Acute coronary syndromes Flashcards

1
Q

describe the term acute coronary syndromes

A

This term covers a spectrum of acute cardiac conditions from unstable angina to varying degrees of evolving myocardial infarction (MI)

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2
Q

how is unstable angina diagnosed?

A

history
ECG
troponin (no significant rise in
unstable angina)

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3
Q

how is unstable angina clinically classified:

A

*Cardiac chest pain at rest
*Cardiac chest pain with crescendo pattern
*New onset angina

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4
Q

how can acute myocardial infarction be diagnosed- ST elevation?

A

ST-elevation MI can usually be diagnosed on ECG at presentation

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5
Q

how can acute myocardial infarction be diagnosed- non ST elevation?

A

*Non-ST-elevation MI is a retrospective diagnosis made after troponin results and sometimes other investigation results are available

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6
Q

how can myocardial infarction be defined?

A

retrospectively as non-Q wave or Q-wave MI on the basis of whether new pathological Q waves develop on the ECG as a result of it

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7
Q

what are ST MIs and LBBB MIs associated with?

A

with larger infarcts unless effectively treated (and therefore more likely to lead to pathological Q wave formation, heart failure or death)

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8
Q

symptoms presenting for myocardial infarction

A

*Cardiac chest pain
* unremitting
*usually severe but may be mild or absent
*occurs at rest
*associated with sweating, breathlessness, nausea and/or vomiting
*one third occur in bed at night

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9
Q

what does myocardial infarction usually cause?

A

-permanent heart muscle damage although this may not be detectable in small MIs
- early mortality
- late mortality

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10
Q

what is a higher risk of myocardial infarction associated with?

A

higher age,
diabetes,
renal failure,
left ventricular systolic dysfunction (elevated NT- proBNP level)
and other risk factors

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11
Q

which patients have the highest mortality risk?

A

Patients presenting with cardiogenic shock or requiring ventilation following out-of-hospital cardiac arrest have the highest mortality risk

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12
Q

how are myocardial infarctions initially managed?

A

*Get in to hospital quickly – 999 call
*Paramedics – if ST elevation, contact primary PCI centre for transfer for emergency coronary angiography
*Take aspirin 300mg immediately
*Pain relief

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13
Q

what hospital management is done for myocardial infarctions?

A

*Make diagnosis
*Oxygen therapy only if hypoxic *Pain relief – opiates/ nitrates *Aspirin +/- platelet P2Y12 inhibitor *Consider beta-blocker
*Consider other antianginal therapy
*Consider urgent coronary angiography e.g. if troponin elevated or unstable angina refractory to medical therapy

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14
Q

what are the causes of ACS?

A

*Rupture of an atherosclerotic plaque and consequent arterial thrombosis is the cause in the majority of cases
*Myocardial infarction due to atherothrombosis is known as ‘type 1’ myocardial infarction
*Other causes of myocardial infarction usually fall under the umbrella of ‘type 2’ myocardial infarction

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15
Q

what are the causes of type 2 MI

A
  • Myocardial oxygen demand/supply mismatch caused by sepsis, acute lung pathology, thyrotoxicosis, pulmonary embolism, anaemia, haemorrhage or other causes of hypotension/hypovolaemia – underlying stable coronary artery disease may or may not be a contributing factor
  • coronary vasospasm without plaque rupture
  • drug abuse (amphetamines, cocaine)
  • dissection of the coronary artery related to defects of the vessel connective tissue
  • thoracic aortic dissection
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16
Q

what is tako- tsubo cardiomyopathy?

A

Stress-induced cardiomyopathy that can masquerade as myocardial infarction.

17
Q

what causes tako- tsubo cardiomyopathy?

A

Often caused by acute stress such as extreme emotional distress in susceptible individuals

18
Q

what does tako- tsubo cardiomyopathy cause?

A

Causes transient left ventricular systolic dysfunction, typically ballooning of the left ventricular apex during systole that recovers over days or a few weeks with limited or no permanent damage

19
Q

what is troponin?

A

A protein complex consisting of troponin C, troponin I and troponin T that regulates actin:myosin contraction.

