Coronary heart disease (CHD) is the abbreviation for coronary heart disease, which is a heart disease with or without symptoms caused by atherosclerosis of the coronary arteries, resulting in narrowing or blockage of the coronary arterial lumen, or/and coronary artery function (spasm) leading to myocardial ischemia, hypoxia, or necrosis. Because the vast majority of the coronary artery atherosclerosis is caused on the basis of the coronary artery atherosclerosis, so the narrow sense of the coronary atherosclerotic heart disease referred to as coronary heart disease. As early as 1979, WTO divided coronary heart disease into five clinical types: asymptomatic myocardial ischemia, angina pectoris, myocardial infarction, ischemic cardiomyopathy, and sudden death, and has been used until now. However, this retrospective typing has limited value for clinical guidance of treatment, therefore, at present, the two clinical typing of stable coronary heart disease and unstable coronary heart disease (acute coronary syndrome ACS) are more often used, the former including: asymptomatic myocardial ischemia, stable angina pectoris, and cardiac insufficiency, and the latter including: unstable angina pectoris, acute myocardial infarction, and sudden death. It should be noted that: coronary heart disease can be manifested as various types of angina pectoris, but not all angina pectoris is coronary heart disease, because, angina pectoris refers to the clinical syndrome due to the imbalance of myocardial oxygen supply and demand for oxygen caused by the aortic stenosis or closure of the aorta or insufficiency, syphilitic aortitis, or aortic coarctation involving the opening of the coronary arteries can also lead to angina pectoris. Coronary angiography has long been considered the “gold standard” for the diagnosis of coronary artery disease. The degree of coronary stenosis can be simply categorized into grades I-IV based on the ratio of the cross-section of the lumen with the most severe stenosis under coronary angiography/the lumen surface of that segment, with grade I being less than 25%, grade II being 26-50%, grade III being 51-75%, and grade IV being 76-100%. Generally speaking, in the absence of coronary artery spasm factors and vulnerable plaque, stenosis due to grade I-II atherosclerosis will not cause a reduction in coronary blood flow and induce myocardial ischemia, and this asymptomatic mild atherosclerosis has no relationship with the onset of coronary artery disease. Because of the diversity of clinical manifestations of coronary artery disease, the complexity of the mechanism of occurrence, the subjectivity of the judgment of the degree of stenosis under the contrast, the existence of eccentric plaques, diffuse lesions, and vulnerable plaques, etc., the diagnosis of coronary artery disease does not depend entirely on the presence of coronary atherosclerosis and the degree of stenosis of the coronary artery by coronary artery contrast, and it is not possible to exclude those who do not have or who have a mild degree of coronary atherosclerosis by coronary artery contrast. The diagnosis of coronary artery disease, which may have diffuse lesions, soft plaques and vulnerable plaques of coronary artery disease patients missed, ignoring the value of intravascular ultrasound (IVUS) or optical coherence imaging technology (OCT) for the diagnosis of coronary artery disease, is not conducive to the early diagnosis and prevention of coronary artery disease. Of course, we cannot simply consider all people with coronary atherosclerosis as coronary heart disease, especially for mild coronary atherosclerosis and stenosis without clinical significance (stenosis of 20-30%) seen on coronary angiography, which will lose the clinical significance of coronary artery disease staging and the diagnostic value of coronary angiography for coronary heart disease. In the diagnostic process of coronary artery disease, the first step is to determine whether the symptoms are ischemic; this time, it is necessary to assess whether the symptoms are acute ischemic symptoms or stable symptoms; and once again, to identify whether it is angina pectoris or myocardial infarction (MI)? Is the presumed coronary lesion a mechanical blockage or a dynamic or thrombotic (acute unstable plaque) blockage? Is it an episode of myocardial ischemia or has necrosis occurred? Stable coronary artery disease is easily diagnosed by the presence of a fixed clinically significant narrowing of the coronary lumen, and in those with symptoms of exertional angina (angina CCS classification that is relatively stable and has been in place for more than 1 month), the ECG can be altered at rest and during episodes/exercise, and therefore the diagnosis can easily be made by combining the history, the ECG, an exercise plate or a load test, and, if necessary, a coronary angiogram. In asymptomatic