Myocardial infarction is a medical term, commonly known as a heart attack that occurs when a portion of the heart muscle (myocardium) is damaged because of sudden occlusion of one of the coronary arteries that supply the oxygen rich blood to the heart muscle.
Pathophysiology of myocardial infarction:
An acute myocardial infarction occurs by developing a thrombus also called blood clot in a coronary artery previously affected by atherosclerosis. Cholesterol deposition in the wall of the artery is the main mechanism of atherosclerosis. This deposited cholesterol ultimately forms a plaque in the wall of the artery called atherosclerotic plaque. Many years are required to establish a plaque. Sometimes atherosclerotic plaque may rupture or erode and can trigger clotting mechanism in the blood to form a blood clot. This blood clot impaired blood flow to heart muscle lasts long enough to damage myocardial cells.
Types of myocardial infarction:
Myocardial infarction is classified into two types;
ST-segment elevation myocardial infarction (STEMI):
It occurs by complete occlusion of a major coronary artery that produces an entire thickness damage of heart muscle. STEMI is also called transmural infarction due to its full thickness involvement. This entire thickness damage of heart muscle produces an ECG (electrocardiography) change of ST-segment elevation. It can be sub classified into anterior, antero-septal, posterior, inferior, lateral, high lateral or antero- lateral myocardial infarction (according to left ventricular wall damage), and RV type (according to right ventricular wall damage).
Non ST-segment elevation myocardial infarction (NSTEMI):
NSTEMI is usually due to complete occlusion of a minor coronary artery or partial occlusion of a major coronary artery that produces a partial thickness damage of heart muscle. Here, the damage of heart muscle is confined to the inner ⅓ rd – ⅔ rd of the left ventricular wall. For this reason, it is also called subendocardial infarction. ST-segment elevation in ECG is not developed in this myocardial infarction because of partial thickness damage of heart muscle. Here, this muscle damage is demonstrated by an elevation of cardiac markers (CK-MB or Troponin) in the blood.
Symptoms of myocardial infarction:
Chest pain: Chest pain is the cardinal symptom of acute myocardial infarction. Pain is constricting, choking, squeezing or heavy in character, develops gradually over several minutes, usually located in the center of the chest, but may radiate to neck, jaw, shoulder, back, and arms (most commonly left arm). Occasionally, pain may be felt only at the sites of radiation. In older patient patients or those with diabetes mellitus, painless myocardial infarction may occur (also called silent myocardial infarction). Pain conducting nerve fiber is degenerated (autonomic neuropathy) in old age and in diabetes.
Shortness of breath: It may develop due to ischemic left ventricular dysfunction or dynamic mitral regurgitation.
Nausea, vomiting, and sweating: Due to upset of autonomic nervous system.
Syncope (sudden loss of consciousness): Sometimes patients may present with syncope, usually due to an arrhythmia or severe hypotension.
Tachycardia (high pulse rate): Due to sympathetic nerve activation.
Bradycardia (low pulse rate): Patients with inferior myocardial infarction may present with bradycardia due to vagus nerve activation.
Cardiogenic shock: Some patients may present with shock due to impaired myocardial function.
Diagnosis of myocardial infarction:
Many people develop chest pain that is not due to a myocardial infarction. Therefore, tests are usually done to confirm the diagnosis of a myocardial infarction. These are:
ECG findings of STEMI are ST-segment elevation, pathological Q-wave formation and T-wave inversion. ST-segment elevation must be greater than 2 mm in chest leads (v1 – v6) or greater than 1 mm in limb leads (I, II, III, aVL and aVF). A new onset left bundle branch block (LBBB) in ECG is also considered as ST-segment elevation myocardial infarction. NSTEMI is usually associated with ST-segment depression or T-wave inversion in ECG.
(2) Cardiac markers
Cardiospecific isoenzyme CK-MB (creatine kinase myocardial band), and cardiospecific proteins troponin T and troponin I are rises in acute myocardial infarction. CK-MB starts to rise at 4-6 hours and falls to normal within 48-72 hours. Troponin T and troponin I start to rise at 4-6 hours and remain high for up to two weeks.
