STEMI (ST-segment elevation myocardial infarction) is one type of heart attack. It is defined as the development of cardiac muscle necrosis results from an acute interruption of blood supply to a part of the heart that is demonstrated by the presence of ST-segment elevation in electrocardiography (ECG) and an elevation of cardiac markers (CK-MB or Troponin) in the blood. Presence of ST-segment elevation in ECG indicates full thickness damage of heart muscle occur in this type of myocardial infarction. For this reason, STEMI is more severe heart attack compared to NSTEMI (non-ST segment elevation myocardial infarction) where partial thickness damage of heart muscle occurs.


STEMI usually develops by formation of an occlusive thrombus in a coronary artery previously affected by atherosclerosis. The most common cause is rupture or erosion of an atherosclerotic plaque that triggers platelet aggregation and fibrin deposition, which lead to formation of an occlusive thrombus in a coronary artery at the site of the atherosclerotic plaque. This arterial occlusion causes interruption of blood supply to part of the myocardium (heart muscle), profound changes take place in the myocardium (heart muscle) that lead to irreversible changes and death of myocardial cells, and as a result STEMI develops.

Clinical symptoms and signs:

Chest pain: Chest pain is the cardinal symptom of STEMI. Pain is constricting, dull, choking or heavy in character, usually located in the centre of the chest, but may radiate to neck, jaw, shoulder, back, and arms (most commonly left arms). Occasionally, pain may be felt only at the sites of radiation.
Difficulty in respiration: Sometimes breathing difficulty develops due to ischemic left ventricular dysfunction or dynamic mitral regurgitation.

Nausea, vomiting, and sweating: Due to autonomic upset.

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 STEMI may present with bradycardia due to vagus nerve activation.

Shock: Some patients may present with shock due to impaired myocardial function.


Diagnosis of STEMI is done by clinical symptoms and signs with following investigations:

Electrocardiography (ECG): ECG finding of STEMI is usually associated with ST-segment elevation, pathological Q-wave formation and T-wave inversion.

Cardiac markers: Cardiospecific isoenzyme CK-MB (creatine kinase myocardial band), and cardiospecific proteins troponin T and troponin I are rises in STEMI. 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.

Full blood count: Elevation of WBC count is usual. Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) may elevate.

Chest X-ray: Assess for signs of lung edema.

Echocardiography : It is done for assessing ventricular function and for detecting important complications.

Early complications:

Early complications of STEMI are as followings:

(A) Arrhythmias: Many patients with STEMI may develop following form of arrhythmia:

  1. Ventricular fibrillation
  2. Ventricular tachycardia
  3. Ventricular ectopics
  4. Accelerated idioventricular rhythm
  5. Atrial fibrillation
  6. Atrial tachycardia
  7. Atrioventricular block
  8. 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 STEMI. 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 infracted heart muscle, thrombus often forms. This thrombus may lodge and lead to development of systemic embolism that occationally causes stroke or ischemic limp.

(F) Mechanical complications: It is due to tear or rupture of part of infarct area of heart muscle.

  1. Severe mitral regurgitation – it is due to rupture of papillary muscle.
  2. Cardiac tamponate – it is due to rupture of ventricle.
  3. Right heart failure – it is due to rupture of interventricular septum.

Late complications:

  1. Post MI syndrome (Dressler’s syndrome): It usually occurs 1-3 weeks after STEMI, 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 STEMI, part of the infracted area of ventricle becomes dilate and moves paradoxically during systole. Ventricular aneurysm can be minimized by use of ACE inhibitor and beta-blocker.


Patients should be admitted immediately to hospital, preferably to a cardiac care unit because there is a significant risk of death.

(1) Bed rest with continuous monitoring by ECG.

(2) Inhaled oxygen therapy.

(3) Relief of pain by opiate analgegic: Intravenous morphine 10 mg or diamorphine 5 mg is usually used and may have to be repeated to relieve severe pain.

(4) Antiplatelet therapy: Antiplatelet drugs prevent platelet aggregation within coronary artery. A 300 mg tablet of aspirin should be given orally as early as possible then 75 mg daily should be continued indefinitely if there are no side effects occur. Aspirin reduces the mortality rate of STEMI by approximately 25%. In combination of aspirin, clopidogrel 600 mg should be given orally as early as possible, followed by 150 mg daily for 7 days and 75 mg daily thereafter, gives a further reduction in mortality. Ticagrelor 150 mg followed by 90 mg two times daily is more effective than clopidegrol. High risk patients, especially patients with diabetes mellitus or patients who undergo percutaneous coronary intervention (PCI), should also be considered for intake of glycoprotein IIb/IIIa receptor blocker (block the final common pathway of platelet aggregation), such as tirofiban, abciximab, or eptifibatide.

(5) Anticoagulant therapy: Anticoagulant drugs prevent 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:

  1. Enoxaparin: 1 mg/kg body weight two times daily usually for 8 days by subcutaneous injection.
  2. Dalteparin: 120 units/kg body weight two times daily usually for 8 days by subcutaneous injection.
  3. Fondaparinux: 2.5 mg daily usually for 8 days by subcutaneous injection.

(6) Beta-blockers: Beta-blockers reduce arrhythmias, heart rate, blood pressure and myocardial oxygen demand, and relive pain. Oral beta-blocker atenolol 25-50 mg twice daily, metoprolol 25-50 mg twice daily, or bisoprolol 5 mg once daily are usually adequate. Patients with heart rate more than 90 beats/minute or patients with hypertension (systolic blood pressure more than 150 mmHg or diastolic more than 90 mmHg), intravenous beta-blockers (atenolol 5-10 mg or metoprolol 5-15 mg over 5 minutes) can be given. Beta-blockers should be avoided if there is heart failure, heart block, hypotension, or bradycardia.

(7) Nitrates: Nitrates act as a vasodilator and relief pain. Nitrates 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. Oral or sublingual nitrates can be used once the pain has resolved.

(8) Statins: Irrespective of serum cholesterol level, all patients should receive statin such as atorvastatin, simvastatin, or rosuvastatin after STEMI.

(9) ACE (angiotensin converting enzyme) inhibitors or ARBs (angiotensive receptor blockers): An ACE inhibitor such as ramipril, enalapril, captopril, or lisinopril is started 1 or 2 days after STEMI. ACE inhibitor therapy reduces ventricular remodeling, prevent the onset of heart failure, and reduce recurrent infarction. ARBs (valsartan, candesartan, losartan, olmesartan etc.) are suitable alternatives in patients with STEMI intolerant of ACE inhibitors.

(10) Reperfusion therapy: All patients with STEMI should be considered for primary PCI (percutaneous coronary intervention). Where PCI is not available or primary PCI cannot be achieved within 120 minutes of diagnosis, thrombolytic therapy such as alteplase, tenecteplase, reteplase,or streptokinase should be administered.

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