Acute coronary syndromes - therapy Flashcards
Name examples of acute coroary syndromes
- sudden cardiac death
- STEMI
- Non- STEMI
- unstable angina
Causes of ACS
- atherslerotic rupture > platelet aggregation ? thrombus > vasospasm and vasoconstriction > transient total occlusion of vessel
Goal of pharmacoptherapy of ACS
- increase myocardial O2 supply through coronary dilation
- decrease myocardial oxygen demand ( decrease in HR, BP, preload/myocardial contractility)
What condition predisposes a patient to coronary thrombus?
Patients with STEMI have a liklihood of a coronary thrombus occluding the infarct artery
ACS with STEMI treatment + explain how they work
ACS with STEMI ; thrombolysis
- serine proteases that work by converting plasminogen into plasmin.
- This breaks down the fibrinogen and fibrin contained in the clot
Fibrolytic categories
- Fibrin specific agents
- Non fibrin specific agents
Name fibrin-specific agents + their function
- altepase
- reteplase
- tenecteplase
All catalyses conversion of plasminogen > plasmin in abscence of fibrin
Name non-fibrin specific agents
-streptokinase
Catalyses systemic fibrinolysis
Contraindictions to fibrinolysis
- prior intracranial hemorrhage
- known structural cerebral vascular lesion
- known malignant intracranial neoplasm
- ischaemic stroke within 3 months
- suspected aortic dissection
- active bleeding/bleeding diathesis (excluding menses)
- signifficant closed head trauma/facial trauma within 3 months
Thrombolysis + aspirin
geater reduction in mortality/increased survival rate
Treatment for no evidence of a STEMI
- aspirin
- tigagrelor/clopidogrel
- fondaparinux/LMW heparin
- IV nitrate
- analgesia
- beta blockers
Others
- prasugrel
- Bllibllla receptor blockers
- statins
Treatment to reduce risk from NSTEMI
- PCI or CABG
- Aspirin
- Clopidogrel, prasugrel, ticagrelor, ticlopidine or cilostazol
- Heparin (LMWH)
- Fondaparinux
- GIIb/IIIa receptor blockers
- Statins
- B blockers
Name Antiplatelet agents
-low dose aspirin ( 75-150mg)
How does aspirin work in preventing platelet aggregation
- asprin inhibits platelet aggregation by inhibiting thromboxane A2 production
- thromboxane stimulates platelet aggregation + vasoconstriction.
- formation of PA leads to angina, unstable angina + acute MI
The effect of using aspirin in the treatment of acute MI, unstable+ secondary prevetation
Unstable angina
-reduces MI and death by 50%
Acute MI
-in combination with thrombolysis reduces mortality by 42% and reinfarction by 52%
Doses of aspirin and its effect
- no difference between higher and lower dose
What is clopidogrel? What does it do
- a prodrug that inhibits P2Y12 ADP receptor which is involved in PA and crosslinking by fibrin
- always used in combination with aspirin ( risk reduction)
Effect of blocking ADP receptor
-blocking of receptor inhibits platelet aggregation by blocking activation of GP IIa/IIa pathway
What is llb/llla complex?
- a receptor for fibrinogen, fibronectin and von WF
- Activation of this receptor complex is the ‘ final pathway ‘ for platelet aggregation and crosslinking of platelets by fibrin
Side effects of clopidogrel
GI bleeding
-prevented when using PPI
Explain why clopidogrel resistance occurs
-activated by CYP2C19 and 14% of the population have low levels and demonstrates resistance to clopidogrel
Name ADP receptor inhibitors
-clopidogrel, prasugrel
members of thienopyridine class
What is the difference between prasugrel and clopidogrel?
- prasugerel inhibits ADP-induced aggregation more rapidly
What is low molecular weight heparin?
-also a component of ACS protocol
