Acute Coronary Syndrome: Definition
Acute Coronary Syndrome (ACS)= a group of conditions that result when atherosclerotic thrombus blocks a coronary artery. A type coronary artery disease??
- There are three types of acute coronary syndrome:
- Unstable angina
- Non-ST-elevation myocardial infarction (NSTEMI)
- ST-elevation myocardial infarction (STEMI)
When a thrombus forms in a fast-flowing artery, it is formed mainly ofplatelets. This is whyantiplatelet medications(eg. aspirin,clopidogrelandticagrelor)are the mainstay of treatment.
ACS: Symptoms
- central, constricting chest pain
- Pain radiating to the jaw or arms
- Shortness of breath
- Palpitations
- Nausea and vomiting
- Sweating and clamminess
- A feeling of impending doom
Symptoms should continue at rest for more than 15 minutes
Asilent myocardial infarctionis when someone does not experience typical chest pain duringacute coronary syndrome. Common in diabetes.
ACS: Investgations
- Baseline bloods
- FBC (anaemia)
- U&Es (required before starting an ACE inhibitor and other medications)
- LFTs (required before starting statins)
- Lipid profile
- Thyroid function tests (hypothyroidism or hyperthyroidism)
- HbA1C and fasting glucose (diabetes)
- Troponin blood tests - raised in NSTEMI
Troponin is non-specific. Alternative causes of a raised troponin include:- Chronic kidney disease
- Sepsis
- Myocarditis
- Aortic dissection
- Pulmonary embolism
- Chest x-rayto investigate for pulmonary oedema and other causes of chest pain
- Echocardiogramonce stable to assess the functional damage to the heart, specifically theleft ventricular function
- ECG - different ecg changes depending on STEMI or NSTEMISTEMI:
- troponin may be raised
- ST-segment elevation
- New left bundle branch block
- raised troponin
- Normal ECG
- Other ECG changes (ST segment depression or T wave inversion)
- normal troponin
- normal ECG
- Other ECG changes (ST depressionorT wave inversion)
ACS: Classification
Types of Myocardial Infarction
Knowing the types of myocardial infarction is helpful for exams. These terms are not frequently used in everyday practice as they may be confusing for those that are not familiar with them.
- Type 1: Traditional MI due to an acute coronary event
- Type 2: Ischaemia secondary to increased demand or reduced supply of oxygen (e.g. secondary to severe anaemia, tachycardia or hypotension)
- Type 3: Sudden cardiac death or cardiac arrest suggestive of an ischaemic event
- Type 4: MI associated with procedures such as PCI, coronary stenting and CABG
You could remember these with the “ACDC” mnemonic:
- Type 1:A–ACS-type MI
- Type 2:C–Can’tcope MI
- Type 3:D–Dead by MI
- Type 4:C–Caused by us MI
Troponinis a protein in cardiac muscle (myocardium) and skeletal muscle. The specific type of troponin, normal range and diagnostic criteria vary based on different laboratories, so check the local policy. A rise in troponin is consistent withmyocardial ischaemia, as they are released from the ischaemic muscle tissue.
ACS: Immediate Management
**Initial Management: MONA
M- Morphine if in severe pain
O- Oxygen 15L non-rebreathe mask (sats <94% or unknown)
N- Nitrate (GTN), use with caution if patient is hypotensive
A- Aspirin 300mg
STEMI: attempt reperfussion of tissue if within 12 hours of onset
- PCI via radial artery - within 2 hours (aspirin and prasugel or clopidogrel if already on oral anticoagulant)
- Thrombolysis (eg. alteplase) (and antithrombin drug eg. fondaparinux)
An ECG should be repeated after 60-90 minutes to see if the ECG changes have resolved. If patients have persistent myocardial ischaemia following fibrinolysis then PCI should be considered.
