Acute MI (Myocardial Infarction) / Heart Attack

Acute MI (Myocardial Infarction) / Heart Attack

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Introduction
Myocardial infarction is the irreversible necrosis of heart muscle secondary to prolonged ischemia. This is usually due to an imbalance in oxygen supply and demand, which is most often due to plaque rupture with thrombus formation in a coronary vessel, resulting in an acute reduction of blood supply to a portion of the myocardium.

Epidemiology
  • Average incidence of MI for those aged between 30 and 69 years is about 600 per 100,000 for men, and 200 per 100,000 for women.
  • Mortality rates after ST elevation MI are equal at 30 days, if both sexes receive equivalent care. Mortality rates become significantly higher for women three years after discharge.
  • Premenopausal women appear to be protected from atherosclerosis.
  • Incidence increases with age and elderly people also tend to have higher rates of morbidity and mortality from MI.
Pathophysiology
  • Coronary arterial thrombosis is the direct cause of acute MI. This thrombotic event occurs when a pre-existing atherosclerotic plaque ruptures or fissures, thereby exposing underlying thrombogenic material to the circulation.
  • Platelets are thus activated and the clotting cascade is initiated. A previously stable atherosclerotic plaque fissures or ruptures due to release of vasoactive substances from activated platelets, coronary arterial vasomotion, mechanical stress fatigue of the atherosclerotic plaque, and rupture of vasa vasorum within the atherosclerotic plaque.
  • The resultant cessation of myocardial blood flow produces specific biochemical and physiological alterations secondary to myocardial ischemia. Diastolic compliance is markedly reduced by ischemia followed by cessation of systolic contractile activity.
  • Prolonged ischemia leads to delayed biochemical and physiological recovery and/or cell necrosis.
Etiology

Risk factors for acute MI due to atherosclerosis:
Fixed
  • Age
  • Male
  • Positive family history
  • Deletion polymorphism in the angiotensin-converting
  • enzyme (ACE) gene (DD)
Potentially modifiable
  • Cigarette smoking
  • Hyperlipidaemia
  • Hypertension
  • Diabetes mellitus
  • Blood coagulation factors – high fibrinogen, factor VII
  • C-reactive protein
  • Homocysteinaemia
  • Lack of exercise
  • Obesity
  • Drugs, e.g. contraceptive pill, nucleoside analogues, COX-2 inhibitors, rosiglitazone
  • Heavy alcohol consumption
  • Gout
Causes of acute MI other than atherosclerosis
  • Coronary artery emboli, secondary to cholesterol, air, or the products of sepsis
  • Coronary occlusion secondary to vasculitis
  • Ventricular hypertrophy (eg, left ventricular hypertrophy, idiopathic hypertrophic subaortic stenosis [IHSS], underlying valve disease)
  • Coronary trauma
  • Congenital coronary anomalies
  • Primary coronary vasospasm (variant angina)
  • Drug use (eg, cocaine, amphetamines, ephedrine)
  • Arteritis
  • Coronary anomalies
  • Infected cardiac valve through a patent foramen ovale (PFO)
  • Significant gastrointestinal bleeding
  • Factors increasing oxygen requirement, such as heavy exertion, fever, or hyperthyroidism
  • Factors decreasing oxygen delivery, such as hypoxemia of severe anemia
  • Aortic dissection, with retrograde involvement of the coronary arteries.
Clinical features

Symptoms

  1. Prolonged cardiac pain in chest, throat, arms, epigastrium or back
  2. Nausea and vomiting
  3. Anxiety and fear of impending death
  4. Breathlessness
  5. Collapse or syncope.
Physical signs
  1. Signs of sympathetic activation: pallor, tachycardia, sweating
  2. Signs of vagal activation: vomiting, bradycardia
  3. Signs of impaired myocardial function:
  4. Hypotension, cold peripheries, oliguria
  5. Narrow pulse pressure
  6. Raised JVP
  7. Diffuse apical impulse
  8. Quiet first heart sound
  9. Third heart sound
  10. Lung crepitations
  11. Signs of tissue damage: fever
  12. Signs of complications: e.g. mitral regurgitation, pericarditis.
Investigations

Electrocardiography

Typical ECG changes in ST- segment elevation MI (STEMI):

Infarct site
Leads showing ST elevation
Anterior:

Small
V3–V4
Extensive
V2–V5
Anterolateral
V4–V6, I, AVL
Anteroseptal
V1–V3
Lateral
I, AVL
Inferior
II, III, AVF
Posterior
V1, V2 (reciprocal)
Right ventricle
VR4
Subendocardial
Any lead
 In NSTEMI (Non- ST segment elevation MI) the ST segment is not elevated, but ST depression and T inversion are seen in ECG.

