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ESC Guidance for ACS Flashcards

1
Q

What high-risk features would suggest against a delayed invasive strategy in NSTEMI?

A
  • Hemodynamic instability
  • Severe heart failure
  • Ventricular arrhythmias
  • Ongoing ischaemic pain
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2
Q

What risk factors, if present in a NSTEMI diagnosis, would prompt an early invasive strategy?

A
  • Hemodynamic instability
  • Severe left ventricular dysfunction
  • High-risk score (e.g., GRACE)
  • Recurrent or persistent angina despite medical therapy
  • Significant ST-segment depression
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3
Q

What does the GRACE score predict in patients with NSTEMI/UA?

A

Risk of adverse cardiovascular events

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4
Q

Name cardiovascular risk factors that are optimised in secondary prevention

A
  • Hypertension
  • Diabetes
  • Hyperlipidaemia
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5
Q

What is the purpose of optimising cardiovascular risk factors in secondary prevention?

A

To reduce complications

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6
Q

What are the components of secondary prevention after ACS?

A

Lifestyle modifications
Pharmacotherapy

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7
Q

What is the primary focus of secondary prevention after ACS?

A

Reduce complications and risk factors

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8
Q

What is the default DAPT duration for ACS patients? When might shorter DAPT durations be considered?

A

12 hours
In high bleeding risk patients

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9
Q

What therapy typically follows DAPT after 12 months?

A

Lifelong aspirin monotherapy

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10
Q

Which P2Y12 inhibitors might be considered for patients with high bleeding risk (HBR)?

A

Ticagrelor or clopidogrel

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11
Q

Why is aspirin + prasugrel the preferred DAPT for patients undergoing or following PCI?

A

Greater potency, faster onset, reduced thrombosis

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12
Q

What is the preferred DAPT for patients undergoing or following PCI?

A

Aspirin + prasugrel

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13
Q

Is pre-treatment with P2Y12 inhibitors recommended in ACS?

A

No, evidence does not support early efficacy

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14
Q

Why is unfractionated heparin (UFH) typically first-line for ACS?

A

Rapid onset, reversibility, proven efficacy

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15
Q

Which antithrombotic agent is typically first-line for ACS?

A

Unfractionated heparin (UFH)

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16
Q

According to the ESC guide, what is ACS caused by?

A

Acute myocardial ischaemia

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17
Q

What is the underlying issue in acute myocardial ischemia?

A

Reduced blood flow in the coronary arteries

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18
Q

What conditions are included within the spectrum of ACS?

A
  • Unstable angina (UA)
  • Non-ST-elevation myocardial infarction (NSTEMI)
  • ST-elevation myocardial infarction (STEMI)
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19
Q

In the context of ACS, what does a “stable patient” refer to?

A

Patients without cardiogenic shock

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20
Q

What is the consequence of cardiogenic shock?

A

Reduced perfusion to bodily tissues

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21
Q

What are some complications associated with ACS?

A

Heart failure (HF)
Severe arrhythmias

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22
Q

What are the key components of the diagnostic process for ACS conditions?

A

Clinical presentation
ECG
Biomarkers
Risk stratification

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23
Q

What ECG finding is characteristic of STEMI? What ECG findings are associated with NSTEMI/UA?

A

ST-segment elevation
ST depression, T-wave changes

24
Q

What does a rise and fall in troponin levels indicate?

A

Myocardial necrosis

25
According to ACS pathways, what characterizes STEMI?
- ST elevation - Total occlusion - Requires immediate reperfusion (PCI or fibrinolysis)
26
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
27
How is unstable angina diagnosed in relation to troponin levels?
Troponin levels remain below the 99th percentile
28
Why does STEMI require immediate reperfusion?
Medical emergency
29
What is the preferred reperfusion strategy for STEMI if performed promptly?
Primary PCI
30
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
31
After fibrinolysis, how is ECG monitored to assess effectiveness in STEMI?
60-90 minutes after IV bolus
32
What reduction in ST-segment elevation after fibrinolysis indicates the need for PCI?
<50%
33
Why is time delay critical in STEMI management?
It contributes to mortality and poor outcomes
34
How does NSTEMI management differ from STEMI management regarding time restrictions?
NSTEMI has less time restrictions
35
What characterises NSTEMI with a very high risk of complications?
Immediate invasive strategy
36
How soon is routine invasive angiography performed in an early invasive strategy for NSTEMI?
Within 24 hours
37
How soon is invasive angiography typically performed in a delayed invasive strategy?
Within 48 hours
38
For which patients is a delayed invasive strategy typically used?
Low-risk patients without high-risk features
39
What is the initial event in acute coronary syndromes (ACS)?
Plaque rupture or plaque erosion
40
What happens during plaque rupture or erosion?
Underlying thrombogenic material is exposed
41
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
42
What is the role of fibrin in clot formation?
Stabilises the clot
43
What type of therapy should all patients with ACS be started on upon hospital admission?
Antithrombotic therapy
44
Why is unfractionated heparin (UFH) typically first-line for ACS?
Rapid onset, reversibility, proven efficacy
45
Which factor mediates the linking of platelets to collagen?
Von Willebrand Factor
46
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
47
What prothrombotic molecule is released by activated platelets?
Adenosine diphosphate (ADP)
48
What does ADP induce by binding to its receptors?
Aggregation and recruitment of more platelets
49
What is another mediator of platelet activation and aggregation?
Thromboxane
50
What effect does thromboxane have on platelets?
They crosslink with each other
51
What causes platelet activation to snowball?
Interlocking mechanisms
52
What does thrombin stimulate in relation to platelets? What does thrombin induce the formation of?
Platelet activation Fibrin
53
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
54
What do activated platelets release to promote clot formation?
Prothrombotic molecules
55
How does thrombin further stimulate platelet activation? What happens to the clot as platelet activation snowballs?
Through a continuous feedback loop Clot grows rapidly

Pharmacy 302 (31 decks)

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