STEMI is a shorthand medical term for ST-segment elevation myocardial infarction. It is one type of heart attack that can be defined as a development of full thickness cardiac muscle damage resulting from an acute interruption of blood supply to a part of the heart and can be demonstrated by ECG (electrocardiography) change of ST-segment elevation.
Here, ST-segment elevation appears in ECG due to full thickness damage of cardiac muscle. Therefore, STEMI is more severe type of myocardial infarction compared to NSTEMI (non-ST segment elevation myocardial infarction) in which partial thickness damage of heart muscle develops.
STEMI usually develops by formation of an occlusive thrombus (blood clot) in a major coronary artery previously affected by atherosclerosis. Cholesterol deposition within 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. Atherosclerotic plaque formation is a long term process, required many years to establish. Sometimes this plaque may rupture or erode, and can trigger platelet aggregation and fibrin deposition, which lead to formation of an occlusive thrombus in a coronary artery. This occlusive thrombus completely block a coronary artery and interrupts blood supply to part of the myocardium (heart muscle), profound changes take place in the myocardium that lead to irreversible changes and death of myocardial cells, and ultimately ST-segment elevation myocardial infarction develops.
Chest pain: Chest pain is the cardinal symptom of STEMI. Pain is often described by patients as a tightness, heaviness or constriction in the chest. It is usually located in the center 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.
Breathing difficulty: Sometimes breathing difficulty develops due to left ventricular dysfunction or dynamic mitral regurgitation.
Profuse sweating, nausea and vomiting may occur due to nervous 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.
Cardiogenic 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:
The typical ECG findings of STEMI are ST-segment elevation with pathological Q-wave formation. Sometimes T-wave inversion may be found but it is a non-specific feature. ST-segment elevation indicates full thickness cardiac muscle injury, pathological Q-wave indicates muscle necrosis and T-wave inversion indicates muscle ischemia.
Troponin T and troponin I, and CK-MB (creatine kinase myocardial band) are rises in blood in STEMI. Troponin T and troponin I start to rise at 4-6 hours and remain high for up to two weeks. CK-MB starts to rise at 4-6 hours and falls to normal within 48-72 hours. Cardiac markers should rise above two times the upper limit of the reference range.
Full blood count:
Elevation of White blood cell (WBC) count is usual. Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) may elevate.
It is done for assessing pulmonary edema.
Immediate echocardiography is not essential, but is helpful if the ECG cannot evaluate the diagnosis of STEMI. A regional wall motion defect is found in infarct area of the heart. It also can assess ventricular function and can detect important complications.
According to wall of cardiac muscle involvement, STEMI may be different types. To read about specific type click on the link below.
It refers to infarction of the anterior wall of left ventricle. It occurs by occluding the left anterior descending artery (LAD) branch of left coronary artery. ECG findings are ST-segment elevation in lead V1 – V6 with reciprocal ST-segment depression in inferior leads (II, III and aVF). Anterior STEMI carries bad prognosis due to large territory infarction.
It develops when anteroseptal wall (area between the left and right ventricles) is damaged due to occlusion of septal branches of left anterior descending artery (LAD). ECG features are ST-segment elevation in lead V1 – V4 with reciprocal ST-segment depression in inferior leads (II, III and aVF).
It refers to infarction of the lateral wall of left ventricle. It is due to blockage of the first diagonal branch of the left anterior descending artery (LAD) and the obtuse marginal branch of the left circumflex artery (LCX). ECG changes are ST-segment elevation in lead I, aVL, V5 and V6 with reciprocal ST-segment depression in inferior leads (II, III and aVF).
High lateral STEMI
It occurs when the superior portion of the lateral wall of left the ventricle, supplied by first diagonal branch of the left anterior descending artery (LAD) is occluded by a thrombus. ECG changes are ST-segment elevation in leads I and aVL with reciprocal ST-segment depression in inferior leads (II, III and aVF).
It refers to infarction of the anterior and lateral wall of the left ventricle. It is due to occlusions of the proximal left anterior descending artery (LAD) or combined occlusions of the left anterior descending artery (LAD) and the left circumflex artery (LCX). ECG changes are ST-segment elevation in leads I, aVL, V4 – V6 with reciprocal ST-segment depression in inferior leads (II, III and aVF).
It occurs when the inferior wall of left ventricle is infarcted by blocking of the right coronary artery (RCA). ECG findings are ST-segment elevation in leads II, III and aVF, with reciprocal ST-segment depression in leads I and aVL. In general, inferior STEMI has a good prognosis. Approximately 40% of patients with inferior STEMI have a concomitant right ventricular (RV) infarction. These patients may develop severe hypotension or cardiogenic shock and generally have a bad prognosis. Sometimes inferior STEMI may associate with a posterior STEMI. These patients also have a bad prognosis.