Laboratory studies
  1. Cardiac biomarkers/enzymes:
    • The most sensitive markers of myocardial cell damage are the cardiac troponins T and I, which are released within 4–6 hours and remain elevated for up to 2 weeks.
    • Creatine kinase (CK) levels: CK-MB levels increase within 3-12 hours of the onset of chest pain, reach peak values within 24 hours, and return to baseline after 48-72 hours
    • Myoglobin levels: Myoglobin is released more rapidly from infarcted myocardium than is troponin; urine myoglobin levels rise within 1-4 hours from the onset of chest pain
    • The elevation of these markers is often mild in NSTEMI compared with STEMI. 
  2. Complete blood count- A leucocytosis is usual, reaching a peak on the first day. The erythrocyte sedimentation rate (ESR) is also elevated.
  3. Chemistry profile
  4. Lipid profile - usually reveals dyslipidemia
  5. C-reactive protein and other inflammation markers – elevated.
Chest X-ray

It may demonstrate pulmonary oedema. The heart size is often normal but there may be cardiomegaly due to pre-existing myocardial damage.

Echocardiography

It is useful for assessing ventricular function and for detecting important complications, such as mural thrombus, cardiac rupture, ventricular septal defect, mitral regurgitation and pericardial effusion. 

Diagnosis

Criteria for acute Myocardial infarction (MI):

Acute MI should be said when there is evidence of myocardial necrosis in a clinical setting which is consistent with acute myocardial ischaemia. Under these conditions, any one of the following criteria meets the diagnosis for MI:
  1. Detection of an increase and/or decrease of cardiac biomarker values (preferably cardiac troponin (cTn)), with at least one value above the 99th centile upper reference limit (URL) and with at least one of the following:
    • Symptoms of ischaemia
    • New or presumed new significant ST segment–T wave (ST–T) changes or new left bundle branch block (LBBB)
    • Development of pathological Q waves in ECG
    • Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality
    • Detection of an intracoronary thrombus by angiography or post-mortem
  2. Cardiac death with symptoms suggestive of myocardial ischaemia and presumed new ischaemic ECG changes or new LBBB, but death occurred before cardiac biomarkers were obtained, or before cardiac biomarker values would be increased
  3. Percutaneous coronary intervention (PCI)-related MI is arbitrarily defined by elevation of cTn values (> 5 × 99th centile URL) in patients with normal baseline values (≤ 99th centile URL) or a rise of cTn values > 20% if the baseline values are increased and are stable or decreasing. In addition, either (i) symptoms suggestive of myocardial ischaemia, or (ii) new ischaemic ECG changes, or (iii) angiographic findings consistent with a procedural complication, or (iv) imaging demonstration of new loss of viable myocardium or new regional wall motion abnormality are required
  4. Stent thrombosis associated with MI when identified by coronary angiography or post-mortem in the setting of myocardial ischaemia and with a rise and/or fall of cardiac biomarker values with at least one value above the 99th centile URL
  5. Coronary artery bypass grafting (CABG)-related MI is arbitrarily defined by increasing of cardiac biomarker values (> 10 × 99th centile URL) in patients with normal baseline cTn values (≤ 99th centile URL). In addition, either (i) new pathological Q waves or new LBBB, or (ii) angiographic documented new graft or new native coronary artery occlusion, or (iii) imaging evidence of new loss of viable myocardium or new regional wall motion abnormality. 
D/D: 
  • Acute Aortic Dissection
  • Unstable Angina
  • Acute Pericarditis
  • Anxiety Disorders
  • Aortic Regurgitation
  • Cardiogenic Shock
  • Esophageal Spasm
  • Gastroesophageal Reflux Disease
  • Heart Arrhythmias
  • Infective Endocarditis
  • Myocarditis
  • Pulmonary Embolism 
Management
  1. Early medical management
Accident and emergency
    • 150–300 mg chewed and 300 mg oral gel 
    • Sublingual glyceryl trinitrate 0.3–1 mg. Repeatation as per need 
Caution:
Main adverse effects of glyceryl trinitrate – dizziness, headache, feeling light-headed, low blood pressure.
    • Oxygen through nasal cannula 2–4 L/min if hypoxia is present
    • Brief history to detect risk factors.
    • Physical examination
    • Intravenous (IV) access & blood for markers (plus FBC, biochemistry, lipids, glucose)
    • 12-lead ECG
    • Intravenous opiate, e.g. diamorphine (or morphine) 2.5–5 mg + antiemetic, e.g. metoclopramide 10 mg 
Caution:
Main adverse effects of diamorphine – drowsiness and mental clouding, sedation, nausea and vomiting and sweating. 
    • The American Heart Association (AHA) recommends starting of beta blockers to all patients with STEMI (unless beta blockers are contraindicated) 
    • If primary PCI is available, administration of GP IIb/IIIa inhibitor. Alternatively, thrombolysis.
Percutaneous coronary intervention (PCI)

PCI is performed by passing a fine guide wire across a coronary stenosis under radiographic control and using it to position a balloon, which is then inflated to dilate the stenosis.

