Unstable angina Flashcards
What is ACS
encompasses unstable angina, non-ST elevation myocardial infarction (NSTEMI) and ST-elevation myocardial infarction (STEMI).
What does ACS typically manifest as
sudden, new-onset angina, or an increase in the severity of an existing stable angina.
What are the clinical classifications for unstable angina?
- 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
Epidemiology
- STEMI = 5/1000 per annum in UK
- M>F
Non modifiable RFs for ACS
- Age (>65 years of age)
- Male
- Family history of premature coronary heart disease
- Premature menopause
Modifiable RFs
- Smoking
- Diabetes mellitus
- Hyperlipidaemia
- Hypertension
- Obesity
- Sedentary lifestyle
Pathophysiology: Atherosclerotic plaque formation
- 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
What is a dianosis of angina based on?
history
ECG
troponin (no significant rise in unstable angina)
Occlusions
- Unstable angina + NSTEMI: Partial occlusion
- STEMI - occlusion is complete
Signs
- 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
Symptoms
-
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
Investigations
- 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.
ECG findings
- 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
Other investigations
- Coronary angiogram:aim to carry out angiography within 90 minutes if required; diagnostic investigation of choice
- FBC
- UEs
- CXR
- Echocardiogram
- HbA1C
Unstable angina + NSTEMI Immediate management
- 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
Immediate STEMI Management
- 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
If ineligible for PCI management for STEMI
-
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
ECG for STEMI MI
If the ECG shows residual ST elevation after 60-90 minutes of thrombolysis, offer immediate angiography and PCI
2ndary prevention of CVD
- 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
Early complications of Angina
- 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
Later complications
-
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
Type of MI
- 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
What are ST elevation MI and MI assosciated with LBBB related to?
larger infarcts
unless effectively treated more likely to lead to pathological Q wave formation, heart failure or death
R wave MI
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
What is the initial management for acute coronary syndrome?
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
Hospital management for MI
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
What is troponin?
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
Positive troponine is found in?
gram negative sepsis
pulmonary embolism
myocarditis
heart failure
arrhythmias
cytotoxic drugs
Agonists for platelet activation
Thrombin > Coagulation
Thromboxane A2
Collagen
5HT
ADP
ATP
Fibrinogen > Fibrin
Aspirin effect
Irreversible inactivation of cyclo-oxygenase 1
Stops conversion of collagen to Thromboxane A2
What does thrombin do?
activates platelets – final factor in coagulation cascade as it cleaves fibrin from fibrinogen
What is the fibrinolytic system?
Endothelium releases tissue plasminogen activator (TPA)
TPA > Plasminogen > plasmin > Fibrin to fibrin degradation products
What is P2Y12 and what is its antagonists / inhibitors
- important amplification process in platelet activation -Makes response of platelets much more aggressive
- Clopidogrel, ticagrelor, prasugrel
What do P2Y12 inhibs do?
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
What are adverse effecrs of P2Y12 inhibs
Bleeding e.g. epistaxis, GI bleeds, haematuria
Rash
GI disturbance
Dyspnoea
What are some GPIIb/IIIa antagonists?
Abciximab
Tirofiban
Eptifibatide
What do GPIIb/IIIa antagonists do?
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
What do anticoagulants do?
- Used in addition to antiplatelet drugs
- Target formation and activity of thrombin
- Inhibit both fibrin formation and platelet activation
When is fondaparinux used?
used in NSTE ACS prior to coronary angiography = safer than heparins as low level of anticoagulation used
When do you use full dose anticoagulation
- used during PCI: options are:
- heparins (usually unfractionated heparin; some centres use enoxaparin, a low-molecular-weight heparin)
- direct thrombin inhibitor: bivalirudin
When is high dose heparin used
cardiopulmonary bypass for CABG surgery
When is a coronary angiography usually performed?
for patients with troponin elevation or unstable angina after medical therapy
What is the most used revascularisation procedure?
PCI
