Acute myocardial infarction (AMI) is a serious threat to human life and health, timely and accurate diagnosis is the key to active treatment, reduce mortality, and improve the prognosis.The clinical manifestations of AMI are intricate, and electrocardiogram (ECG) is the most important examination tool for the early diagnosis of AMI. ECG has been used in clinical practice for more than 100 years, and is still the most commonly used diagnostic method for AMI because of its non-invasive nature, simple operation, good reproducibility, and the ability to make a diagnosis in a short period of time at the bedside. If the ECG is analyzed in combination with clinical data, early diagnosis can be made in 70% to 80% of AMI. In recent years, with the continuous improvement of clinical diagnostic level, some new points of view and new indexes for diagnosing AMI have been put forward, which further improve the ability of electrocardiogram to diagnose AMI. 1, the evolution of acute myocardial infarction (AMI) electrocardiogram classification: 1.1. recent classification: AMI according to the electrocardiogram performance is divided into Q-wave AMI and non-Q-wave AMI, and from the pathological anatomy is divided into subendocardial and transmural AMI. the vast majority of transmural AMI in the first hours after the onset of the manifestation of ST-segment elevation, and some patients in the hyperpolar period manifested as a high T-wave, followed by the emergence of Q-wave. The majority of transmural AMIs show ST-segment elevation in the first few hours after onset. In subendocardial infarction, ST-segment depression occurs in the early stage, followed by T-wave inversion, and Q-wave rarely occurs; only repeated subendocardial necrosis, when the necrotic myocardium accumulates to a certain degree and exceeds half of the thickness of the ventricular wall, can also be manifested as Q-wave AMI. The time of T-wave inversion in subendocardial infarction is generally more than 24 hours, and those with less than 24 hours are usually caused by transient myocardial ischemia. Some patients in the very early manifestation of ST-segment elevation transmural ischemia, but soon due to thrombus autolysis or thrombolytic therapy to make the infarction-related vascular recanalization, the amount of myocardial necrosis is less than the formation of Q-wave, at this time should also be referred to as a non-Q-wave AMI. 1.2.The latest classification: AMI should be classified into ST-segment elevation infarction (STEMI) and non-ST-segment elevation infarction (NSTEMI) according to the electrocardiogram in the early stage of the presence or absence of ST-segment elevation. (In early AMI, only ST-segment changes appear, and pathologic Q waves usually appear in 8 to 12 hours after the onset of AMI, and in 14% of cases, they appear in 72 hours after the onset of AMI. Therefore, Q-wave infarction or no Q-wave infarction cannot be diagnosed in the early stage of AMI. Prediction of Q-wave or no Q-wave infarction on the basis of ST-segment elevation or depression is unreliable. Successful thrombolytic therapy prevents the occurrence of Q-waves, which currently do not appear pathologically in the evolution of STEMI in about 40% of cases. It has a guiding role in treatment: STEMI reflects thrombotic occlusion of coronary arteries and should be treated with thrombolysis; while NSTEMI reflects incomplete occlusion of coronary arteries caused by platelet-based white blood clots and should be treated with antiplatelet drugs, and thrombolysis is not beneficial. 2, the specificity and sensitivity of electrocardiography in the diagnosis of AMI: Due to the progress of serologic examination, especially the CK-MB isomer determination (CK-MB1, CK-MB2/MB1) and the application of troponin combined with the clinic, the sensitivity reaches 100%. ECG is lower, with a specificity and sensitivity of 69% and 81%, respectively. According to Sgarbossa, 15% to 18% of patients with AMI have no changes on the first tracing of the ECG, and 25% have atypical changes on the ECG.The absence of changes on the ECG or atypical changes on the ECG in patients with AMI may be due to the following five conditions: (1) infarct size is too small; (2) occlusion of the left ileoad; (3) tracing too early and failing to perform a series of tracings; and (4) left ileoad branch occlusion: no changes on the conventional 12-lead ECG in 50% of cases; (5) too early tracing and failing to perform a series of tracings; (6) too small an area of infarct size. (4) inappropriate tracing time: around 12 to 24 hours after the onset of AMI, from the super-acute phase to the acute phase, the elevated ST segment can be lowered to baseline, while the pathological Q wave has not yet appeared, the electrocardiogram can be a transient pseudo-normalization; (5) infarction site special: single right ventricle, posterior wall infarction, such as the failure to carry out the 18-lead electrocardiogram. 