A posterior STEMI occurs when the posterior area of the left ventricle, usually supplied by posterior descending artery (a branch of right coronary artery in 80% cases) is occluded by a thrombus. Isolated posterior STEMI is rare. The majority of cases it occurs with inferior STEMI or lateral STEMI. Posterior area of the left ventricle is not directly visualized by the standard 12-lead ECG. For this reason, typical ECG changes are not seen in a posterior STEMI. In standard 12-lead ECG, it may shows tall R wave with ST-segment depression in lead V1 – V4. The ST-segment depressions in lead V1 – V4 can be observed as mirrored ST-segment elevations and the tall R waves are the Q waves. Posterior STEMI is confirmed in 15 leads ECG by the presence of ST-segment elevation in leads V7 – V9 (posterior leads). Leads V7 – V9 are placed on the posterior chest wall (V7 on the left posterior axillary line, V8 on the tip of left scapula and V9 on the left paraspinal region; all are placed in the same horizontal plane as V6).
RV (right ventricular) infarction
Isolated RV infarction is uncommon. It occurs with inferior STEMI. In ECG, it may show ST-segment elevation in lead V1 (lead V1 looks directly at the right ventricle). RV infarction is confirmed by the presence of ST-segment elevation in the right sided chest leads (V3 R– V6 R). The most sensitive lead is V4 R. Leads placement are V1 and V2 to their usual position, and V3 – V6 to the right side of chest in a mirror-image position of the left side of chest. Patients with RV infarction may present with severe hypotension or cardiogenic shock due to poor right ventricular contraction. This hypotension or shock is treated with fluid loading (usually normal saline).
Both early and late complications may occur in STEMI.
These develop within one week. Early complications of STEMI are as followings:
Arrhythmias are disturbance of the electrical rhythm of the heart in which heartbeat may be too fast, too slow or irregular. In most of cases arrhythmias are mild and transient. But, life threatening arrhythmias may develop that are the major cause of death during the first 24 hours after an attack. Arrhythmias that may develop in STEMI are ventricular fibrillation, ventricular tachycardia, ventricular ectopics, accelerated idioventricular rhythm, atrial fibrillation, atrial tachycardia, atrioventricular block and sinus bradicardia.
Acute heart failure
It may occur due to left ventricular dysfunction.
It is due to extensive left ventricular damage.
Pericarditis develops on second or third days after attack. Patient may feel a different type of chest pain that tends to be worse or sometimes only feel on inspiration.
The endocardial surface (inner surface) of infarcted heart muscle is rough that may triggers platelet aggregation and often forms thrombus. This thrombus may dislodged from heart and may cause stroke (if reach in the brain) or ischemic limb (if reach in the limb).
It is due to tear or rupture of infarcted heart muscle. It includes-
- Severe mitral regurgitation – it is due to rupture of papillary muscle.
- Cardiac tamponate – it is due to rupture of ventricle.
- Right heart failure – it is due to rupture of interventricular septum.
These develop after one week of attack and include:
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 (pain killer), high dose aspirin or even corticosteroids.
Left ventricular aneurysm
Aneurysm means abnormal dilatation. In STEMI, aneurysm may develop in left ventricular wall due to full thickness cardiac muscle damage in which infarcted heart muscle may dilate and moves paradoxically during systole (when heart pump). Left ventricular aneurysm can be minimized by early use of ACE inhibitor and beta-blocker.
It develops gradually over time after an attack in which the heart muscle cannot pump enough blood to meet the body’s demand.
STEMI is more serious form of heart attack. Therefore, patients need immediate hospitalization, preferably to a cardiac care unit.
(1) Complete bed rest with continuous monitoring by ECG.
(2) Inhaled high flow oxygen therapy.
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 STEMI 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.
(4) Relief of pain by opiate analgegic
Intravenous morphine 10 mg or diamorphine 5 mg is usually used along with anti-emetic drug and may have to be repeated to relieve severe pain.
All patients with STEMI should be considered for primary PCI (percutaneous coronary intervention) immediately. It is treatment of choice for ST-segment elevation myocardial infarction. It reduces a significant mortality, infarct size and further infarction. Where PCI is not available or primary PCI cannot be achieved within 120 minutes of diagnosis, thrombolytic therapy should be given.
