1st Line Treatment of Prinzmetal's Angina

DHP- Amlodipine, Nifedipine (Short Acting), Felodipine

SE - Flushing, dizziness, peripheral edema, headache, reflex tachycardia

NON-DHP- Diltiazem, Verapamil

SE - Decreased HR, AV Block, Heart Failure, Constipation

NON-DHP Contraindicated in Sick Sinus Syndrome, Bradycardia, Uncompensated Heart Failure

Treatment of Chronic Angina

MOA: Inhibits late sodium current which reduces calcium overload preserving cardiac cellular function.

Minimal Effect on HR, BP, coronary blood flow

Contraindicated in prolonged QT interval

Anticoagulant- ACS, DVT, PE

MOA: INDIRECT, binds to and promotes the effect of Antithrombin III (inactivation of clotting factors IXa, Xa, XIa, and XIIa)

Monitored by aPTT(Activated Partial Thromboplastin Time)

Reversed by antidote Protamine Sulfate

SE - Heparin Induced Thrombocytopenia (HIT)

Anticoagulant - Low Molecular Weight Heparin

ACS, DVT, PE

MOA: Dependent on ATIII, more anti-factor Xa than IIa.

Advantages over Heparin - Greater bioavailability, longer DOA, more predictable, no lab monitoring, less toxicity.

Anticoagulant - Low Molecular Weight Heparin

ACS, DVT, PE

MOA: Dependent on ATIII, more anti-factor Xa than IIa.

Advantages over Heparin - Greater bioavailability, longer DOA, more predictable, no lab monitoring, less toxicity.

Anticoagulant - Factor X Inhibitor

DVT and ACS

MOA: Indirect factor X, pentasaccharide that binds to ATIII

SE - Bleeding

Route - Injectable

Anticoagulant - Factor X Inhibitor

DVT, PE, Postoperative thromboprophylaxis, CVA Prevention in nonvalvular a-fib

MOA: Direct factor X inhibitor

Rapid onset of action

Route: Oral

Anticoagulant - Factor X Inhibitor

DVT, PE, Postoperative thromboprophylaxis, CVA Prevention in nonvalvular a-fib

MOA: Direct factor X inhibitor

Rapid onset of action

Route: Oral

Anticoagulant - Factor X Inhibitor

DVT, PE, Postoperative thromboprophylaxis, CVA Prevention in nonvalvular a-fib

MOA: Direct factor X inhibitor

Rapid onset of action

Route: Oral

Anticoagulant - Direct Thrombin Inhibitor

HIT/PCI (Percutaneous coronary Intervention)

MOA: Inhibit thrombin by directly binding to the active site of thrombin, without depending on ATIII

Route: Parenteral

Anticoagulant - Direct Thrombin Inhibitor

HIT/PCI (Percutaneous coronary Intervention)

MOA: Inhibit thrombin by directly binding to the active site of thrombin, without depending on ATIII

Route: Parenteral

Anticoagulant - Direct Thrombin Inhibitor

HIT/PCI (Percutaneous coronary Intervention)

MOA: Inhibit thrombin by directly binding to the active site of thrombin, without depending on ATIII

Route: Parenteral

Anticoagulant - Direct Thrombin Inhibitor

DVT, PE, Stoke prevention in non-valvular AF, post-op thromboprophylaxis

Route: Oral

Anticoagulant

DVT, PE, AF

MOA: Inhibits the synthesis of vitamin k dependent clotting factos II, VII, IX, and X by inhibiting Vitamin K Epoxide Reductase

Delayed onset (3-5 days), Narrow therapeutic index.

Must monitor INR (International normalized Ratio) - should be between 2.5-3.5

Antiplatelet

ACS, PCI, Other Thrombotic Events

MOA - Inhibit COX, decrease TXA2 levels

Antiplatelet - ADP (P2Y12) Receptor Inhibitor

ASC, PCI

Thienopyridine, Irreversible binding to ADP receptor.

Antiplatelet - ADP (P2Y12) Receptor Inhibitor

ASC, PCI, Other thrombotic events (CVA)

Thienopyridine, Irreversible binding to ADP receptor.

Antiplatelet - ADP (P2Y12) Receptor Inhibitor

ASC, PCI

Thienopyridine, Irreversible binding to ADP receptor.

Antiplatelet - ADP (P2Y12) Receptor Inhibitor

ASC, PCI

Non- Thienopyridine, Reversible binding to ADP receptor.

Antiplatelet - ADP (P2Y12) Receptor Inhibitor

ASC, PCI

Non- Thienopyridine, Reversible binding to ADP receptor.

Antiplatelet - GP IIb/IIIa Inhibitor

ACS, PCI

Most effective of all Antiplatelet therapies.

MOA: Bind to GP IIb/IIIa and inhibit the binding of fibrinogen to platelet GP IIb/IIIa receptor

Route: Parenteral

Antiplatelet - GP IIb/IIIa Inhibitor

ACS, PCI

Most effective of all Antiplatelet therapies.

MOA: Bind to GP IIb/IIIa and inhibit the binding of fibrinogen to platelet GP IIb/IIIa receptor

Route: Parenteral

Antiplatelet - GP IIb/IIIa Inhibitor

ACS, PCI

Most effective of all Antiplatelet therapies.

MOA: Bind to GP IIb/IIIa and inhibit the binding of fibrinogen to platelet GP IIb/IIIa receptor

Route: Parenteral

Antiplatelet - Thrombin Receptor Inhibitor

Reduction of Thrombotic cardiovascular events in patients with a history of myocardial infarction or PAD.

MOA: Antagonist of PAR-1 (Protease activated recptor type 1) Inhibits thrombin induced platelet aggregation

Thrombolytic Drug

Acute MI, Massive PE, acute Ischemic Stroke

Human recombinant tPA (r-tPA)

Specific to fibrin bound plasminogen

Short Half-life

Thrombolytic Agent

Acute MI

Recombinant mutant variants of tPA

SPECIIC FOR FIBRIN BOUND PLASMINOGEN???

Thrombolytic Agent

Acute MI

Recombinant mutant variants of tPA

SPECIIC FOR FIBRIN BOUND PLASMINOGEN???

Thrombolytic

MOA: Forms a complex with plasminogen that converts plasminogen to plasmin

Lacks fibrin specificity

Antigenic

Thombolytic

Human Enzyme formed by kidneys

Catalyzes conversion of plasminogen to plasmin

Lacks fibrin specificity

Non-Antigenic