if not within 12hours, then manage medically with ticagrelor nor clopidogrel if high bleeding risk/already on anticoag
NSTEMI
B- Base descision about PCI on the GRACE Score
A- Aspirin 300mg
T- Ticagrelor 180mg stat dose (clopidogrel if high bleeding risk, on anticoagulant), antiplatelet
M- morphine for pain control
A- Antithrombin with fondaparinux, unless high risk bleed
N- Nitrate (GTN)
O- Oxygen if less than 95%
GRACE SCORE= 6-month probability of death after NSTEMI
- 3% or less - low risk - ticagrelor
- more than 3% + haemodynamically stable - medium to high risk - PCI within 72 hours of admission + prasugrel/ticagrelor or clopidogrel
- more than 3% + haemodynamically unstable - medium to high risk - immediate PCI
Unstable NSTEMI: Immediate Coronary angiography
ACS: Long Term Management
Remember using 6A’s:
- Aspirin 75mg daily
- Ticagrelor/Clopidogrel for 12 months (Another antiplatelet
- Atorvastatin 80mg daily - check LFTs
- ACE Inhibitor (eg. ramipril) - titrated as high as tolerated
- Atenolol or beta blocker
- Aldosterone antagonist - for those with heart failure
Echocardiogram, cardiac rehabilitation, secondary prevention med
- monitor renal function (U+Es) when takingACE inhibitorsandaldosterone antagonists as both can causehyperkalaemia(raised potassium).
- aldosterone agonist + ACEi or ARB has a risk of fatal hyperkalaemia.
ACS: Complications
The complications of a myocardial infarction can be remembered with the “DREAD” mnemonic:
- D–Death (shock or ventricular fib)
- R–Rupture of the heart septum or papillary muscles
- E–**“oEdema”**(heart failure)
- A–Arrhythmia andAneurysm
- D–**Dressler’s Syndrome and damage to kidneys
- Dressler’s Syndrome - pericarditis that occurs 2-3 weeks after MI. ECG shows (global ST elevationandT wave inversion). Management is withNSAIDs(e.g.,aspirinoribuprofen) and, in more severe cases steroids (eg. prednisolone).
- Kidney damage - monitor kidney function (urine output, U+Es, creatinine, eGFR)
- Organ damage, usually brain and kidneys first as they are the most well-perfused organs
left ventricular aneurysm - after months- persistent ST elevation and LV failure- anticoag as thrombus may form
LV free wall rupture- 1-2 weeks after MI. Acute heart failure secondary to cardiac tamponade (raised JVP, pulsus paradoxus, diminished heart sounds). Urgent pericardiocentesis and thoracotomy are required.
Ventricular septal defect- 1 week after. acute heart failure with pan-systolic murmur
acute MR - ischaemia or papillary muscles - acute hupotension and pulmonary oedema - end-to-mid systolic murmur - vasodilator therapy or emergency surgical repair
Stable Angina: Management
immediate symptomatic relief
GTN
long-term symptomatic relief:
Beta-blocker/ rate-limiting CCB (verapamil or diltiazem) monotherapy
Beta-blocker + long-acting dihydropyridine CCB (amlodipine, modified-release nifedipine)
Increase to max dose.
A specialist may consider other options:
- Long-acting nitrates(e.g.,isosorbide mononitrate)
- Ivabradine
- Nicorandil
- Ranolazine
avoid verapamil and diltiazem in patients with heart failure. Avoid beta-blocker in asthma
If a patient has an inadequate response to verapamil then adding a long-acting nitrate is a suitable next step. beta blocker and verapamil should not be prescribed together - risk of complete herat block
Nitrate tolerance
many patients who take nitrates develop tolerance and experience reduced efficacy
standard-release isosorbide mononitrate should use an asymmetric dosing interval to maintain a daily nitrate-free time of 10-14 hours to minimise the development of nitrate tolerance
this effect is not seen in patients who take once-daily modified-release isosorbide mononitrate
secondary prevention(“four As”) mnemonic:
- A–Aspirin 75mg once daily
- A–Atorvastatin 80mg once daily
- A–ACE inhibitor (if diabetes, hypertension, CKD or heart failure are also present)
- A–Already on abeta blockerfor
ACS: prognostic factors
Poor prognostic factors
age
development (or history) of heart failure
peripheral vascular disease
reduced systolic blood pressure
Killip class*
initial serum creatinine concentration
elevated initial cardiac markers
cardiac arrest on admission
ST segment deviation
Killip class Features 30 day mortality
I No clinical signs heart failure 6%
II Lung crackles, S3 17%
III Frank pulmonary oedema 38%
IV Cardiogenic shock 81%
To do:
acs: immediate management
angina: drug management
