Acute Coronary Syndrome (ACS)

Universal definition of myocardial infarction

The term ‘myocardial infarction’ should be used when there is evidence of myocardial necrosis in a clinical setting consistent with myocardial ischaemia, in which case any one of the following meets the diagnosis for MI:

Detection of rise and/or fall of cardiac biomarkers (preferably troponin), with at least one value above the 99thpercentile of the upper reference limit, together with at least one of the following:

Symptoms of ischaemia

ECG changes indicative of new ischaemia (new ST-Tchanges or new left bundle branch block)

Development of pathological Q waves

Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality

Sudden unexpected cardiac death, involving cardiac arrest, often with symptoms suggestive of myocardialischaemia,and accompanied by presumably new ST elevation or new left bundle branch block, and/or evidence of fresh thrombus by coronary angiography and/or at autopsy, but death occurring before blood samples could be obtained or before the appearance of cardiac biomarkers in the blood

Pathological findings of an acute MI

Pathogenesis of ACS

ACS may present as a new phenomenon or against a background of chronic stable angina.

The culprit lesion is usually a complex ulcerated or fissured atheromatous plaque with adherent platelet rich thrombus and local coronary artery spasm.

This is a dynamic process whereby the degree of obstruction may either increase leading to MI or regress spontaneously due to platelet disaggregation and endogenous fibrinolysis.

Clinical features of acute coronary syndrome

Symptoms

Prolonged cardiac pain: chest,throat,arms,epigastrium or back

• Anxiety and fear of impending death

• Nausea and vomiting

• Breathlessness

• Collapse/syncope

Physical signs

Signs of sympathetic activation: pallor, sweating, tachycardia

• Signs of vagal activation: vomiting, bradycardia

• Signs of impaired myocardial function

Hypotension, oliguria, cold peripheries

Narrow pulse pressure

Raised JVP

Third heart sound

Quiet first heart sound

Diffuse apical impulse

Lung crepitations

• Signs of tissue damage: fever

• Signs of complications: e.g. mitral regurgitation, pericarditis

Timely intervention is vital

Sudden death from VF or asystole may occur immediately and often within first hour.

If patient survives this most critical phase then liabilities to dangerous arrhythmias remains, but diminishes as each hour goes by.

It is vital that the patient knows not to delay calling for help if symptoms occur.

Early intervention can save life,myocardium.

Differential diagnosis of chest pain

Anxiety/emotion

Cardiac

Myocardial ischaemia (angina)

MI

Myocarditis

Pericarditis

Mitral valve prolapse

DD chest pain

Aortic

Aortic dissection

Aortic aneurysm

Oesophageal

Oesophagitis

Esophageal spasm

Mallory–Weiss syndrome

Lungs/pleura

Bronchospasm

Pulmonary infarct

Pneumonia

Tracheitis

Pneumothorax

Pulmonary embolism

Malignancy

Tuberculosis

Connective tissue disorders (rare)

Musculoskeletal

Osteoarthritis

Rib fracture/injury

Costochondritis (Tietze’ssyndrome)

Intercostal muscle injury

Epidemic myalgia(Bornholm disease)

Neurological

Prolapsed intervertebral disc

Herpes zoster

Thoracic outlet syndrome

Diagnostic workup of ACS

Serial ECGs

Serial measurements of CKMB and trop T and trop I

Other blood tests

Lipid profile

CXR

Echocardiography

Management of acute MI

Urgent admission to CCU

Medical treatment aspirin,clopidogrel,anticoagulation and angina therapy.

Management of pain and vomiting

Oxygen

Thrombolysis

Cardiac monitoring and management of arrythmias

PCI or CABG

Oral antiplatelet agents in acute coronary syndromes

Aspirin alone (75–325 mg/day) reduces the risk of death, MI and stroke in acute coronary syndromes . The addition of clopidogrel (75 mg daily) to aspirin causes a further modest reduction in these events.

Anti coagulation in acute coronary syndromes

Aspirin plus low molecular weight heparin is more effective than aspirin alone in reducing the combined endpoint of death,MI, refractory angina and urgent need for revascularisation. In comparison to low molecular weight heparin, the pentasaccharide,fondaparinux (2.5 mg s.c.), is associated with lower bleeding rates and better overall survival.

Relative contraindications to thrombolytic
therapy: potential candidates for primary angioplasty

Active internal bleeding

Previous subarachnoid or intracerebral haemorrhage

Uncontrolled hypertension

Recent surgery (within 1 mth)

Recent trauma (including traumatic resuscitation)

High probability of active peptic ulcer

Pregnancy

Complications of MI

Arrythmias

Post infarction angina

Acute circulatory failure and cardiogenic shock

Pericarditis

Mechanical complications

Rupture of papillary muscles,interventricular septum or ventricle.

Thromboembolism

Ventricular anuerysm