Myocardial Infarction

By

Prof. Dr. Aliaa Aly El Aghoury

Prof. of Internal Medicine Endocrinology Unit Faculty of Medicine, Alex. University

Myocardial infarction (MI)

MI is almost always due to the formation of

occlusive thrombus at the site of rupture or erosion of an atheromatous plaque in a coronary artery.
The thrombus often undergoes spontaneous

lysis over the course of the next few days, although by this time irreversible myocardial damage has occurred.

Clinical features of myocardial infarction

Symptoms : Prolonged cardiac pain (chest, throat, arms,

epigastrum or back)

Anxiety and fear of impending death

Nausea and vomiting

Breathlessness Collapse/syncope

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Physical signs :
Signs of sympathetic activation :

Pallor, sweating, tachycardia

Signs of vagal activation :

Vomiting, tachycardia

Myocardial Infarction N.B. :

The pain occurs in the same sites as angina but is usually

more severe and lasts longer, it is often described as a tightness, heaviness or constriction in the chest. Painless or silent myocardial infarction is common in older or diabetic patients. Sudden death from ventricular fibrillation or asystole may occur immediately and many deaths occur within the first hour.

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Investigations I. Electrocardiography
Is usually helpful in confirming the diagnosis.

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II. Plasma biochemical markers

MI causes a detectable rise in the plasma concentration of enzymes and proteins that are normally within cardiac cells. The most widely used are creatine kinase (CK). A cardio-specific isoform of this enzyme (CK-MB) and the cardiospecific proteins troponin T & I.

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Serial (usually daily) estimations are particularly helpful because it is the change in plasma concentrations of these markers that is of diagnostic value.

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CK starts to rise at 4-6 hours, peaks at about 12 hours and falls to normal within 48-72 hours. Troponin T and I are released within 4-6 hours and remain elevated for up to 2 weeks.

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III. Other blood tests 1. Leucocytosis 2. ESR 3. CRP (C-reactive protein)

IV. Chest X-ray : Cardiomegaly, pulmonary oedema

V. Echocadiography

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Management:
Early management of acute myocardial infarction (AMI) require immediate access to medical and paramedical care and defibrillation facilities.

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I. Immediate measures
High-flow oxygen I.V. access ECG monitoring 12-lead ECG I.V. analgesia (opiates) and antiemetic
Intravenous opiates e.g. morphine sulphate and antiemetics (metoclopramide) should be administered through an intravenous cannula and titrated by giving repeated small aliquots until the patient is comfortable.

Aspirin 300 mg

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2. Acute reperfusion therapy Thrombolysis: successful thrombolysis leads to reperfusion with relief of pain, resolution of acute ST elevation. The sooner the patient is treated the better the results will be, any delay will only increase the extent of myocardial damage (minutes mean muscle).

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Streptokinase 1.5 million U in 100 ml of saline given as an intravenous infusion over 1 hour is a widely used regimen. Streptokinase is antigenic and occasionally causes serious allergic manifestations, it may also cause hypotension.

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Altephase (human tissue plasminogen activator or tPA) is a genetically engineered drug that is not antigenic and seldom causes hypotension. The major hazard of thrombolytic therapy is bleeding. (PCI) Primary percutaneous coronary intervention is the treatment of choice.

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3. Maintaining vessel patency
Antiplatelet therapy Aspirin 75-300 mg/d Clopidogrel 75 mg/d Anticoagulant: subcutaneous heparin twice daily (low molecular weight heparin is now available).
N.B blockers and nitrates can be used as Adjunctive therapy

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N.B

Complications of infarction Arrythmias Ventricular fibrillation Atrial fibrillation Sinus bradycardia Acute circulatory failure Embolism

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II. Late Management:

Life-style modification - Stop smoking - Regular exercise - Diet (weight control, lipid lowering).

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Secondary prevention drug therapy - Antiplatelet therapy - Statin b blocker - ACE inhibitor - Control diabetes and hypertension III. Rehabilitation