3.New criteria for diagnosing AMI on electrocardiogram For a long time, the emergence of new pathologic Q waves and ST-segment elevation in 2 adjacent leads have been regarded as reliable indicators for the diagnosis of acute myocardial infarction (AMI), but there is no consistency in the specific degree of pathologic Q waves and ST-segment elevation requirements. The European Society of Cardiology/American College of Cardiology suggests the following diagnostic criteria for reference. 3.1 Progressive AMI: ① ST-segment elevation ≥0.2 mV (leads V1-V3), ST-segment elevation ≥0.1 mV (leads other than aVR); ② The above changes occur in 2 or more leads. 3.2. Established AMI: ① Q wave duration ≥ 30ms depth ≥ 0.1mV; ② The above changes occur in 2 or more leads. 4, the concept and significance of isotropic Q wave Myocardial infarction does not appear pathological Q wave, but can cause characteristic morphological changes in QRS wave, these electrocardiographic changes and pathologic Q wave can diagnose myocardial infarction, this characteristic change in QRS wave is called isotropic Q wave. It includes: ① small q wave: V1 ~ V2 leads rS wave before the appearance of small q wave, if you can exclude right ventricular hypertrophy, left anterior branch block, more suggestive of anterior interstitial wall infarction; V3 ~ V6 leads appear Q wave, did not meet the diagnostic criteria for pathological Q wave, but the following characteristics: QV3> V4 or QV4>V5>V6, more suggestive of anterior wall infarction; ② progressive Q wave: refers to the original Q wave changes (widening or deepening). (Widening or deepening) or the appearance of new Q waves in the original non-Q wave leads; ③ pathological Q wave region: Q waves can be recorded around the infarcted area of the leads (up and down or left and right); ④ abnormal changes in the R wave is lost: the R wave of the thoracic leads in reverse increment, the difference in the amplitude of the R wave of the two neighboring thoracic leads is more than 50%, and the amplitude of the R wave of a certain lead declines progressively; the beginning of the QRS wave appears to be a cut, a pause, or an infarct-related lead. Presence of a negative R wave of ≥0.05 mV in the infarct-related leads. When one or a combination of the above five conditions exists, the diagnosis of myocardial infarction should be considered. 5, some of the special use of ECG to diagnose AMI 5.1.ST segment depression in anterior thoracic leads to diagnose AMI: Individual ST segment depression ≥1mm (measured 80ms after the J-point) in more than 6 leads has a specificity of 96.6%; ST segment depression is most pronounced in leads V2-V3, suggesting occlusion of the left ileocardiographic branch has a specificity of 96%; ST segment depression is most pronounced in leads V4-V6, accompanied by an upright rather than inverted T wave, suggesting occlusion of the left anterior descending branch has a specificity of 96%. ST segment depression is most obvious in leads V4-V6, accompanied by upright rather than inverted T waves, suggesting subendocardial ischemia caused by subtotal occlusion of the left anterior descending branch. 5.2. AMI combined with left bundle branch block or ventricular pacing: left bundle branch block is similar to the depolarization and repolarization of ventricular muscle caused by AMI, and often masks the electrocardiographic changes of AMI. Sgarbosso et al. proposed three indexes: ST segment elevation in the leads with the upward QRS wave is ≥1mm (counted as 5); ST segment depression in leads V1-V3 is ≥1mm (counted as 3); ST segment elevation in the leads with the downward QRS wave is ≥1mm (counted as 3); and ST segment elevation in leads V4-V6 is ≥1mm (counted as 2). ST-segment elevation in leads with QRS main wave downward ≥ 5 mm (counted as 2); 90% specificity for diagnosis of AMI if the total score is ≥ 3, and 80% if the total score is ≥ 2. 5.3. The diagnostic value of aVR lead for AMI: anterior wall AMI with ST segment elevation in aVR lead suggests that left anterior descending branch occlusion occurs in the proximal side of the first septal branch, with a specificity of 95%; lower wall AMI with ST segment depression in aVR lead suggests large infarct size and poor prognosis; anterior side wall AMI with ST segment depression in aVR lead suggests large infarct size and high rate of congestive heart failure; angina pectoris is associated with a high rate of congestive heart failure; angina is associated with a high rate of congestive heart failure; angina is associated with high rate of congestive heart failure; angina is associated with high rates of congestive heart failure. In angina pectoris, ST-segment depression in leads Ⅰ, Ⅱ, and V4-V6 with ST-segment elevation in aVR leads suggests left main stem lesions. 