In order to understand the global uniform definition of myocardial infarction more comprehensively and to update the thinking on the diagnosis and treatment of acute myocardial infarction, the authors analyzed the new content of the global uniform definition of myocardial infarction, interpreted the diagnostic value of the new definition based on troponin elevation and the new clinical staging, applied the clinical examination of myocardial infarction rationally, diagnosed acute myocardial infarction rapidly and accurately, and analyzed the impact of the new definition on clinical efficacy determination, treatment strategy and the development of We also analyzed the impact of the new definition on clinical efficacy, treatment strategy and the development of Chinese medicine research. The new definition emphasizes the centrality of troponin elevation in acute myocardial infarction and identifies the definition of myocardial infarction associated with PCI and CABG. The authors go on to suggest that the new definition of infarction should be used as a diagnostic basis to advance clinical and scientific research on acute myocardial infarction. The European Society of Cardiology (ESC), the American College of Cardiology (ACC), the American Heart Association (AHA), and the World Heart Federation (WHF) jointly promulgated a unified global definition of myocardial infarction in Circulation on October 19, 2007, which incorporates a biochemical marker of greater sensitivity and specificity – Troponin (cTn) was included as a core item in the diagnosis of myocardial infarction. The previous WHO definition of diagnostic criteria for myocardial infarction included ischemic symptoms, abnormal electrocardiogram (ECG) changes and serum myocardial enzymatic changes, emphasizing the chest pain symptoms of typical myocardial infarction, the dynamic changes of ECG during myocardial ischemia and the dynamic evolution of serum enzymes mainly AST, CK, CK-MB and LDH. Because some patients with acute myocardial infarction may not have typical clinical manifestations of myocardial ischemia, and some patients such as diabetic patients may not have any chest pain; electrocardiographic changes are not seen in a small number of patients with acute myocardial infarction; in addition, the traditional so-called “myocardial enzyme profile” is not entirely derived from myocardial tissue. The specificity and sensitivity are low. In view of the above, the definition of myocardial infarction should be updated by adapting the pathological changes of myocardial infarction and combining them with newly discovered markers of myocardial necrosis, which is consistent with the current understanding of myocardial infarction. I. Deepen the comprehensive understanding of myocardial infarction 1. Classification of new definition of central infarction The new definition divides myocardial infarction into five types according to etiology. Type I: Spontaneous ischemia-related myocardial infarction caused by a primary coronary event (such as plaque erosion/rupture, fissure or entrapment). Type II: ischemia-related myocardial infarction secondary to increased oxygen consumption or decreased oxygen supply (e.g., coronary spasm, coronary embolism, anemia, arrhythmia, hypertension, or hypotension). Type III: Sudden cardiac death (including cardiac arrest), usually with symptoms of myocardial ischemia, accompanied by new ST-segment elevation or new LBBB, and/or evidence of new thrombus confirmed by coronary angiography or autopsy, but death often occurs prior to obtaining a blood specimen or elevated cardiac markers. Type IV: 1. Type IVa: Myocardial infarction associated with PCI; 2. Type IVb: Myocardial infarction associated with stent thrombosis confirmed by autopsy or coronary angiography. Type V: myocardial infarction associated with CABG. It is also emphasized that sometimes patients may present with more than one type of myocardial infarction simultaneously or sequentially. Myocardial infarction does not include myocardial cell death due to mechanical injury in CABG, nor does it include myocardial necrosis due to other confounding factors, such as renal failure, heart failure, electrical resuscitation, electrophysiological ablation, sepsis, myocarditis, cardiotoxic drugs or infiltrative disease. Previously, the WHO did not specify the clinical type of myocardial infarction and listed sudden cardiac death as a separate category from acute myocardial infarction, but this new definition clearly diagnoses sudden death associated with myocardial ischemia as myocardial infarction; the special features of the new definition not only highlight ischemia-related spontaneous myocardial infarction caused by primary coronary events, but also include myocardial infarction secondary to increased oxygen consumption or decreased oxygen supply leading to ischemia in the clinical in the staging. Types IV and V myocardial infarction as clinical types of myocardial infarction associated with intervention and coronary artery bypass grafting are highlights of the new definition. Intervention and bypass are both therapeutic operations on the coronary arteries, and the myocardial damage caused by these operations has not been objectively recognized and has been intentionally or unintentionally ignored by clinicians. The new definition of myocardial infarction of medical origin into the scope of myocardial infarction fills the gap, and also reminds clinicians that inappropriate vascular operations may bring new damage to patients, which needs clinical attention. 