1. Acute coronary syndrome (ACS)
Domina Petric, MD

2. Introduction
ACS includes unstable angina and evolving myocardial infarction (MI) that can be STEMI (MI with ST elevation) and NSTEMI (MI without ST elevation).

3. plaque rupture thrombosis inflammation Underlying pathology
ACS may be rarely due to emboli
or coronary spasm in normal coronary
arteries.
Underlying pathology
plaque rupture
thrombosis
inflammation

4. Unstable angina Unstable plaque!
Plaque disruption and platelet aggregation!
Thrombus formation!
Blood vessel is not completely occluded.

5. NSTEMI Ruptured plaque and thrombus formation!
Thrombus occludes blood vessel completely,
but not all the time.
There may be some blood flow through
the vessel at the time.
ECG may show ST depression, T wave inversion or can even be normal
(non Q wave or subendocardial MI).

6. STEMI ECG shows ST elevation or there is a new onset of LBBB.
Blood vessel is completely occluded
and all the time.
Without intervention, there can not be
any blood flow through the vessel.
Damage to heart muscle is severe.
ECG shows ST elevation or there is a new onset of LBBB.

7. Risk factors can be devided into three groups:
NON MODIFIABLE
MODIFIABLE
CONTROVERSIAL

8. Non modifiable risk factors
Age
Gender
Family history of ischaemic heart disease (especially MI in first degree relative younger than 55 years)

9. Modifiable risk factors
smoking
hypertension
diabetes mellitus
hyperlipidaemia
obesity
sedentary lifestyle
cocaine use

10. Controversial risk factors
stress
type A personality
left ventricular hyperthrophy
increased levels of fibrinogen
hyperinsulinaemia
increased levels of homocysteine
ACE genotype

11. Symptoms
Acute central chest pain lasting more than 20 minutes and it is often associated with nausea, sweatiness, dyspnoea and palpitations.
Silent infarction presents without chest pain, usually in elderly, diabetics or women.
In silent infarction symptoms include syncope, pumonary oedema, epigastric pain and vomiting (especially in inferior MI), post operative hypotension or oliguria, acute confusional state, stroke and hyperglycaemic states.

12. Signs
Most common signs include distress, anxiety, pallor, sweatiness, tachycardia, hypertension or hypotension and presence of fourth heart sound.
There may be signs of heart failure like increased jugular venous pressure (JVP), third heart sound and basal crepitations.
There can be pansystolic murmur present that usually means papillary muscle dysfunction or rupture or ventricular septal defect caused by MI.
Low grade fever may also be present.
Later signs can be pericardial friction rub and peripheral oedemas.

13. In STEMI there is evolution of ECG changes: hyperacute (tall) T waves
ST elevation or new LBBB occur within hours of transmural infarction
T wave inversion and development of pathological Q waves that follow over hours to days

14. Hyperacute T waves in STEMI!
Image source: lifeinthefastlane.com

15. Localisation of MI Type of infarction (localisation)
ST segment elevation
Septal MI
V1, V2
Anterior MI
V3, V4
Anteroseptal MI
V1-V4
Lateral MI
DI, aVL, V6
Anterolateral MI
DI, aVL, V3-V6
Anterior extended MI
DI, aVL, V1-V6
High lateral MI
DI, aVL
Inferior MI
DII, DIII, aVF
Anteroinferior (apical) MI
DII, DIII, aVF + at least one of V1-V4
Posterior MI
Tall R with ST denivelation in V1, V2 (mirror image in V1, V2)

16. Posterior MI: ST depression in V1-V2 (V3)
If you turn ECG upside down and back, there will be ST elevation in V1-V2!
This is called mirror test. Image source: lifeinthefastlane.com

17. widened mediastinum (in aortic rupture)
Chest X ray
cardiomegaly
pulmonary oedema
widened mediastinum (in aortic rupture)

18. Myoglobin levels rise within 1-4 hours from the onset of pain.
Cardiac enzymes
Myoglobin levels rise within 1-4 hours from the onset of pain.
Myoglobin is highly sensitive, but not specific.

