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THERAPY IN
CORONARY
ARTERY
DISEASE.
As per ESC 2017 guidelines.
By Dr SUMEDH RAMTEKE
Ticagrelor
Cilastazole
Clopidogrel,
Prasugrel , Ticagrelor
Aspirin
ECOSPRIN
Irreversible inhibitor of COX ( needeed for production of PG and
ThXA2).
Bioavailability- 80-100%.
Protein binding- 80-90%.
Metabolism – Liver (CYPC2C19, CYP3A).
Elimination half life-2-3 hr for low dose, 15-30 hr for large dose.
Excretion- urine (80-100%), sweat, saliva, faeces.
When to stop before surgery-7 days.
C/I- allergic to NSAIDs, NSAID induced bronchospasm, peptic ulcer.
Aspirin is known to cause hemolytic anaemia in G6PD Def patients.
Avoid in hyperuricemia/gout.
Associated with Rey’s Syndrome in children.
Major Trials: ISIS-2, CURRENT OASIS-7
CLOPIDOGREL
Thienopyridine group, Irreversible P2Y12 ADP
receptor antagonist
Bioavailability- >50%
Protein Binding- 94-98%
Metabolism- Liver
Onset of action- 2 hrs
Elimination Half life-7-8 hrs
Duration of action – 5 days
Excretion – 50% kidney, 46% biliary
When to stop before surgery- 5 days.
Major Trials: CURE, COMMIT, CLARITY TIMI28, PCI-CURE,
CREDO, PCI-CLARITY, CURRENT OASIS-7, GRAVITAS,
PRASUGREL
Thienopyridine group, Irreversible P2Y12 ADP receptor antagonist
Bioavailability- >79%
Protein binding -98%
Half life – 7 Hr
Peak plasma time - 30 min.
Absorption >79%
Metabolism via CYP3A4 and CYP2B6
Excretion –urine 68%, faeces 27%
When to stop before surgery- 7 days
C/I- active bleeding, H/o TIA, Stroke, Age > 75, weight <60 kg,TTP.
Major Trials: TRITON TIMI 38, TRIOLOGY-ACS, ACCOAST
TICAGRELOR
Chemical class- cyclopentyl-triazolo-pyrimidine(CPTP)
Reversible P2Y12 ADP receptor antagonist
Bioavailability-36%
Protein binding - >99%
peak plasma time- 1.5 hr, 2.5 hr (AM)
metabolized by CYP3A4
Half life- 7 hr, 9 hr(AM)
excretion- 58%faeces, 26% urine
When to stop before surgery- 3 days.
C/I- major bleeding, COPD/Asthma, Bradyarrhythmia, sick sinus
syndrome,severe hepatic impairment.
Major Trials: PLATO, ATLANTIC, PEGASUS – TIMI54.
CILASTOZOLE
Class- Phosphodiaesterase 3 inhibitor
Mechanism- inhibit platelet aggregation induced by collagen, 5’
ADP, epinephrine and Arachidonic acid.
Protein binding- 95-98%.
Metabolism- Liver ( CYP3A4, CYP249).
Elimination time half – 11-13 hr.
Excretion – kidney.
SAFARI-STEMI- In STEMI + primary PCI, radial
access was not superior to femoral access.
DUAL ANTIPLATELET THERAPY IN CORONARY ARTERY DISEASE.
DUAL ANTIPLATELET THERAPY IN CORONARY ARTERY DISEASE.
DUAL ANTIPLATELET THERAPY IN CORONARY ARTERY DISEASE.
DUAL ANTIPLATELET THERAPY IN CORONARY ARTERY DISEASE.
DUAL ANTIPLATELET THERAPY IN CORONARY ARTERY DISEASE.
DUAL ANTIPLATELET THERAPY IN CORONARY ARTERY DISEASE.
DUAL ANTIPLATELET THERAPY IN CORONARY ARTERY DISEASE.
DUAL ANTIPLATELET THERAPY IN CORONARY ARTERY DISEASE.
DUAL ANTIPLATELET THERAPY IN CORONARY ARTERY DISEASE.
DUAL ANTIPLATELET THERAPY IN CORONARY ARTERY DISEASE.
DUAL ANTIPLATELET THERAPY IN CORONARY ARTERY DISEASE.
DUAL ANTIPLATELET THERAPY IN CORONARY ARTERY DISEASE.
DUAL ANTIPLATELET THERAPY IN CORONARY ARTERY DISEASE.
DUAL ANTIPLATELET THERAPY IN CORONARY ARTERY DISEASE.
DUAL ANTIPLATELET THERAPY IN CORONARY ARTERY DISEASE.
DUAL ANTIPLATELET THERAPY IN CORONARY ARTERY DISEASE.
DUAL ANTIPLATELET THERAPY IN CORONARY ARTERY DISEASE.
DUAL ANTIPLATELET THERAPY IN CORONARY ARTERY DISEASE.
