Acute Coronary Syndrome

» Cardiology

Overview

Overview Coronary artery obstruction or rupture can result in a variety of ischaemic condition which fall under the term of acute coronary syndrome. This does not include stable angina. Ischaemic heart disease is the leading cause of death world wide. The mortality of myocardial infarction is believed to be 45% with 70% of these deaths occurring before reaching medical care. It is important to reopen the artery and re-establish flow as soon as possible. This may be achieved by:

percutaneous coronary intervention (PCI) - transluminal coronary balloon angioplasty and stenting
fibrinolytic therapy

Watch Acute Coronary Syndrome DETAILED Overview

Definitions
Acute myocardial Infarction: Death of myocardial tissue because of inadequate blood flow
ST- segment elevation myocardial infarction (STEMI): MI as defined as in acute myocardial infarction, with ST-segment elevation more than 0.1 mV in two or more contiguous leads, and elevated cardiac biomarkers.
Non-ST segment elevation myocardial infarction (NSTEMI): MI, but without ST-segment elevation. May have other ECG changes, such as ST-segment depression or T-wave inversion. Will have elevated cardiac biomarkers.
Unstable angina is defined by the absence of biochemical evidence of myocardial damage. It is characterised by specific clinical findings of prolonged (>20 minutes) angina at rest; new onset of severe angina; angina that is increasing in frequency, longer in duration, or lower in threshold; or angina that occurs after a recent episode of MI.

Remember Stable Angina is not part of Acute Coronary syndrome

Risk Factors

Modifiable	Non-modifiable
Smoking	Increasing age
Hypertension	Male sex
Dyslipidaemia	Family history
Diabetes mellitus	Ethnicity
Obesity
Physical inactivity
High calorie intake diet
Psychological stress

Signs and Symptoms

Clinical Presentation Retrosternal Pain (for at least 30min), which radiates to the neck, arms and jaw. The pain is described as crushing, heaviness or like a tight band. Worse with physical or emotional exertion. Not relieved by rest. Nitrate spray (within a couple of minutes) may not always relieve the pain. Acute coronary syndrome may be accompanied with diaphoresis, feeling of impending doom and breathless.

Remember Patients classically clinch their fist and hold it on their chest to describe the pain (Levine's Sign)

Think If patient has stable angina, with rest the pain will go

Examination

Signs of impaired myocardium

Hypotension, Oligouria
Raised JVP
Narrow pulse pressure
Third heart sound
Lung crepitation (pulmonary edema)

Differential Diagnosis

CAUSES OF CHEST PAIN BY BODY SYSTEMS
Cardiac	Respiratory	Gastrointestinal	Musculoskeletal	Psychogenic
Acute Coronary Syndrome	Pulmonary Embolism	Oesophageal rupture	Rib Fracture	Anxiety
Aortic dissection	Pneumothorax	Pneumomediastinum	Herpes Zoster	Panic attack
Pericarditis	Pulmonary Hypertension	Cholecystitis	Costochondritis
Stable Angina	Pneumonia	GERD
Endocarditis	Lung Cancer	Peptic ulcer disease
Cardiac tamponade	Bronchiectasis	Acute Pancreatitis

Investigation

Chest pain with high suspicion of Acute Coronary syndrome (history, examination and risk factors)

ECG - tall T-wave, ST elevation or new Left Bundle Brach Block
FBC
EUC
Glucose
Lipid profile
Cardiac Enzymes
- Troponin T (cTNT) and Troponin (cTNl) are proteins virtually exclusive to cardiac myocytes. They are highly specific and sensitive, but are only maximally accurate after 12 hours.
- Creatinine Kinase - CK-MM, CK-BB, CK-MB

Think Don’t be fooled by normal cardiac enzymes. A fresh MI (< 30 minutes) may not yet show elevated blood levels.

Remember Troponin can be released into blood when cardiac muscle is damaged by pericarditis, PE with a large clot or sepsis. Renal failure also reduces the rate of troponin excretion.

Diagnosis (at least two of the following):

Typical chest pain persisting for more than 30 minutes
Typical ECG findings
- ST elevation
- Pathological Q wave
Elevated cardiac biomarker levels.
- Troponin (peaks in 1 -2 days) lasts 2 weeks
- CK-MB - rises 4-6 hours peaks at 12 and at 2 days drops off

ECG

ECG is an important investigation tool for the identification and diagnosis of ACS and other cardiovascular diseases. Record ECG as soon as possible in suspected MI. Look at ST segment and look for:

ST elevation
ST depression

ECG Changes in Acute Coronary Syndrome
STEMI	Hyperacute T waves, which are tall, peaked, and symmetric Elevation of the ST segment (>1mm) in contiguous leads, depending upon the location of the MI.
NSTEMI	T wave flattening or inversion typically precedes ST segment depression Q waves are typically absent but can occur, and the duration of the ST and T wave changes is variable.
Unstable Angina

Remember The deeper the q- wave the longer the infarction has been.

ST Elevation Infarction of cardiac muscles results in ECG changes that evolve over hours, days and weeks in relatively predictable fashion.

Location of myocardial infarction can be identified with the ECG leads.