Drug used for thrombolysis is alteplase, tenecteplase, reteplase, or streptokinase. These drugs break the occlusive thrombus within the coronary artery and clear the arterial lumen. The benefit of thrombolytic therapy is very time dependent. Major benefit is seen in those patients who are present within three hours of onset of chest pain. It may also be given in patients who present within 12 hours of pain. Thrombolytic therapy reduces hospital mortality by 25 to 50% and also reduces infarct size. The survival benefit of thrombolytic therapy is maintained for at least 10 years. The main hazard of this therapy is hemorrhage. Therefore, it should be avoided for patients with active bleeding, previous hemorrhagic stroke or subarachnoid hemorrhage, uncontrolled hypertension, any major surgery within one month, recent major trauma, active peptic ulcer and pregnancy. Among the thrombolytic therapy, tissue plasminogen activators such as alteplase, tenecteplase and reteplase are best. Among the tissue plasminogen activators, tenecteplase have a lower incidence of hemorrhage.
In patients who fail to achieve coronary arterial reperfusion following thrombolytic therapy or thrombolytic therapy is contraindicated, early (within 6 hours of symptom onset) emergency PCI may be considered, particularly who develop cardiogenic shock.
Treatment for maintaining arterial patency:
Further occlusion of coronary artery following reperfusion therapy is common in ST-segment elevation myocardial infarction. Therefore, maintaining arterial patency after successful reperfusion is essential.
(1) Antiplatelet therapy
Aspirin 75 mg daily should be taken indefinitely if there are no side effects occur. In combination of aspirin, clopidogrel 75 mg daily should be given orally. Both aspirin and clopidogrel inhibit platelet aggregation and prevent further occlusion. Ticagrelor 90 mg two times daily may be given instead of clopidegrol. Patients with STEMI who undergo primary PCI, glycoprotein IIb/IIIa receptor blocking drug such as tirofiban, abciximab, or eptifibatide are the best antiplatet drug.
(2) Anticoagulant therapy
In general, anticoagulant therapy is not required after PCI (Glycoprotein IIb/IIIa inhibitor is infused for 18 hours after PCI). Usually, anticoagulant therapy is given for 48 hours following thrombolytic therapy with tissues plasminogen activator because a rebound procoagulant effect may appear following thrombolysis. In contrast, streptokinase has persistant anticoagulant effect for 24-48 hours after administration due to its different pharmacological mechanism. Therefore, anticoagulant therapy following streptokinase has no additional benefits.
If patients with STEMI not treated with PCI or thrombolytic therapy, anticoagulant therapy should be given for 5-8 days. These drugs prevent reinfarction and reduce the risk of thromboembolic complications. Available anticoagulation drugs are unfractionated heparin, fractionated heparin also called low molecular weight 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 a day by subcutaneous injection.
- Dalteparin: 120 units/kg body weight two times a day by subcutaneous injection.
- Fondaparinux: 2.5 mg daily by subcutaneous injection.
In the absence of bradycardia, heart failure, heart block or hypotension, all patients with ST-segment elevation myocardial infarction should be considered for beta-blocker. Beta-blockers reduce arrhythmias, relive pain and further attack. Atenolol 25-50 mg twice daily, bisoprolol 5 mg once daily or metoprolol 25-50 mg twice daily may be given orally. Initially intravenous beta-blocker (atenolol 5-10 mg or metoprolol 5-15 mg over 5 minutes) can be given if heart rate ˃ 90 beats/minute, or systolic blood pressure ˃ 150 mmHg or diastolic ˃ 90 mmHg.
ACE (angiotensin converting enzyme) inhibitors or ARBs (angiotensive receptor blockers):
An ACE inhibitor such as enalapril, ramipril, lisinopril or captopril is started 1 or 2 days after attack. An ACE inhibitor reduces ventricular remodeling, reduce recurrent infarction and prevent the onset of heart failure. An ARB such as valsartan, olmesartan candesartan, or losartan is suitable alternatives in patients who are intolerant of ACE inhibitors.
All patients with STEMI should receive statin such as atorvastatin, simvastatin or rosuvastatin irrespective of their serum cholesterol level.
Nitrate spray may be used sublingually or buccally if patients feel chest pain.
Approximately 25% of patients die within a few minutes after an attack without medical care. The prognosis is much better of those who survive to reach hospital, with a 28-day survival of more than 85%. Of those patients who survive an acute episode, more than 80% survive for 1 year, about 75% for 5 years, 50% for 10 years and 25% for 20 years. The prognosis is better for inferior than anterior STEMI.