ESC Guidance for ACS Flashcards
What high-risk features would suggest against a delayed invasive strategy in NSTEMI?
- Hemodynamic instability
- Severe heart failure
- Ventricular arrhythmias
- Ongoing ischaemic pain
What risk factors, if present in a NSTEMI diagnosis, would prompt an early invasive strategy?
- Hemodynamic instability
- Severe left ventricular dysfunction
- High-risk score (e.g., GRACE)
- Recurrent or persistent angina despite medical therapy
- Significant ST-segment depression
What does the GRACE score predict in patients with NSTEMI/UA?
Risk of adverse cardiovascular events
Name cardiovascular risk factors that are optimised in secondary prevention
- Hypertension
- Diabetes
- Hyperlipidaemia
What is the purpose of optimising cardiovascular risk factors in secondary prevention?
To reduce complications
What are the components of secondary prevention after ACS?
Lifestyle modifications
Pharmacotherapy
What is the primary focus of secondary prevention after ACS?
Reduce complications and risk factors
What is the default DAPT duration for ACS patients? When might shorter DAPT durations be considered?
12 hours
In high bleeding risk patients
What therapy typically follows DAPT after 12 months?
Lifelong aspirin monotherapy
Which P2Y12 inhibitors might be considered for patients with high bleeding risk (HBR)?
Ticagrelor or clopidogrel
Why is aspirin + prasugrel the preferred DAPT for patients undergoing or following PCI?
Greater potency, faster onset, reduced thrombosis
What is the preferred DAPT for patients undergoing or following PCI?
Aspirin + prasugrel
Is pre-treatment with P2Y12 inhibitors recommended in ACS?
No, evidence does not support early efficacy
Why is unfractionated heparin (UFH) typically first-line for ACS?
Rapid onset, reversibility, proven efficacy
Which antithrombotic agent is typically first-line for ACS?
Unfractionated heparin (UFH)
According to the ESC guide, what is ACS caused by?
Acute myocardial ischaemia
What is the underlying issue in acute myocardial ischemia?
Reduced blood flow in the coronary arteries
What conditions are included within the spectrum of ACS?
- Unstable angina (UA)
- Non-ST-elevation myocardial infarction (NSTEMI)
- ST-elevation myocardial infarction (STEMI)
In the context of ACS, what does a “stable patient” refer to?
Patients without cardiogenic shock
What is the consequence of cardiogenic shock?
Reduced perfusion to bodily tissues
What are some complications associated with ACS?
Heart failure (HF)
Severe arrhythmias
What are the key components of the diagnostic process for ACS conditions?
Clinical presentation
ECG
Biomarkers
Risk stratification
What ECG finding is characteristic of STEMI? What ECG findings are associated with NSTEMI/UA?
ST-segment elevation
ST depression, T-wave changes
What does a rise and fall in troponin levels indicate?
Myocardial necrosis
According to ACS pathways, what characterizes STEMI?
- ST elevation
- Total occlusion
- Requires immediate reperfusion (PCI or fibrinolysis)
What ECG findings might be observed in NSTEMI patients? In NSTEMI, what accompanies the ECG findings?
Transient ST elevation, ST depression, T-wave abnormalities
Rise and fall in troponin
How is unstable angina diagnosed in relation to troponin levels?
Troponin levels remain below the 99th percentile
Why does STEMI require immediate reperfusion?
Medical emergency
What is the preferred reperfusion strategy for STEMI if performed promptly?
Primary PCI
How soon should primary PCI be performed from first medical contact for STEMI? If PCI is unavailable, how soon should fibrinolysis be administered after hospital arrival for STEMI?
Within 120 minutes
Within 10 minutes
After fibrinolysis, how is ECG monitored to assess effectiveness in STEMI?
60-90 minutes after IV bolus
What reduction in ST-segment elevation after fibrinolysis indicates the need for PCI?
<50%
Why is time delay critical in STEMI management?
It contributes to mortality and poor outcomes
How does NSTEMI management differ from STEMI management regarding time restrictions?
NSTEMI has less time restrictions
What characterises NSTEMI with a very high risk of complications?
Immediate invasive strategy
How soon is routine invasive angiography performed in an early invasive strategy for NSTEMI?
Within 24 hours
How soon is invasive angiography typically performed in a delayed invasive strategy?
Within 48 hours
For which patients is a delayed invasive strategy typically used?
Low-risk patients without high-risk features
What is the initial event in acute coronary syndromes (ACS)?
Plaque rupture or plaque erosion
What happens during plaque rupture or erosion?
Underlying thrombogenic material is exposed
How do activated platelets bind to each other? What is formed when activated platelets bind to each other?
Via glycoprotein IIb/IIIa receptors
A platelet-rich clot
What is the role of fibrin in clot formation?
Stabilises the clot
What type of therapy should all patients with ACS be started on upon hospital admission?
Antithrombotic therapy
Why is unfractionated heparin (UFH) typically first-line for ACS?
Rapid onset, reversibility, proven efficacy
Which factor mediates the linking of platelets to collagen?
Von Willebrand Factor
Which molecules exposed at the site of vessel injury recruit platelets? What change in platelet shape indicates its activation?
Collagen and von Willebrand Factor
Change into dendritic form
What prothrombotic molecule is released by activated platelets?
Adenosine diphosphate (ADP)
What does ADP induce by binding to its receptors?
Aggregation and recruitment of more platelets
What is another mediator of platelet activation and aggregation?
Thromboxane
What effect does thromboxane have on platelets?
They crosslink with each other
What causes platelet activation to snowball?
Interlocking mechanisms
What does thrombin stimulate in relation to platelets? What does thrombin induce the formation of?
Platelet activation
Fibrin
What kind of process is platelet activation in clot formation? Why is platelet activation an obvious therapeutic target?
Self-reinforcing
It is crucial in blood clot formation
What do activated platelets release to promote clot formation?
Prothrombotic molecules
How does thrombin further stimulate platelet activation? What happens to the clot as platelet activation snowballs?
Through a continuous feedback loop
Clot grows rapidly
