What Is an ST Elevation Myocardial Infarction?

ST-segment elevation myocardial infarction (STEMI) refers to a type of acute ischemic chest pain that lasts for more than 20 minutes. Serum myocardial necrosis markers increase in concentration and evolve dynamically. Myocardial infarction.

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Niu Hongxia

job title

Deputy Chief Physician

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Causes of ST-segment elevation myocardial infarction

The pathological basis of STEMI is the induction of acute occlusive thrombosis based on coronary plaque damage. In most patients with acute myocardial infarction (AMI), thrombus formation on the basis of atherosclerotic plaques can occlude the lumen. Occlusion of the left anterior descending coronary artery occludes the anterior wall of the left ventricle, the apex, the inferior wall, the anterior septum, and the anterior papillary muscle of the mitral valve. Occlusion of the right coronary artery causes the left ventricular diaphragm (when the right coronary artery is dominant), posterior septum, and right ventricular infarction, and can affect the sinoatrial node and the atrioventricular node. Occlusion of the left coronary circumflex branch can cause the left ventricle's high lateral wall, the plantar plane (when the left coronary artery is dominant), and the left atrium infarction, which may affect the atrioventricular node. Occlusion of the left coronary artery caused extensive left ventricular infarction. Right ventricular and left and right atrium infarctions are rare.

Clinical manifestations of ST segment elevation myocardial infarction

Aura

Most patients have fatigue, chest discomfort, and palpitations, shortness of breath, irritability, and angina pectoris during activities a few days before the onset of illness. Among them, new angina pectoris (primary angina pectoris) or exacerbation of angina pectoris (deteriorating angina pectoris) is the most prominent. Angina pectoris is more frequent, more severe, longer lasting, nitroglycerin is less effective, and the inducing factors are not obvious.

2. Symptoms

(1) Pain: This is the first symptom to appear. The location and nature of the pain are the same as those of angina pectoris, but it usually occurs during quietness or sleep. The pain is more severe and has a wider range. The duration can be up to several hours or days. Resting or containing nitroglycerin tablets can not relieve the patient. Patients are often upset, sweating, fearing, and have a sense of dying. Some patients are pain-free, mostly diabetic patients or the elderly, and present with shock or acute heart failure from the beginning; a few patients have no pain or other symptoms during the entire process, and have only found myocardial infarction afterwards.

(2) Systemic symptoms: fever, accompanied by tachycardia, increased white blood cell count, and increased red blood cell sedimentation rate, are caused by the absorption of necrotic substances. It usually appears 24-48 hours after the onset of pain, and the degree is often positively correlated with the infarct range. The body temperature is generally around 38 ° C, rarely exceeding 39 ° C, and lasts for about a week.

(3) Gastrointestinal symptoms: about 1/3 of patients with pain, accompanied by nausea, vomiting, and epigastric pain in the early stages of onset, are related to vagus nerves with necrotic myocardial stimulation and reduced cardiac output, and insufficient tissue perfusion; intestine Flatulence is not uncommon; hiccups can occur in severe cases.

(4) Arrhythmia: seen in 75% -95% of patients, most often within 1-2 weeks after onset, especially within 24 hours.

(5) Hypotension and shock: When pain occurs, it will cause blood pressure to drop, which can last for several weeks before rising, and often cannot return to previous levels. If the pain is relieved and the systolic blood pressure is lower than 80mmHg, the patient is irritable, pale, skin is cold and cold, the pulse is thin and fast, heavy sweating, decreased urine output, mental retardation, and even fainting are manifested in shock.

(6) Heart failure: It is mainly acute left heart failure, which can occur within the first few days after the onset or in the stage of pain and shock improvement. Patients have difficulty breathing, coughing, cyanosis, irritability, etc. In severe cases, pulmonary edema or right heart failure may occur, and jugular vein irritation, hepatomegaly, and edema may occur. Right ventricular myocardial infarction, right heart failure can appear at the beginning.

Examination of ST segment elevation myocardial infarction

Physical sign

Heart signs Heart dullness can be normal or slightly to moderately increased; heart rate increases faster, and a few can slow down; the first heart sound in the apical region weakens; fourth heart sound (atrial) running horse rhythm can occur, a few There is a third heart sound (ventricular) galloping rhythm; a small number of patients appear pericardial friction sounds on the 2nd to 3rd days after onset, which are caused by reactive fibrinous pericarditis; rough systolic murmurs or contractions may appear in the apical area Late Karat, caused by dysfunction or rupture of the mitral papillary muscles; may have various arrhythmias.