19. Cardiac enzymes
Cardiac troponin levels (T and I troponine) are the most sensitive and specific markers of myocardial necrosis.
Serum levels of TrT and TrI start to rise within 3-12 hours from the onset of chest pain.
Peak levels are at hours.
TrT and TrI levels decrease to baseline over 5-14 days.

20. Cardiac enzymes
Creatin kinase has 3 isoenzymes: CK-MM, CK-BB and CK-MB.
CK-MM is found mainly in skeletal muscle.
CK-MM levels are increased after trauma (falls, seizures), in prolonged exercise, myositis and hypothyroidism.
CK-BB is predominantly in the brain.
CK-MB is mainly in the heart.
CK-MB levels increase within 3-12 hours of pain onset, reach peak values within 24 hours and return to baseline after hours.
Levels peak earlier if reperfusion occurs.
Sensitivity is 95% with high specificity.

21. Clevelandclinicmeded.com

22. Differential diagnosis
angina
pericarditis
myocarditis
aortic dissection
pulmonary embolism
oesophageal reflux or spasm

23. Pre-hospital management
Morphine 5-10 mg iv. + metoclopramide 10 mg iv.
Oxygen (if saturation is low)
Nitroglycerine (except in severe hypotension)
Aspirin 300 mg chewed

24. STEMI (in hospital)
Prasugrel (60 mg per os if there is no history of stroke/TIA) or ticagrelor (180 mg per os) or clopidogrel (300 mg per os).
Morphine 5-10 mg iv. (repeat after 5 minutes if necessary) with anti-emetic iv.
Oxygen if patient has SaO2 <95%, if breathless or in acute left heart failure.
Primary PCI should be offered to all patients who present with an acute STEMI preferably within 120 minutes of first medical contact.
Fibrinolysis is contraindicated after 24 hours from onset of symptoms.

25. NSTEMI (in hospital)
The aim of therapy is to optimize anti-ischaemic and antiplatelet therapy.
For high risk patient invasive strategy is prefered: infusion of GPIIb/IIIa antagonist and refer for angiography.
High risk patients have rise in troponin, dynamic ST segment or T wave changes and/or secondary criteria (diabetes, LVEF<40%, early angina post MI, recent PCI, prior CABG and chronic kindey disease).
Conservative strategy for low risk patients with no recurrence of chest pain, no signs of heart failure, normal ECG, negative baseline hours troponin and no inducible ischaemia.

26. Subsequent management in ACS
Bed rest for 48 hours with continous ECG monitoring.
Daily examination!
Prophylaxis against thromboembolism until the patient is fully mobile.
Aspirin 100 mg per os.
Long term beta blockers lower mortality rate (heart rate should be 60 or less).
ACE-inhibitors!
Statins!
Address modifiable risk factors!
Assess LV function!

27. Complications of MI cardiac arrest cardiogenic shock bradycardias
heart block
tachyarrhythmias
right ventricular failure or right heart infarction
pericarditis
deep venous thrombosis
pulmonary embolism
systemic embolism
cardiac tamponade
mitral regurgitation
ventricular septal defect
late malignant ventricular arrhythmias
Dressler´s syndrome
left ventricular aneurysm

28. Dressler´s syndrome
Recurrent pericarditis, pleural effusions, fever, anaemia and increased erythrocyte sedimentation rate 1-3 weaks after MI.

29. Coronary artery bypass graft (CABG)
Indications:
A) To improve survival
left main stem disease
triple vessel disease involving proximal part of the left anterior descending
B) To relieve symptoms
angina unresponsive to drugs
unstable angina
if angioplasty is unsuccessful

30. Literature
Oxford Handbook of Clinical Medicine. Longmore M. Wilkinson I. B. Baldwin A. Elizabeth W. Ninth edition.
Lifeinthefastlane.com
Clevelandclinicmeded.com