(3) Full blood count
Elevation of WBC count is usual. Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) may elevate.
(4) Chest X-ray
It is done to assess for signs of lung edema.
Regional ventricular wall motion abnormalities on an echocardiogram are also suggestive of a myocardial infarction. It also assesses ventricular function and detects important complications.
Early complications of myocardial infarction :
Early complications of myocardial infarction are as followings:
(A) Arrhythmias: Many patients with myocardial infarction may develop following form of arrhythmia:
- Ventricular fibrillation
- Ventricular tachycardia
- Ventricular ectopics
- Accelerated idioventricular rhythm
- Atrial fibrillation
- Atrial tachycardia
- Atrioventricular block
- Sinus bradicardia
In majority of cases arrhythmia is transient. Rest, pain relief and correction of hypokalaemia may prevent them.
(B) Left ventricular failure: It is due to extensive myocardial infarction.
(C) Cardiogenic shock: It is due to left ventricular dysfunction.
(D) Percarditis – pericarditis develop on the second or third days after myocardial infarction. Patient may feel a different type of pain that tends to be worse or sometimes only feel on inspiration.
(E) Embolism: On the endocardial surface of infarcted heart muscle, thrombus often forms. This thrombus may lodge and lead to development of systemic embolism that occationally causes stroke or ischemic limp.
(F) Mitral regurgitation – it is due to papillary muscle infarction.
Late complications myocardial infarction:
(1) Post MI syndrome (Dressler’s syndrome): It usually occurs 1-3 weeks after myocardial infarction, and is characterized by fever, pericarditis and pleuritis, and is probably due to myocardial antigens released after infarction. Management is with NSAIDs, high dose aspirin or even corticosteroids.
(2) Left ventricular aneurysm: In myocardial infarction, part of the infarcted area of ventricle becomes dilate and moves paradoxically during systole. Ventricular aneurysm can be minimized by use of ACE inhibitor and beta-blocker.
Treatment of myocardial infarction:
A myocardial infarction requires immediate hospitalization and medical attention.
(1) Complete bed rest with continuous monitoring by ECG.
(2) Inhaled oxygen therapy.
(3) Aspirin and clopidogrel
A 300 mg tablet of aspirin is given orally as early as possible. It can be given intravenously to patients who cannot swallow or who are unconscious. Aspirin reduces the mortality rate of myocardial infarction by approximately 25%. In combination of aspirin, clopidogrel 300 mg should be given orally as early as possible. Small mortality benefit is seen in combination of aspirin and clopidogrel. Ticagrelor 150 mg orally may be given instead of clopidogrel. Aspirin, clopidogrel and ticagrelor all are antiplatelet drugs that prevent the aggregation of platelets within the blood vessels.
(4) Pain relief
Nitrate and opiate analgegic are used to relief pain. Nitrate act as a vasodilator and relief pain. Nitrate should first be given buccally or by sublingual (under tongue) spray. If the patient experiencing persistent ischemic chest pain after 3 doses given 5 minutes apart, then intravenous glyceryl trinitrate 0.6-1.2 mg/hour or isosorbide dinitrate 1-2 mg/hour can be given until pain relieved or systolic blood pressure falls to less than 100 mgHg. Intravenous opiate analgegic such as morphine 10 mg or diamorphine 5 mg is usually used for severe pain and may have to be repeated.
Treatment to restore blood supply in the occluded coronary artery (re-perfusion therapy):
The part of the heart muscle does not die immediately after occlusion of coronary artery. If blood supply is restored within a few hours, much of the affected area of the heart muscle will be saved from damaging. There are two therapies that can restore blood supply back through the occluded coronary artery:
(1) Primary percutaneous coronary intervention (PCI):
It is treatment of choice for ST-segment elevation myocardial infarction. It should be done within 120 minutes of symptoms starting. Where PCI is not available or primary PCI cannot be achieved within 120 minutes of diagnosis, thrombolytic therapy should be administered.
