Acute Coronary Syndrome Flashcards
Describe the spectrum ACS? (4 points )
- Unstable angina
- Non-ST elevation myocardial infarction
- ST-elevation myocardial infarction
- Sudden cardiac death
Common pathogenesis of ACS?
- Atherosclerotic plaque rupture or erosion
- Superimposed platelet aggregation and thrombosis
- Vasospasm, and vasoconstriction
What are the two goals of pharmacotherapy?
- Increase myocardial oxygen supply
- Decrease myocardial oxygen demand
How do you increase myocardial oxygen supply?
-Through coronary vasodilation
How do you decrease myocardial oxygen demand?
- Decrease in heart rate
- Decrease blood pressure
- Decrease preload or myocardial contracility
What do patients with STEMI have a high likelihood of?
A Coronary thrombus occulding the infarct artery
How does STEMI usually occur?
Coronary artery occlusion due to formation of thrombus overlying an atheromatous plaque
What thrombolytic agents are available today?
Serine proteases
How do thrombolytic agents work?
converting plasminogen to the natural fibrinolytic agent plasmin
What does plasmin act on?
fibrinogen
What are the two categories of thrombolytic agents?
- Fibrin-specific agents
2. Non-fibrin specific agents
name 3 fibrin specific agents?
- Alteplase
- Reteplase
- Tenecteplase
How to fibrin specific drugs work?
All catalyse conversion of plasminogen to plasmin in the absence of fibrin
Where are streptokinases taken from?
from mycobacterium (causes sensitation so only one dose available)
When would you not give thrombolytic drugs? (7)
- Prior intracranial hemorrhage
- Known structural cerebral vascular lesion
- Known malignant intracranial neoplasm
- Ischaemic stroke within 3 months
- Suspected aortic dissection
- Active bleeding/diathesis
- Significant closed-head trauma or facial trauma within 3 months
What do you do if there is no evidence of a STEMI ACS?
- Aspirin
- Tigagrelor/clopidogrel-antiplatlete
- Fondaparinux/LMW heparin
- IV nitrate
- Analgesia
- Beta Blockers
What is the dose given of aspirin?
low ( 75-100mg)
What is aspirin is apotent inhibitor of what?
Platelet thromboxane A2 production
what can the daily use of aspirin reduce the risk of?
ACute MI (mortality 23%) Unstable angina (death 50%) Secondary prevention (reduce reinfarction by 32% and combines vascular events by 25%)
What is clopidogrel?
a Pro-drug
How does clopidogrel work?
Inhibits ADP receptor activated platelet aggregation
What receptor does clopidogrel act on?
P2Y12 ADP
What is P2Y12 ADP responsible for?
Important in aggregation of platelets and cross linking by fibrin
What is Clopidogrel activated by?
CYP2C19
How much of the population have low levels of CYP2c19?
14%
What is the IIb/IIIa complex?
it is a receptor fibrinogen, fibronectin and von WF
What happens when IIb/IIIa complex is activated?
“final common pathway” for platelet aggregation and cross-linking of platelets by fibrin
What is clopidrogrel always used in combination?
aspirin
What is more effective than clopidogrel with aspirin?
Ticagrelor and aspirin
What is more rapid and consistent in than clopidogrel in inhibiting the ADP- platelet aggregation
Prasugrel
What are clopdiogrel and prasugrel members of?
Thienopyridine class of ADP receptor inhibitors
Name the four low molecular weight heparin?
- Enoxaparin
- Dalteparin
- Tinzeparin
- Fondaparinux
What is the most safe in terms of major bleeds of the low molecular weight heparin?
Fondaparinux
Why is fondaparinux a good choice?
- Single chemical entity
- Synthetic pentasaccaride
- Highly selective for antithrombin
- Once-daily administration
- No need for platelet monitoring
What are beta blockers used for?
- In treatment of cute MI
- For secondary prevention in the survivors of an acute MI
How do beta blockers work?
Competitvely inhibit the myocardial effects of circulating catecholamines and reduce myocardial oxygen comsumption by lowering heart rate, blood pressure and myocardial contractility.
How much does atenolol or metoprolol reduce mortality by?
10-15%
