fibrin specificity

reduces sensitivity to PAI-1

longer t1/2

complet of protein bound streptokinase

Thombolytic activity due to release of streptokinase

MOA: binds to antithombin to increase activity (catalyst)

Dosing: IV bolus 5000 U followed by CI 30,000-35,000 U/d

Contraindicated: surgery w/in 10 d, active bleed, serious GI bleed, previous stroke

ADR- hemorrhage, thrombocytopenia, osteoporosis

Dose: 5000 U SC q8-12hr

No monitoring required

Heparin antidoe

binds heparin sulfate groups inhibiting heparin/antithrombin complex

IV- rapid onset (5 min)

Fractionated heparin/low molecular weight

MOA: increased inhibition of Xa

decreased inhibition of thrombin

Easier to administer, predictable response, no monitoring, longer t1/2, QD-BID dosing, lower incidence of thrombocytopenia, lower osteoporosis

Factor Xa selective inhibitor

MOA: binds antithrombin to inhibit Xa

doesn't inhibit thrombin

increased efficacy relative to LMWH- shows reduced major bleeding and improved long term mortality in ACS

No antidote

Hirudin analogs

Argatroban (Acova)

Bivalirudin (Angiomax)

Desirudin (Ipravask)

Lepirudin (Refludan)

MOA: direct inhibitor of thrombin

independent of antithrombin III

effectively inhibit thrombin bound to fibrin (in the thrombus)

MOA: direct thrombin inhibitor

Oral aanticoagulant

prodrug- ester hydrolyzed

peak plasma concentrations within 2 hours

QD- 150-220 mg

Approve in the reduction in the risk of stroke and systemic embolism non-valvular a.fib

Breaks down in moisture- keep in packaging

MOA: inhibits the synthesis of vit K dependent coagulation factors (prothrombin, VII, IX, X)

interferes with cyclic inter-conversion of vit K epoxide to the active form of vitamin K

Dose- 5-10mg/d then adjust for INR 2.0-3.0

4 days of therapy required before a clinical response occurs

MOA: irreversible inhibitor of COX-1 (at low doses)

Onset: 5 min

Duration: days

MOA: antiplatelet by inhibiting the ADP dependent pathway of paltelet activation

Irreversible antagonists of platelet ADP receptor

Delayed onset- 10 days

ADR: neutropenia and thrombocytopenia

MOA: binds irreversibly to the ADP P2Y12 receptor to inhibit:

Platelet signaling events

Platelet granule release

GP IIb/IIIa receptor activation

Platelet aggregation

MOA: irreversible antagonist of platelet ADP receptors

Metabolism- a single step

MI decreased but bleeding increased

Reversible antagonist of ADP receptor

NO metabolic activation

No inter-patient variability in efficacy

Rapid onset- 2 hours (rather than days)

Investigational

reversible P2Y12 receptor antagonist

IV- onset in minutes

Effects stopped quickly by stopping infusion

optimal for PCI

reversible, RGD mimetic peptide

GP IIb/IIIa receptor antagonist

inhibits platelet aggregation

reversible, non-peptide RGD-mimetic

GP IIb/IIIa inhibitor

prevents platelet aggregation

peptides with specific sequence of fibrinogen to bind to receptor but doesn't illicit response

Antiplatelet agent

Phosphodiesterase inhibitor

Aspirin 25mg and ER dipyridamole 200mg

Phosphodiesterase inhibitor

Diphyridamole alone: not effective antiplatelet drug

coronary vasodilation

myocardial perfusion studies

Antiplatelet agent

Phosphodiesterase inhibitor

vasodilator

intermittent claudication

thrombolytic agent

Investigational

greater selectivity for fibrin bound plasminogen

Investigational

degrades fibrinogen in the circulation

decreases blood viscosity

anti-fibrinolytic that blocks the activation of plasminogen by inhibiting plasminogen activators

reduces degradation of fibrin by plasmin

CCB that works better in the brain to relax smooth muscle

favorable effect on the severity of neurological deficits caused by cerebral vasospasm following subarachnoid hemorrhage

MOA: inhibits the Na/K ATPase pump

reversibly binds to a subunit of the Na/K ATPase on the extracellular surface of cardiac cells

increases availability of intracellular calcium`