Except that blood pressure can increase in very early stages, almost all patients have lower blood pressure. People with hypertension before the onset of blood pressure can drop to normal and may no longer return to the level before the onset of the disease.

2. ECG

The typical early ECG of STEMI manifests as the ST-segment arch is raised upward (in a one-way curve) with or without pathological Q-wave and R-wave reduction (the ST-segment change may not be obvious during a posterior myocardial infarction). The electrocardiogram during the super-acute phase can appear as abnormally tall and two asymmetric T waves. When the first electrocardiogram fails to confirm the diagnosis, it needs to be reviewed after 10 to 30 minutes.

3. Laboratory inspection

(1) Serum enzyme: Determination of serum phosphocreatine kinase (CK or CPK) appeared within 6 hours of onset, peaked at 24 hours, disappeared after 48 to 72 hours, and the positive rate reached 92.7%. Aspartate aminotransferase (AST or GOT) increased 6 to 12 hours after onset, peaked at 24 to 48 hours, and returned to normal after 3 to 6 days. Lactate dehydrogenase (LDH) increased 8 to 12 hours after the onset, peaked in 2 to 3 days, and returned to normal in 1 to 2 weeks. In recent years, -hydroxybutyrate dehydrogenase (-HBDH), -glutamyl phosphotranspeptidase (-GTP), and pyruvate kinase (PK) can also be determined.

(2) Determination of myoglobin: Urinary myoglobin excretion and determination of serum myoglobin content are the most specific and sensitive markers of myocardial injury for the diagnosis of myocardial necrosis. Urinary myoglobin is excreted 5 to 40 hours after infarction, and lasts for an average of 83 hours. The rise of serum myoglobin occurs slightly earlier than the appearance of CK, at about 4 hours, the peak disappears faster than CK, and most of them return to normal within 24 hours.

(3) Other serological tests: Myosin light or heavy chain, serum free fatty acids, all increased after acute myocardial infarction. Patients with significantly increased free fatty acids in serum are prone to severe ventricular arrhythmias. In addition, in acute myocardial infarction, due to the stress response, blood glucose can be increased, glucose tolerance can be temporarily reduced, and it returns to normal after 2 to 3 weeks.

4. Imaging examination

Imaging tests such as echocardiography are helpful for the differential diagnosis and risk stratification of patients with acute chest pain. Symptoms and ECG can clearly diagnose STEMI. Patients do not need to wait for myocardial injury markers and / or imaging results, but should give reperfusion and other related treatments as soon as possible.

Treatment of ST segment elevation myocardial infarction

(A) treatment principles

Restore myocardial blood perfusion as soon as possible to save the dying myocardium, prevent infarction from expanding or reducing the scope of myocardial ischemia, protect and maintain heart function, and deal with severe arrhythmia, heart failure and various complications in time to prevent sudden death.

(Two) reperfusion treatment

Thrombolytic therapy

In hospitals without PCI conditions or when the FMC to PCI time is significantly delayed due to various reasons, intravenous thrombolysis is still a good choice for patients with STEMI who have indications. For patients within 3 hours of onset, the immediate effect of thrombolytic therapy is basically similar to direct PCI. Thrombolytic drugs are recommended to use specific plasminogen activators such as recombinant tissue plasminogen activators alteplase, lanteplase, reteplase, and tenaiplase.

2. Interventional Therapy

Including direct PCI, remedial PCI and post-thrombotic PCI.

Within 12 hours of onset (including posterior posterior wall myocardial infarction) or patients with acute STEMI with newly emerged left bundle branch block, direct PCI is recommended (, A); with cardiogenic shock or heart failure, 12-hour patients still recommend direct PCI (I, B).

3. Emergency Coronary Artery Bypass Grafting (CABG)

Patients with acute STEMI have persistent or repeated ischemia, cardiogenic shock, severe heart failure, and the anatomy of the coronary artery is not suitable for PCI or mechanical complications of myocardial infarction may require emergency CABG.

(Three) antithrombotic therapy

Antiplatelet therapy

(1) Aspirin: All patients with STEMI without contraindications should immediately take water-soluble aspirin or chew enteric-coated aspirin.

(2) P2Y12 receptor inhibitors: Patients with STEMI direct PCI should be given a load of ticagrelor or clopidogrel for at least 12 months (I, A).