2. Recognize the correlation between pathological features of myocardial infarction and clinical manifestations The pathological definition of myocardial infarction is the death of myocardial cells caused by prolonged ischemia, and myocardial infarction in coronary heart disease is the death of myocardial cells triggered by ischemia of the supplied myocardium due to coronary artery lesions. Myocardial infarction can be classified according to area: focal necrosis, small area (less than 10% of the left ventricular myocardium), medium area (10%-30% of the left ventricular myocardium) and large area (greater than 30% of the left ventricular myocardium) necrosis. The clinical presentation of patients with myocardial infarction correlates with the size of the myocardial infarction. Focal myocardial necrosis may be without ST-T changes on the ECG, and small areas of myocardial infarction may cause atypical ST-T changes in a single lead or abnormal Q waves or nonspecific ST-T changes in adjacent leads. A medium-sized right ventricular myocardial infarction is more likely to be admitted with clinical manifestations of hypotension or shock and may be accompanied by severe bradycardia. The dynamic evolution of a typical acute myocardial infarction is seen in medium to large left ventricular myocardial infarction. 3. Inconsistency between pathological and clinical staging of myocardial infarction Myocardial infarction is pathologically divided into acute, healing and old stages. However, clinical staging is generally divided into progressive phase (<6 hours), acute phase (6 hours to 7 days), healing phase (7 days to 28 days) and old phase (≥29 days) according to ECG and disease process. The clinical and ECG-documented infarct staging does not always correspond exactly to the actual pathological staging. If the patient still has dynamic ST-T changes on ECG and myocardial necrosis markers are still higher than normal, the clinical indication is that the infarction is still in the acute phase, but only mononuclear cells and fibroblasts are seen on myocardial pathology, and no polymorphonuclear leukocytology is seen, suggesting that the pathologic staging may already be in the healing phase. If patients enter the healing phase from the acute stage relatively early, AMI patients can be out of danger earlier and can also be transferred from the intensive care unit to the general ward for treatment to speed up the cardiac rehabilitation process. Second, update the thinking of diagnosis and treatment of acute myocardial infarction The update of the definition of myocardial infarction has prompted us to update the thinking of diagnosis and treatment of acute myocardial infarction, rapid and accurate diagnosis and scientific treatment. 1. Correct application of clinical examination of myocardial infarction for rapid and accurate diagnosis Myocardial cTn is currently the most specific and sensitive marker of choice for the diagnosis of myocardial necrosis. This definition takes the elevation of cTn as the core index for the diagnosis of acute myocardial infarction. It also emphasizes that elevation of cTn indicates myocardial injury, but the diagnosis of acute myocardial infarction cannot be made simply on the basis of this. If there is no clinical evidence of myocardial ischemia, other causes of myocardial injury, such as aortic coarctation, myocarditis, pulmonary embolism, heart failure and renal failure, should be considered and excluded. Any degree of myocardial necrosis caused by ischemia should be classified as myocardial infarction, but it should be emphasized that there is a significant difference between subtle injury and massive infarction. The former is characterized by elevated cTn but not other biochemical markers (e.g., CK-MB); the latter may present with complications such as heart failure, shock, and fatal arrhythmias. The diagnosis should be accompanied by a description of other cardiac states, such as the functional status of the left ventricle, the severity of the coronary lesion, and the stability of progression of the disease. In the early diagnosis of acute myocardial infarction, clinically used cardiac enzyme indices such as AST, LDH, HBDH, CK, etc. should be discarded in the diagnosis of AMI because they are not specific and highly sensitive, considering the health economic significance. In addition, when conducting clinical research on acute myocardial infarction, it will not be necessary to perform myocardial enzyme profiles, which will reduce research expenditures and facilitate clinical research. Although the specificity of myoglobin is very poor, the advantage of this index is its timeliness and sensitivity. Myoglobin is the earliest marker elevated in myocardial necrosis and can be detected as early as half an hour after the onset of infarction, which has differential significance for the early diagnosis of AMI. ECG changes have always been an important tool for diagnosing myocardial infarction and determining its location and area, but not all acute myocardial infarction will have abnormal ECG changes, it is only an alternative but not a necessary item to confirm the diagnosis of myocardial infarction. Because ECG is the most convenient test and can detect acute myocardial infarction with ST-segment elevation or depression at the first visit, it is the most popular and important clinical test and is a mandatory test for the diagnosis of acute myocardial infarction. Imaging techniques such as echocardiography can detect abnormalities in ventricular wall motion, which can help in the diagnosis of myocardial infarction and the detection of complications of myocardial infarction. The widespread use of echocardiography for early diagnosis of acute myocardial infarction is greatly limited by the limitations of the instrumentation and the skill level of the diagnostic technicians. In the recovery phase of myocardial infarction, imaging is useful in evaluating left ventricular function and confirming the presence or absence of surviving myocardium, which is a good guide for developing treatment and secondary prevention strategies. In acute myocardial infarction, myoglobin, troponin and CK-MB, and electrocardiogram are the first necessary tests. When patients have ischemic chest pain, elevated myoglobin is highly suspected of acute myocardial infarction; elevated troponin confirms the diagnosis of acute myocardial infarction without the need for ischemic changes in the ECG. On the other hand, in patients without symptoms of ischemic chest pain, an abnormal elevation of troponin, even a small one, still needs to be combined with electrocardiographic and imaging changes to exclude or diagnose acute myocardial infarction. Be wary of the clinical inertia of easily excluding cases of mildly elevated troponin from acute myocardial infarction. 