5.4. The morphology of ST-segment elevation in the precordial leads predicts the state of cardiac function: recently Kosnge proposed that the morphology of ST-segment elevation is categorized into concave, linear and convex. The concave type has the best left ventricular function, the linear type is the second best, and the convex type is the worst. 6. electrocardiographic diagnosis of infarct-related arteries and prognosis The new classification method of the electrocardiogram of ST-segment elevation myocardial infarction (STEMI) is closely related to coronary artery anatomy, patient’s clinical presentation and prognosis, and also has a guiding significance for treatment. 6.1. Proximal left anterior descending infarction: proximal occlusion of the first perforating septal branch of the left anterior descending branch, with ST-segment elevation in ECG leads V1 to V6, I and aVL. As the blood supply of the Hi-Po system is affected, newly occurring bundle branch block may be present, with left anterior branch block and right bundle branch block being the most common, and left bundle branch block, two-branch block, or Mohs’ type 2 AV block may also be present. Unless prompt and effective reperfusion therapy is administered, patients may develop pump failure or cardiogenic shock. Patients have a 30-day mortality rate of 19.6% and a 1-year mortality rate of 25.6%. 6.2. Middle left anterior descending infarction: occlusion of the distal first perforating septal branch of the left anterior descending branch and the proximal large diagonal branch, with ST-segment elevation in the V1-V6, I and aVL leads of the electrocardiogram, and no conduction block. Myocardial necrosis is confined to the anterolateral and anteroapical segments, and the septum is not damaged proximally. If cardiogenic shock occurs, there may be pre-existing damage to the myocardium or an extracardiac cause such as hemorrhage. Pump failure may occur, and ventricular wall tumor with apical thrombosis is common. The 30-day morbidity and mortality rate is 9.2%, and the 1-year morbidity and mortality rate is 12.4%. 6.3. Distal left anterior descending branch infarction: the left anterior descending branch of the large diagonal branch is occluded distally, and the electrocardiogram is only ST-segment elevation in the leads of V1-V4, which does not complicate cardiogenic shock, and the pump failure seldom occurs, but due to the disappearance of apical ventricular wall motion, it may be complicated with thrombus formation. The 30-day morbidity and mortality rate of patients is 6.8%, and the 1-year morbidity and mortality rate is 10.2%. 6.4. Left anterior descending branch diagonal branch occlusion infarction: left anterior descending branch diagonal branch occlusion infarction also belongs to the distal left anterior descending branch infarction, and only ST-segment elevation occurs in leads I, aVL, V5 and V6, and serious complications, such as pump failure and serious arrhythmia, rarely occur. The 30-day mortality rate of patients is 4.5%, and the 1-year mortality rate is 6.7%. 6.5. Small inferior wall infarction: usually occlusion of the distal branches of the right coronary artery (posterior lateral branch, posterior descending branch), or it may be occlusion of the branches of the left echogenic branch (left dominant type). ST-segment elevation was seen only in II, III and aVF leads, and complications were rare. Patients have a 30-day mortality rate of 4.5% and a 1-year mortality rate of 6.7%. 6.6. Medium and large inferior wall infarction (posterior, lateral wall and right ventricle): occlusion of the proximal or left echogenic branch of the right coronary artery, ST-segment elevation in ECG leads Ⅱ, Ⅲ and aVF, in addition, one or three of the following changes can occur: ① ST-segment elevation in leads V1, V3R～V4R; ② ST-segment elevation in leads V5 and V6; ③ R/S > 1 in leads V1 and V2. Due to large right ventricular infarction, patients can develop cardiac Due to the large right ventricular infarction, the patient may develop heart failure (right heart failure) and cardiogenic shock, and often has bradycardia and Mohs’ type 1 AV block. Patients have a 30-day mortality rate of 6.4% and a 1-year mortality rate of 8.4%.