chronic myocardial ischemia, heart failure type of CHD can be diagnosed on the basis of evidence of positive exercise plate or load test, myocardial perfusion defects, echocardiographic demonstration of segmental or diffuse left ventricular hypokinesis, and cardiac enlargement. The diagnosis of unstable coronary artery disease, or ACS, is also not difficult. For the diagnosis of unstable angina pectoris (UAP) in ACS, the diagnostic conditions of stable angina pectoris can be referred to, and all types of angina pectoris other than stable angina pectoris can be categorized as unstable angina pectoris.For the diagnosis of acute myocardial infarction (AMI) in ACS, in addition to the diagnosis that can be made directly based on the pathological findings of AMI (which is difficult to achieve in the clinic), the diagnosis of acute myocardial infarction (AMI) can be made, in most cases, by referring to the October 2007 release of the The global unified definition of myocardial infarction released in October 2007, adopting the diagnostic model of “1+1”, 1 necessary condition + 1 sufficient condition, the necessary condition is: cardiac biochemical marker level (cTn optimal) elevated more than the upper limit of the reference value of the 99th percentile value; the sufficient condition is: 1. ischemic symptoms; 2. ECG suggestive of new ischemic ECG suggesting new ischemic changes (new ST-T changes or new LBBB); 3. ECG suggesting pathologic Q-wave formation; and 4. imaging evidence suggesting new localized ventricular wall motion abnormalities or loss of viable myocardium. The requisites of these are the only clinical basis for distinguishing UAP from AMI and are important markers for ACS risk stratification and prognostic assessment. However, the increase in the level of cardiac necrosis markers requires a certain “time window”, and its diagnosis of AMI still has retrospective characteristics, therefore, emphasizing its immediate detection (Point of Care Testing POCT) and re-testing 6-8 hours after the onset of the disease is important for early diagnosis, risk stratification of ACS, guide therapeutic decisions. The new global definition of myocardial infarction also proposes diagnostic criteria for sudden cardiac death (including cardiac arrest) MI, and MI associated with percutaneous coronary intervention (PCI) and coronary artery bypass grafting (CABG), the former of which is defined as: sudden cardiac death/cardiac arrest, accompanied by signs and symptoms of myocardial ischemia, accompanied by new onset of ST-segment elevation or new onset of LBBB and/or evidence of new thrombosis confirmed by coronary angiography or autopsy. evidence of thrombus, but death often occurs before blood specimens are obtained or cardiac markers are elevated; PCI-associated MI is defined as a person with a normal baseline cTn level who undergoes (PCI) and has a cardiac marker level greater than 3 times the URL99 percentile value; the latter is defined as a person with a normal baseline cTn level who undergoes CABG and has a cardiac marker level greater than 5 times the URL99 percentile value, combined with one of the following. New onset of rational Q waves, new onset of LBBB, coronary angiographic confirmation of new bridging vessel or coronary artery occlusion, and new onset of imaging evidence of loss of viable myocardium. In conclusion, the correct diagnosis of coronary artery disease must be based on a correct understanding of the definitions of coronary atherosclerosis, coronary artery disease, angina pectoris, myocardial infarction, and acute coronary syndromes, pathophysiologic processes, and the relationship between them. Because of the lack of diagnostic procedures and methods with high sensitivity and specificity for the diagnosis of coronary heart disease, the phenomena of omission, misdiagnosis and indiscriminate diagnosis of coronary heart disease; omission, misuse and abuse of examination means; and misjudgement and indiscriminate judgment of the examination results still exist, and some doctors have difficulty in grasping the diagnosis of CHD and are at a loss as to what to do. Therefore, CHD should not be understood and diagnosed one-sidedly and in isolation, especially for those without obvious ischemic symptoms or with atypical symptoms, but should be evaluated according to the patient’s clinical manifestations (type), myocardial necrosis markers, electrocardiographic features, exercise load test, echocardiography, and combined with the evidence of imaging (coronary angiography, cardiac myocardial imaging, IVUS, and OCT), etc., so as to make the correct diagnosis and improve the diagnosis of CHD. This will improve the correct rate of coronary heart disease diagnosis, especially the early diagnosis and detection of coronary heart disease, so as to guide the prevention and treatment of coronary heart disease in a more scientific way.