Location of Infarct	ST elevation in leads
Anterior	V2-V5
Antero-lateral	I, aVL, V5, V6
Inferior	III, aVF (sometimes II also)
Posterior
Right ventricular

Pathophysiology

Video: Cardiogenic Shock

Symptoms and signs	Mechanisms
Severe myocardial ischaemia:
Chest pain	Ischaemia
Fourth heart sound	Forceful filling of non-compliant left ventricle
Low grade fever	Inflammation
Leucocytosis and increased levels of inflammatory markers	Inflammation
Increase in troponin levels	Leakage of protein from injured cardiac myocytes
Activation of autonomic nervous system:
Tachycardia and sweating	Sympathetic activation
Bradycardia, nausea, and vomiting	Vagal activation (especially in inferior acute myocardial infarction)

Source: BMJ Clinical Review Acute Coronary Syndrome 2015

Pathology

Type of infarct

Transmural

Affects all of the myocardial wall
ST elevation and Q waves

Subendocardial

Necrosis of <50% of the myocardial wall
ST depression

Think An ST-segment elevation on ECG indicates that the infarction extends through the full thickness of the myocardial wall (transmural). The absence of ST-segment elevation in the setting of cardiac enzymes indicates that the infarction is limited to the subendocardium. NSTEMIs are dangerous in that the patient is still at risk for a full-thickness infarct in that area.

PATHOLOGICAL CHANGES
Time from onset	Gross Findings	Microscopic Findings
1-3 hours	Pallor of mycocardium	No inflammatory cells
4-12 hours	Pallor of mycocardium	Coagulation necrosis, inflammation (oedema, oesoinophil and neutrophil infiltration)
<24 hours	Coagulation necrosis	Coagulation necrosis
1-3 days	Central area of yellow discoloration surrounded by a thin rim of highly vascularized hyperemia	Macrophage infiltration
3-7 days		Fibroblast infiltration
Days 7 - 21

Management STEMI

Definition
PCI: Percutaneous coronary intervention (angioplasty and/or stenting).
Thrombolytics: Drugs such as tissue plasminogen activator (tPA), streptokinase, and reteplase (r-PA), which act to lyse fibrin thrombi in order to restore patency of the coronary artery when PCI is contraindicated or is not available

Must consider the following in managing ACS:

The suspicion of acute MI based on the clinical and ECG findings
Deciding whether the patient has indications or contraindications for thrombolytics or primary percutaneous coronary intervention
Excluding other diagnoses that might mimic acute MI but would not benefit from or might be worsened by anticoagulation or thrombolysis (eg, acute pericarditis, aortic dissection).

Acute management

Admission to coronary care unit
Explain to patient what has happened
Morphine
Oxygen
Nitrates
Aspirin
Clopidogrel
Acute management Reperfusion therapy
- Percutaneous coronary intervention (PCI) OR Fibrinolytic therapy (thrombolysis)

Remember MONAC Morphine (+/- antiemetic), Oxygen, Nitrates, Aspirin, Clopidogrel

Acute management Reperfusion therapy

Early reperfusion with PCI or thrombolytics reduces mortality and preserves ventricular function in patients who have ST-segment elevation, have no contraindications, and receive treatment within the first 6 to 12 hours

PCI should be performed within:
- 60min if patient presents within the first hour of symptom onset
- 90min if patient presents between 1-3hrs after symptom onset
- 90 to 120 minutes for patients presenting between 3 and 12 hours
If these targets cannot be reached, fibrinolysis should be given within 30 minutes of arrival in hospital
Fibrinolytic therapy (Thrombolysis) within 24 hours, contraindication >24hours
- Alteplase OR
- Reteplase
Anticoagulant therapy
- Hepain
Heart Bypass

Indications for reperfusion therapy

Ischaemic/infarction symptoms of longer than 20 minutes (chest pain-radiating to shoulder or jaw, sweating, feeling of doom

Symptoms commenced within 12 hours

ST elevation or presumed new left bundle branch block on ECG

No contraindications to reperfusion therapy.

Pharmacology Thrombolytics break down/dissolve clots. It is used to treat stroke, pulmonary embolism and myocardial infarction. Three main thrombolytic drugs: tissue plasminogen activator, streptokinase, andurokinase. Side effects: major bleeding, cardiac arrhythmias, cholesterol embolus syndrome, anaphylactoid reaction, cerebrovascular accident, intracraneal hemorrhage. Steptokinase specific adverse effects: Non-cardiogenic pulmonary edema, hypotension, fever and shivering.

Contraindication and cautions for thrombolysis use in STEMI

Risk of Bleeding (active bleeding, haemorrhage ophthalmic condition, known bleeding diathesis, suspected aortic dissection)

Risk of intracranial haemorrhage

Recent Major trauma, surgery, head injury <3weeks

Aortic Dissection

Pregnancy

On-going management Non-pharmacological

Smoking cessation
Alcohol limitation
Diet modification
Lose weight

On-going management pharmacological (ABAS)

ACE inhibitors OR Angiotensin Receptor Blocker
Beta-blockers
Aspirin + clopidogrel
Statins

Long-term anticoagulation to prevent emboli from left ventricular mural thrombus should be considered in patients who have suffered a large myocardial infarction, particularly if a large akinetic/dyskinetic area is present.

Pharmacology Aspirin is a COX 1/2 inhibitor. It prevents the production of Prostagladins (inflammation: fever and pain) and thromboxane (clotting). It is used to treat fever, osteoarthritis, heart conditions and stroke. Side effects: nausea/vomiting, dyspepsia, stomach ulcer or bleeding problems, headache, dizziness, tinnitus, renal dysfunction and Reye’s syndrome (particularly in children who have taken aspirin)