On the other hand, medium to high risk patients with non-ST segment elevation myocardial infarction should be considered for early coronary angiography and revascularization, either by PCI (percutaneous coronary intervention) or by CABG (coronary artery bypass grafting). Early medical treatment is appropriate in low risk patients, and coronary angiography and revascularization reserved for those who fail to settle with medical treatment. (By using grace score or timi score, patients with non-ST segment elevation myocardial infarction can be categorized into low, medium or high risk group).
(2) Thrombolytic therapy:
It is only indicated for ST-segment elevation myocardial infarction. It is also called clot-busting drug. Available clot-busting drugs are streptokinase, alteplase, tenecteplase and reteplase. These drugs break the blood clot within the coronary artery and clear lumen. It should be given within three hours of onset of chest pain but may be given in patients who present within 12 hours of pain. After 12 hours, thrombolytic therapy appears to be a little benefit and may be harmful. In non-ST segment elevation myocardial infarction, this therapy is totally harmful and should be avoided.
Aspirin 75 mg daily should be given indefinitely if there are no side effects occur. Clopidogrel 75 mg daily should be given orally in combination of aspirin. Both drugs inhibit platelet aggregation and prevent further occlusion. Ticagrelor 90 mg two times daily may be given instead of clopidegrol. Ticagrelor is more effective than clopidegrol. Patients who undergo percutaneous coronary intervention, glycoprotein IIb/IIIa receptor blocking drug such as tirofiban, abciximab, or eptifibatide are the best antiplatet drug.
Anticoagulant therapy is recommended in patients not receiving reperfusion therapy. This therapy prevents reinfarction, and reduces the risk of thromboembolic complications. Anticoagulation can be achieved by using unfractionated heparin, low molecular weight heparin or fractionated heparin (enoxaparin, dalteparin), or a pentasaccharide (fondaparinux). Comparatively low molecular weight heparin is more safety and efficacious than unfractionated heparin, and pentasaccharide is more safety and efficacious than low molecular weight heparin. The dose regimens are:
- Enoxaparin: 1 mg/kg body weight two times daily usually for 8 days by subcutaneous injection.
- Dalteparin: 120 units/kg body weight two times daily usually for 8 days by subcutaneous injection.
- Fondaparinux: 2.5 mg daily usually for 8 days by subcutaneous injection.
Beta-blocker diminishes myocardial oxygen demand by reducing heart rate, blood pressure and myocardial contractility, and reduces chest pain and ventricular arrhythmias. Reduction in heart rate prolongs the diastolic period of the heart and may augment blood flow to the heart muscle. In patients not receiving thrombolytic therapy, early beta-blocker reduces in infarct size and mortality rate. In patients receiving thrombolytic therapy, recent trials have not found a mortality rate reduction, although recurrent ischemia and re-infarction rates were reduced. Oral beta-blocker atenolol 25-50 mg twice daily, metoprolol25-50 mg twice daily, or bisoprolol 5 mg once daily are usually adequate. Beta-blockers should be avoided if there is heart failure, heart block, hypotension, or bradycardia.
Oral or sublingual nitrate can be used if patients feel chest pain.
Irrespective of serum cholesterol level, all patients should receive statin such as atorvastatin, rosuvastatin, simvastatin or pitavastatin.
ACE (angiotensin converting enzyme) inhibitor or ARB (angiotensive receptor blocker):
An ACE inhibitor such as ramipril, enalapril, captopril, or lisinopril is started 1 or 2 days after myocardial infarction. ACE inhibitor therapy reduces ventricular remodeling, prevent the onset of heart failure, and reduce recurrent infarction. An ARB (valsartan, candesartan, losartan or olmesartan) is suitable alternative in patients intolerant of ACE inhibitor.
- Restrict physical activities for four to six weeks – Death tissue of infarct area in heart muscle takes 4-6 weeks to be replaced with fibrous tissue.
- Cessation of cigarette smoking.
- Maintaining an ideal body weight.
- Eating a Mediterranean style diet (diet rich in monounsaturated fatty acids and omega-3 fatty acids, but low in saturated fatty acids).
- Achieving well control of high pressure and diabetes mellitus.
- Taking regular exercise up to, but not beyond, the point of chest discomfort.
- Continue secondary prevention drugs therapy including aspirin, clopidogrel, beta-blocker, ACE inhibitor, and statin.