Unstable angina

Question 1

What is ACS

Answer 1

encompasses unstable angina, non-ST elevation myocardial infarction (NSTEMI) and ST-elevation myocardial infarction (STEMI).

Question 2

What does ACS typically manifest as

Answer 2

sudden, new-onset angina, or an increase in the severity of an existing stable angina.

Question 3

What are the clinical classifications for unstable angina?

Answer 3

• Cardiac chest pain at rest
• Cardiac chest pain with crescendo pattern
• New onset angina – angina out of the blue – somethings happened to the coronary artery

Question 4

Epidemiology

Answer 4

• STEMI = 5/1000 per annum in UK
• M>F

Question 5

Non modifiable RFs for ACS

Answer 5

• Age (>65 years of age)
• Male
• Family history of premature coronary heart disease
• Premature menopause

Question 6

Modifiable RFs

Answer 6

• Smoking
• Diabetes mellitus
• Hyperlipidaemia
• Hypertension
• Obesity
• Sedentary lifestyle

Question 7

Pathophysiology: Atherosclerotic plaque formation

Answer 7

• Accumulation of LDLP cholesterol in inner layer of BV
• Leukocytes adhere to endothelium - gain entry to intima where they combine with lipids to become foam cells
• artery remodelling + calcification + foam cells causes atherosclerotic plaque to form
• plaque rupture causes platelet activation, thrombus formation and coronary artery occlusion
• results in ischaemia and infarction

Question 8

What is a dianosis of angina based on?

Answer 8

history
ECG
troponin (no significant rise in unstable angina)

Question 9

Occlusions

Answer 9

• Unstable angina + NSTEMI: Partial occlusion
• STEMI - occlusion is complete

Question 10

Signs

Answer 10

• Hypotension or hypertension
• Reduced 4th heart sound
• Signs of heart failure: e.g. increased JVP, oedema; **red flag symptom
• Systolic murmur: if mitral regurgitation or a ventricular septal defect develops

Question 11

Symptoms

Answer 11

• Chest pain
  
  • Central, ‘heavy’, crushing pain
  • Radiation to the left arm or neck
  • Symptoms should continue at rest for more than 20 minutes
• Shortness of breath
• Sweating and clamminess
• Nausea and vomiting
• Palpitations
• Anxiety

Question 12

Investigations

Answer 12

• ECG:perform within 10 minutes. Aim to perform serial ECGs every 10 minutes to detect dynamic changes.
• Troponin:for a STEMI and NSTEMI, troponin levels will begin to elevate 4-6 hours after injury and will remain elevated for roughly 10 days. In unstable angina, there isnoelevation in troponin.

Question 13

ECG findings

Answer 13

• Unstable angina: non-specific changes
• NSTEMI: ST-segment depression; T-wave inversion; pathological Q waves; a normal ECG may be seen
• STEMI: ST-segment elevation; T-wave inversion; new left-bundle branch block

Question 14

Other investigations

Answer 14

• Coronary angiogram:aim to carry out angiography within 90 minutes if required; diagnostic investigation of choice
• FBC
• UEs
• CXR
• Echocardiogram
• HbA1C

Question 15

Unstable angina + NSTEMI Immediate management

Answer 15

• Oxygen:only if SpO2is <94%, and aim for 94-98%
• Analgesia:morphine and sublingual glyceryl trinitrate
• Dual antiplatelets: Aspirin +
• Prasugrel, ticagrelor or clopidogrel - if undergoing PCI - just T+ C if not
• Anticoagulation:
• Fondaparinux or unfractionated heparin
• BBs
• Remember ‘MONA’: Morphine,Oxygen,Nitrates,Aspirin

Question 16

Immediate STEMI Management

Answer 16

• Oxygen:only if SpO2is <94%, and aim for 94-98%
• Analgesia:morphine and sublingual glyceryl trinitrate
• Dual antiplatelets: Aspirin +
• Prasugrel, ticagrelor or clopidogrel - if undergoing PCI - just T+ C if fibrinolysis
• Anticoagulation - U Heparin + glycoprotein IIB/IIA inhib

Question 17

If ineligible for PCI management for STEMI

Answer 17

• Thrombolysis e.g. alteplase or tenecteplase
  
  • IV administration of a fibrinolytic agent
  • Offered if symptom onset is greater than 12h OR PCI not available within 120 mins
• Anticoagulation
  
  • An antithrombin agent such as unfractionated heparin is usually given alongside thrombolysis

Question 18

ECG for STEMI MI

Answer 18

If the ECG shows residual ST elevation after 60-90 minutes of thrombolysis, offer immediate angiography and PCI

Question 19

2ndary prevention of CVD

Answer 19

• Lifestyle changes: exercise, diet change, smoking cessation, reducing alcohol intake
• Manage cardiovascular risk factors: lipid, diabetes, hypertension management
• Antiplatelet therapy:
  
  • Aspirin 75mg OD continued indefinitely
  • The second antiplatelet depends on the one chosen in the acute setting i.e. prasugrel, ticagrelor, or clopidogrel, and is usually continued for 12 months.
• Statin
• ACEi