(3) GPIIb / IIIa receptor antagonists: In the case of effective dual antiplatelet and anticoagulant therapy, it is not recommended that STEMI patients routinely use GPIIb / IIIa receptor antagonists before imaging (IIb, B).

Tirofiban or eptifibatide can be administered intravenously to high-risk patients or patients who are angiographically suggesting a heavy thrombus load and have not been given an appropriate load of P2Y12 receptor inhibitors (IIa, B).

For direct PCI, intracoronary injection of tirofiban can help reduce no reflow and improve myocardial microcirculation perfusion (IIb, B).

2. Anticoagulation therapy

(1) Patients with direct PCI: intravenous infusion of unfractionated heparin (70-100U / kg), combined with GPb / a receptor antagonist, intravenous infusion of unfractionated heparin (50-70U / kg) (I, B), or Intravenous bolus 0.75mg / kg of bivalirudin, followed by 1.75mg kg-1 h-1 intravenous infusion (with or without tirofiban) (IIa, A), and maintained until 3-4h after PCI .

In patients with STEMI who have a high risk of bleeding, bivalirudin alone is better than combination of unfractionated heparin and GP IIb / IIIa receptor antagonists (IIa, B). Fondaparinux increases the risk of thrombosis in the catheter and should not be used alone as an anticoagulant option in PCI (III, C).

(2) Patients with intravenous thrombolysis: should receive at least 48 hours of anticoagulation therapy (up to 8 days or until revascularization) (I, A).

(3) Patients with PCI after thrombolysis: can continue to use intravenous heparin, and adjust the dose according to the ACT results and whether to use GPb / a receptor antagonists (I, C). For patients who have used appropriate doses of enoxaparin and need PCI, if the last subcutaneous injection is within 8h, no additional dose is required before PCI. If the last subcutaneous injection is between 8-12h, enoxaparin 0.3 should be injected intravenously mg / kg (I, B).

(4) Patients who have not undergone reperfusion treatment within 12 hours of onset or have an onset of> 12 hours: anticoagulant therapy must be given as soon as possible. Fondaparinux is beneficial to reduce death and reinfarction without increasing bleeding complications (I, B).

(5) Prevention of thromboembolism: Patients with atrial fibrillation with a CHA2DS2-VASc score of 2 or after mechanical heart valve replacement or venous thromboembolism should be treated with warfarin, but attention should be paid to bleeding (I, C). Warfarin anticoagulation is reasonable in patients with asymptomatic left ventricular mural thrombosis (IIa, C). Patients receiving dual antiplatelet therapy after DES should control the INR to 2.0-2.5 when adding warfarin (IIb, C). Patients at high risk of bleeding may be treated with warfarin plus clopidogrel (IIa, B).

(4) Other drug treatments

Anti-myocardial ischemia

(1) Beta-blockers: Patients with STEMI without contraindications should routinely take beta-blockers within 24 hours of onset (I, B). Metoprolol is recommended to be taken orally, starting with a low dose and gradually increasing the dose. If the patient is well tolerated, switch to a corresponding long-acting controlled-release preparation after 2-3 days.

(2) Nitrate: Intravenous infusion of nitrate is used to relieve ischemic chest pain, control hypertension or reduce pulmonary edema (I, B). If the patient has a systolic blood pressure <90mmHg, a decrease of> 30% from the basal blood pressure, severe bradycardia (<50 beats / min), and nitric acid esters should not be used in STEMI patients (, C).

(3) Calcium antagonists: Short-acting dihydropyridine calcium antagonists are not recommended for patients with STEMI; for patients without left ventricular systolic dysfunction or atrioventricular block, if -blockers are ineffective or contraindicated, Non-dihydropyridine calcium antagonists (IIa, C) can be used. When STEMI is combined with difficult-to-control angina, diltiazem (IIa, C) can be used in addition to beta blockers.

2. Other treatments

(1) ACEI and ARB: All patients with STEMI without contraindications should be given long-term treatment with ACEI (I, A). ARB is used in patients who cannot tolerate ACEI (I, B). Routine combination of ACEI and ARB is not recommended; patients with tolerable ACEI are not recommended to routinely replace ACEI with ARB.

(2) Aldosterone receptor antagonists: For patients with LVEF0.40 after STEMI, cardiac insufficiency or diabetes, and no obvious renal insufficiency, aldosterone receptor antagonists (I, A) should be given.

(3) Statins: All STEMI patients without contraindications should start statin treatment as soon as possible after admission, regardless of cholesterol levels.