20
Q

what are Cardiac-specific isoforms of troponin T and troponin I?

A

are highly sensitive markers for cardiac muscle injury

21
Q

what is the Role of soluble platelet agonists in thrombus formation at site of vascular damage?

A

promote healing
prevent bleeding to death
platelets adhere and secrete agonists to activate other platelets and attract them such as ADP ( ADP is the target of the anti platelet plug)
forma plug in the breech- good when needed but bad when responding to atherosclerotic rupture

22
Q

fibronyltic system

A

e
n plasminogen
d I
o I
t I fibrin
h——->tPA—— I I
e Plasmin——–> I
l I
I Fibrin
u degradation products
m

23
Q

when is P2Y 12 Inhibitors used?

A

sed in combination with aspirin in
management of ACS = ‘dual antiplatelet therapy’

24
Q

what are the three oral drugs available of P2Y 12 inhibtors?

A

*Three oral drugs are available: clopidogrel, prasugrel and ticagrelor

PRASUGREL IS MOST EFFICIENT

25
Q

describe the effect of Clopidogrel and prasugrel

A

are thienopyridines that have an irreversible effect on platelets

26
Q

describe the effect of ticagrelor

A

Ticagrelor binds reversibly to P2Y12 receptors so has a more rapid offset of effect than thienopyridines

27
Q

what are the adverse effects common to all of P2Y12 inhibitors ?

A
  • Bleeding e.g. epistaxis, GI bleeds, haematuria * Rash
  • GI disturbance
28
Q

diosyncratic adverse effects of ticagrelor:

A
  • Dyspnoea: usually mild and well-tolerated, but occasionally not tolerated and requires switching to prasugrel or clopidogrel
  • Ventricular pauses: usually sinoatrial pauses, may resolve with continued treatment
29
Q

what are GPIIb/IIIa antagonists used with

A

*Used in combination with aspirin and oral P2Y12 inhibitors in management of patients undergoing PCI for ACS

30
Q

what increased risk do GPIIb/IIIa antagonists have?

A

*Increase risk of major bleeding

31
Q

what do anticoagulants target

A

Target formation and/or activity of thrombin

32
Q

what do anticoagulants inhibit?

A
  • Inhibit both fibrin formation and platelet activation
33
Q

doses of anticoagulants varying on procedure

A

Fondaparinux (a pentasaccharide) used in NSTE ACS prior to coronary angiography = safer than heparins as low level of anticoagulation used
* Full-dose anticoagulation used during PCI: options are heparins (usually unfractionated heparin; some centres use enoxaparin, a low-molecular-weight heparin) or the direct thrombin inhibitor bivalirudin (expensive, little used now)
* High dose heparin used during cardiopulmonary bypass for CABG surgery

34
Q

what is given for initial pain relief in ACS?

A

morphine + metoclopramide, nitrates

35
Q
A
  • Initial pain relief if necessary – morphine + metoclopramide, nitrates
  • Aspirin and P2Y12 inhibitor combination (assuming no contraindications
    and confirmed diagnosis)
  • Anticoagulant: fondaparinux or heparin
  • Consider intravenous glycoprotein IIb/IIIa antagonists for STEMI patient undergoing primary PCI
  • Anti-anginal therapy – beta blocker, nitrates, calcium antagonist
  • Secondary prevention – statins, ACEI, beta blocker, other antihypertensive
    therapy
  • Heart failure patients – diuretic, ACEI, beta blocker, aldosterone antagonist (spironolactone, epleronone)
  • Fibrinolytic therapy may be used for acute STEMI if primary PCI not available
36
Q

when is coronary angiography usually performed?

A

for patients with troponin elevation or unstable angina refractory to medical therapy

37
Q

what is the most frequent revascularisation procedure?

A

PCI

38
Q

Why may some patients have no obstructive coronary artery disease?

A
  • Actual diagnosis not ACS
  • Plaque rupture without significant stenosis and resolution of
    obstructive thrombus by the time of angiography
  • Stress-induced (Tako-Tsubo) cardiomyopathy without obstructive coronary artery disease
39
Q
A