Fibrinolysis 

Double bolus r-PA (reteplase) and single bolus TNK-t-PA (tenecteplase) facilitate rapid administration of fibrinolytic therapy and can be used for pre-hospital thrombolysis. 

Caution:

Main adverse effects of reteplase and tenecteplase - abnormally low blood pressure, bleeding from the genitourinary system, bleeding from the respiratory tract, bleeding of the stomach or intestines. 
    • Patients presenting with no ST-segment elevation should receive anti-ischemic therapy and may be candidates for PCI urgently or during admission and are not candidates for immediate administration of thrombolytic agents.
Coronary artery bypass surgery
Internal mammary arteries, radial arteries or reversed segments of the patient’s own saphenous vein can be used to bypass coronary artery stenosis.
  1. Late management:
  1. Risk stratification and further investigation
  2. Lifestyle modification
    • Increase in physical activity to prevent or control ischemic heart disease
    • Cessation of smoking
    • Regular exercise( at least 30 – 45 minutes of moderate intensity physical activity like walking, jogging, cycling or swimming on most days of the week),
    • Avoiding extra salt
    • No alcohol consumption
    • Controlling body weight.
  3. Dietary modification:
    • Decrease in intake of saturated fat, polyunsaturated fat and trans fatty acids and therefore decrease in intake of butter, fatty meats, margarine, dairy products made from 2% or whole milk.
    • Using oils containing monounsaturated fatty acids and n-3 fatty acids (e.g., canola and olive oil).
    • Eating monounsaturated-rich nuts in moderation.
    • Eating at least five to seven servings of vegetables and fruits daily.
    • Eating soy products and legumes daily.
    • Eating garlic regularly.
    • Increasing intake of soluble fiber (Present in Apples, Barley, Citrus fruits, Strawberries, Carrots, Guar, Legumes).
  4. Secondary prevention
            Drug therapy -
    • Antiplatelet therapy (aspirin and/or clopidogrel)
    • β-blocker
    • ACE inhibitor / ARB (Angiotensin Receptor Blocker) 
Caution:
Significant adverse effects of ACE inhibitor – persistent dry cough.
    • Statins, e.g. , lovastatin, fluvastatin, pitavastatin, pravastatin, simvastatin and rosuvastatin
Caution:
 Adverse effects of statins – muscle pain, digestive problems, liver damage, rash or flushing, neurological side effects, increased blood sugar] 
    • Additional therapy for control of diabetes and hypertension
    • Mineralocorticoid receptor antagonists, g., spironolactone, eplerenone
  1. Rehabilitation
  2. Devices - Implantable cardiac defibrillator (high-risk patients).
Prognosis
  • In about one-quarter of all cases of MI, death occurs within a few minutes without medical care. Half of the deaths occur within 24 hours of the onset of symptoms and about 40% of all affected patients die within the first month. 
  • The prognosis of those who survive to get to hospital is much better, with a 28-day survival of more than 85%. Late outcomes are determined by the extent of myocardial damage, and unfavourable features include poor left ventricular function, AV block and persistent ventricular arrhythmias. 
  • The prognosis is worse for anterior than for inferior infarcts. Bundle branch block and high cardiac marker levels both indicate extensive myocardial damage. Of those who survive an acute attack, more than 80% live for a further year, about 75% for 5 years, 50% for 10 years and 25% for 20 years. 
Complications: 
  1. Heart failure
  2. Myocardial rupture and aneurysmal dilatation
  3. Ventricular septal defect (VSD)
  4. Mitral regurgitation
  5. Cardiac arrhythmias
    1. Ventricular fibrillation
    2. Ventricular tachycardia
    3. Accelerated idioventricular rhythm
    4. Ventricular ectopics
    5. Atrial fibrillation
    6. Atrial tachycardia
    7. Sinus bradycardia (particularly after inferior MI)
    8. Atrioventricular block
  6. Conduction disturbances
  7. Post-MI pericarditis and Dressler’s syndrome.
Further reading
  • Harrison's Principles of Internal Medicine, 19th edition
  • Davidson's Principles and Practice of Medicine, 22nd Edition
  • Kumar and Clark's Clinical Medicine, 8th Edition
  • Current Medical Diagnosis & Treatment, 53rd edition.

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