Question 20

Early complications of Angina

Answer 20

• Post-MI pericarditis:inflammation of the pericardium usually occurs afew dayspost-MI due to irritation of the pericardium; usually benign
• Cardiac arrest/tachyarrhythmias:most commonly**due to ventricular fibrillation
• Bradyarrhythmias:heart block is more common after an inferior myocardial infarction
• Cardiogenic shock:extensive ventricular damage may lead to impaired ejection fraction and the development of cardiogenic shock
• Ventricular septal defect:seen within the first week and may present with acute heart failureand a pansystolic murmur
• Mitral regurgitation

Question 21

Later complications

Answer 21

• Dressler’s syndrome:presents similarly to post-MI pericarditis but occurs2-6 weekspost-MI, and reflects anautoimmuneprocess against neo-antigens formed by the heart
  Diagnosis:ECG(global ST elevationandT wave inversion),echocardiogram (pericardial effusion) and raisedinflammatory markers(CRPandESR).
  Management:NSAIDs(aspirin/ibuprofen) and in more severe cases steroids (prednisolone). May needpericardiocentesisto remove fluid around the heart.
• Heart failure:ventricular dysfunction following extensive damage can lead to chronic heart failure
• Left ventricular aneurysm: bulge or ballooning of a weakened area of the heart

Question 22

Type of MI

Answer 22

• Type 1: a classic MI and occurs due to atheromatous plaque rupture
• Type 2: secondary to ischaemia due toeitherincreased oxygen demandordecreased supply, such as vasospasm, anaemia and sepsis. Management involves treating the underlying cause.
• Type 3: Sudden cardiac death or cardiac arrest suggestive of an ischaemic event
• Type 4: MI associated with PCI / coronary stenting / CABG

Question 23

What are ST elevation MI and MI assosciated with LBBB related to?

Answer 23

larger infarcts
unless effectively treated more likely to lead to pathological Q wave formation, heart failure or death

Question 24

R wave MI

Answer 24

R wave generated by electrically viable myocardium under ECG lead – if we replace this with scar tissue lose R wave and you get pathological R wave

Question 25

What is the initial management for acute coronary syndrome?

Answer 25

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

Question 26

Hospital management for MI

Answer 26

Make diagnosis Bed rest Oxygen therapy 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

Question 27

What is troponin?

Answer 27

Troponin C Troponin I and Troponin T Protein complex regulates actin:myosin contraction Highly sensitive marker for cardiac muscle injury Not specific for acute coronary syndrome May not represent permanent muscle damage

Question 28

Positive troponine is found in?

Answer 28

gram negative sepsis pulmonary embolism myocarditis heart failure arrhythmias cytotoxic drugs

Question 29

Agonists for platelet activation

Answer 29

Thrombin > Coagulation Thromboxane A2 Collagen 5HT ADP ATP Fibrinogen > Fibrin

Question 30

Aspirin effect

Answer 30

Irreversible inactivation of cyclo-oxygenase 1 Stops conversion of collagen to Thromboxane A2

Question 31

What does thrombin do?

Answer 31

activates platelets – final factor in coagulation cascade as it cleaves fibrin from fibrinogen

Question 32

What is the fibrinolytic system?

Answer 32

Endothelium releases tissue plasminogen activator (TPA) TPA > Plasminogen > plasmin > Fibrin to fibrin degradation products

Question 33

What is P2Y12 and what is its antagonists / inhibitors

Answer 33

- important amplification process in platelet activation -Makes response of platelets much more aggressive - Clopidogrel, ticagrelor, prasugrel

Question 34

What do P2Y12 inhibs do?

Answer 34

Used in combination with aspirin in management of ACS = ‘dual antiplatelet therapy’ Increase risk of bleeding so need to exclude serious bleeding prior to administration

Question 35

What are adverse effecrs of P2Y12 inhibs

Answer 35

Bleeding e.g. epistaxis, GI bleeds, haematuria Rash GI disturbance Dyspnoea

Question 36

What are some GPIIb/IIIa antagonists?

Answer 36

Abciximab Tirofiban Eptifibatide

Question 37

What do GPIIb/IIIa antagonists do?

Answer 37

Only intravenous drugs available Used in combination with aspirin and oral P2Y12 inhibitors in management of patients undergoing PCI for ACS Increase risk of major bleeding so used selectively

Question 38

What do anticoagulants do?

Answer 38

- Used in addition to antiplatelet drugs - Target formation and activity of thrombin - Inhibit both fibrin formation and platelet activation

Question 39

When is fondaparinux used?

Answer 39

used in NSTE ACS prior to coronary angiography = safer than heparins as low level of anticoagulation used

Question 40

When do you use full dose anticoagulation

Answer 40

- used during PCI: options are: - heparins (usually **unfractionated heparin**; some centres use enoxaparin, a low-molecular-weight heparin) - direct thrombin inhibitor: bivalirudin

Question 41

When is high dose heparin used

Answer 41

cardiopulmonary bypass for CABG surgery

Question 42

When is a coronary angiography usually performed?

Answer 42

for patients with troponin elevation or unstable angina after medical therapy

Question 43

What is the most used revascularisation procedure?

Answer 43

PCI