DUAL ANTIPLATELET THERAPY IN CORONARY ARTERY DISEASE.
DUAL ANTIPLATELET THERAPY IN CORONARY ARTERY DISEASE.
DUAL ANTIPLATELET THERAPY IN CORONARY ARTERY DISEASE.
DUAL ANTIPLATELET THERAPY IN CORONARY ARTERY DISEASE.
DUAL ANTIPLATELET THERAPY IN CORONARY ARTERY DISEASE.
DUAL ANTIPLATELET THERAPY IN CORONARY ARTERY DISEASE.
DUAL ANTIPLATELET THERAPY IN CORONARY ARTERY DISEASE.
DUAL ANTIPLATELET THERAPY IN CORONARY ARTERY DISEASE.
DUAL ANTIPLATELET THERAPY IN CORONARY ARTERY DISEASE.
DUAL ANTIPLATELET THERAPY IN CORONARY ARTERY DISEASE.
DUAL ANTIPLATELET THERAPY IN CORONARY ARTERY DISEASE.
DUAL ANTIPLATELET THERAPY IN CORONARY ARTERY DISEASE.
DUAL ANTIPLATELET THERAPY IN CORONARY ARTERY DISEASE.
DUAL ANTIPLATELET THERAPY IN CORONARY ARTERY DISEASE.
DUAL ANTIPLATELET THERAPY IN CORONARY ARTERY DISEASE.
DUAL ANTIPLATELET THERAPY IN CORONARY ARTERY DISEASE.
DUAL ANTIPLATELET THERAPY IN CORONARY ARTERY DISEASE.
DUAL ANTIPLATELET THERAPY IN CORONARY ARTERY DISEASE.

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DUAL ANTIPLATELET THERAPY IN CORONARY ARTERY DISEASE.

  • 1. THERAPY IN CORONARY ARTERY DISEASE. As per ESC 2017 guidelines. By Dr SUMEDH RAMTEKE
  • 4. ECOSPRIN Irreversible inhibitor of COX ( needeed for production of PG and ThXA2). Bioavailability- 80-100%. Protein binding- 80-90%. Metabolism – Liver (CYPC2C19, CYP3A). Elimination half life-2-3 hr for low dose, 15-30 hr for large dose. Excretion- urine (80-100%), sweat, saliva, faeces. When to stop before surgery-7 days. C/I- allergic to NSAIDs, NSAID induced bronchospasm, peptic ulcer. Aspirin is known to cause hemolytic anaemia in G6PD Def patients. Avoid in hyperuricemia/gout. Associated with Rey’s Syndrome in children. Major Trials: ISIS-2, CURRENT OASIS-7
  • 5. CLOPIDOGREL Thienopyridine group, Irreversible P2Y12 ADP receptor antagonist Bioavailability- >50% Protein Binding- 94-98% Metabolism- Liver Onset of action- 2 hrs Elimination Half life-7-8 hrs Duration of action – 5 days Excretion – 50% kidney, 46% biliary When to stop before surgery- 5 days. Major Trials: CURE, COMMIT, CLARITY TIMI28, PCI-CURE, CREDO, PCI-CLARITY, CURRENT OASIS-7, GRAVITAS,
  • 6. PRASUGREL Thienopyridine group, Irreversible P2Y12 ADP receptor antagonist Bioavailability- >79% Protein binding -98% Half life – 7 Hr Peak plasma time - 30 min. Absorption >79% Metabolism via CYP3A4 and CYP2B6 Excretion –urine 68%, faeces 27% When to stop before surgery- 7 days C/I- active bleeding, H/o TIA, Stroke, Age > 75, weight <60 kg,TTP. Major Trials: TRITON TIMI 38, TRIOLOGY-ACS, ACCOAST
  • 7. TICAGRELOR Chemical class- cyclopentyl-triazolo-pyrimidine(CPTP) Reversible P2Y12 ADP receptor antagonist Bioavailability-36% Protein binding - >99% peak plasma time- 1.5 hr, 2.5 hr (AM) metabolized by CYP3A4 Half life- 7 hr, 9 hr(AM) excretion- 58%faeces, 26% urine When to stop before surgery- 3 days. C/I- major bleeding, COPD/Asthma, Bradyarrhythmia, sick sinus syndrome,severe hepatic impairment. Major Trials: PLATO, ATLANTIC, PEGASUS – TIMI54.
  • 8. CILASTOZOLE Class- Phosphodiaesterase 3 inhibitor Mechanism- inhibit platelet aggregation induced by collagen, 5’ ADP, epinephrine and Arachidonic acid. Protein binding- 95-98%. Metabolism- Liver ( CYP3A4, CYP249). Elimination time half – 11-13 hr. Excretion – kidney.
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  • 15. SAFARI-STEMI- In STEMI + primary PCI, radial access was not superior to femoral access.