2. Impact on clinical outcomes and treatment strategies A uniform definition of global myocardial infarction is important for clinical work, as it can be used both as an inclusion criterion and as an endpoint in clinical studies. The clinical value of troponin T for the early diagnosis and prognosis of acute non-Q-wave myocardial infarction has been investigated earlier in China. The use of highly sensitive and specific cTn as a clinical diagnostic and efficacy index for acute myocardial infarction, changes in the diagnostic criteria for myocardial infarction can affect the clinical characteristics of the patients enrolled and the number of cardiovascular events with acute myocardial infarction as an endpoint, thus affecting the conclusions of evidence-based studies. Harmonization of the definition of myocardial infarction also contributes to the accuracy of meta-analyses of similar studies and the comparability of findings between different acute myocardial infarction study groups. The absolute value of troponin is directly proportional to the mass of myocardial necrosis. Higher troponin indicates a larger area of myocardial infarction, which also indicates a large number of involved vessels, severe lesions, complications, and a poor prognosis. ECG and imaging can determine the site and area of myocardial infarction more accurately, which is of greater significance for the judgment of the condition and prognosis, and is an important basis for choosing the treatment plan for AMI. For example, in AMI patients with ST elevation, out-of-hospital thrombolysis can open the vessel early and help reduce myocardial necrosis. Another example is that patients with large left ventricular myocardial infarction generally have lesions in the proximal part of the anterior descending branches, which are prone to the formation of ventricular wall tumors and rupture of the left ventricular free wall, with an increased incidence of acute cardiovascular events and potentially worse prognosis. The updated definition of myocardial infarction has led to the diagnosis of acute myocardial infarction in more patients who previously could not be diagnosed with acute myocardial infarction, bringing new clinical issues and the need to clinically differentiate between macrovascular or microvascular lesions and to develop more detailed guidelines for the scientific management of different clinical situations. It is not enough to make the diagnosis of acute myocardial infarction alone, but also to determine the extent of the infarction, the function of the left ventricle, and the severity of the coronary artery lesion, thus predicting the patient's regression. The new definition requires to pay attention to large myocardial infarction, but also to small microvascular myocardial infarction. The significance of this is the early effective intervention of coronary artery disease, comprehensive prevention and treatment for risk factors, as well as early imaging or morphological examination of coronary arteries, early detection of large vessel lesions, prevention of larger myocardial injury, and protection of cardiac function. 3. Impact on the development of TCM research in acute myocardial infarction With troponin as the core index, the number of cases of myocardial damage caused by coronary microvascular lesions has increased. Such patients cannot be effectively treated by interventional methods such as stent implantation or surgical bypass, and the advantages of combining Chinese and Western medicine may be more significant. On the other hand, type IV and type V myocardial infarction are myocardial infarction related to revascularization therapy, and the number of detection of these patients has increased accordingly, making clinicians pay more attention to these two types of myocardial infarction. With the advancement of TCM research, the use of TCM interventions along with revascularization therapy to reduce the incidence of type IV and V myocardial infarction may become a new research direction. With the reconceptualization of the pathology of AMI and the expansion of the scope of diagnosis of AMI, the classification and composition of TCM symptoms of AMI may be affected, and the previously conducted studies of symptoms need to be supplemented with new information to update the understanding. It is possible to use troponin elevation as an endpoint indicator of clinical efficacy in patients with coronary artery disease as a result of TCM interventions, which can help to illustrate the efficacy of TCM treatment of coronary artery disease in a more scientific way. In conclusion, we should comprehensively popularize the new definition of myocardial infarction, adopt new criteria for the diagnosis of acute myocardial infarction, pay attention to medically induced myocardial infarction, and comprehensively promote clinical and scientific research on acute myocardial infarction.