I. Interventional treatment of coronary artery disease and post-treatment medication Coronary interventional treatment includes percutaneous transluminal balloon angioplasty (PTCA) and coronary stent implantation. PTCA is performed by delivering a balloon to the corresponding stenosis of the coronary artery and performing high-pressure dilation to eliminate coronary stenosis. The mechanism of PTCA is due to the irregular tearing of intima and intima due to the high-pressure expansion of the balloon, so PTCA still has its own limitations, such as unsatisfactory expansion and the tendency to have obvious residual stenosis; more importantly, because of the risk of acute occlusion due to the tearing of the vessel wall at the expansion site after simple PTCA, entrapment and elastic retraction of the vessel wall, PTCA is now less often applied in the clinic alone, and generally stents are implanted after PTCA. A coronary stent is a support tube of porous stainless steel (or alloy) that can be opened by balloon expansion, which is attached to the surface of the balloon and delivered by the delivery system to the lesion for release. It solves the problems of tearing and entrapment of the vessel wall after PTCA, as well as elastic retraction and negative remodeling of the vessel. Coronary stents currently consist of two main categories: bare metal stents (BMS) and drug-eluting stents (DES). the BMS metal mesh is completely reendothelialized in a shorter time, but the restenosis rate is higher; the restenosis rate is significantly lower after DES, but the complete reendothelialization time is also greatly delayed. Generally speaking, after coronary artery branch intervention, a stent is implanted, but this is only the beginning of effective treatment. The originally narrowed coronary artery becomes smooth due to the support of the stent, but for the coronary artery to be continuously smooth, long-term medication and long-term treatment must not be relaxed. There are three main purposes of applying drugs after stenting for patients with coronary artery disease: 1. prevention of thrombosis in the stent; 2. secondary prevention of coronary artery disease, i.e., prevention of stenosis in other coronary arteries; 3. control of myocardial ischemic symptoms of coronary artery disease. Anti-platelet therapy is an important measure to prevent platelet aggregation and thrombosis in the stent and other coronary arteries. It is currently believed that effective anti-platelet therapy is a guarantee and prerequisite for the safety of coronary interventions, and its importance for coronary interventions cannot be overemphasized. (A) Medication method After coronary stenting, dual antiplatelet therapy, i.e. aspirin + clopidogrel combination, should be administered. The guidelines for coronary intervention both at home and abroad recommend dual antiplatelet therapy for at least 12 months after coronary implantation of DES, at least 1 month after BMS, and at least 1 month after PTCA alone; for acute For patients undergoing intervention for acute coronary syndromes, dual antiplatelet therapy is recommended for at least 12 months, regardless of the type of stent implanted. Since lifelong administration of enteric aspirin is generally recommended as secondary prophylaxis in patients with coronary artery disease without contraindications, clopidogrel is generally discontinued and enteric aspirin is continued after the end of dual antiplatelet therapy. In some patients, even with the application of standardized duplex antiplatelet therapy, in-stent thrombosis still occurs, and the risk factors include procedure-related factors, lesion-related factors, patient-related factors, etc. Some complex and severe coronary lesions are at high risk and danger of thrombosis after intervention and require stronger antiplatelet therapy, and some patients develop antiplatelet drug resistance (the mechanism of which is unclear, and there is no uniform (the mechanism is unclear and there is no unified standard for detection and judgment), all of the above patients should be intensified with antiplatelet therapy. After interventions for left main stem lesions, chronic occlusive lesions, bifurcation lesions, long lesions, and multiple severe lesions, if there are no bleeding risk factors, dual antiplatelet therapy can be extended appropriately, and if necessary, triple antiplatelet therapy can be used, with cilostazol (Tada) 50-100 mg, 2 times/d, on top of aspirin + clopidogrel orally for 6-12 months. 2. In patients with in-stent thrombosis on top of aspirin + clopidogrel, if there are no risk factors for bleeding, clopidogrel dose can be doubled (150mg/d, changed to 75mg/d after 1-4 weeks), triple antiplatelet therapy, or clopidogrel can be replaced with new generation P2Y12 inhibitors such as prasugrel 60mg load, 10mg/d maintenance, or ticagrelor 180 mg load, 90 mg, 2 times/d maintenance. (ii) Bleeding risk of dual antiplatelet therapy Studies have shown that although dual antiplatelet therapy does not increase the risk of life-threatening bleeding compared with enteric aspirin alone, the incidence of mild bleeding increases from 2.4% to 5.1% and the incidence of major bleeding increases from 2.7% to 3.7%, suggesting that dual or triple antiplatelet therapy can increase the risk of bleeding, and once bleeding occurs, the incidence of adverse cardiovascular Once bleeding occurs, the incidence of adverse cardiovascular events is significantly increased. Therefore, during dual antiplatelet therapy, bleeding risk should be closely monitored, timely measures should be taken to avoid bleeding events, and the optimal balance of antithrombotic and bleeding reduction should be actively achieved. In general, patients of advanced age, women, with a history of bleeding and renal insufficiency are at high risk for both bleeding and in-stent thrombosis. In this population, the best way to achieve a balance between antithrombotic and bleeding reduction is to try to use the simplest interventional strategy and BMS. The main risk factors for stenting for GI bleeding risk are: previous history of GI bleeding, age >65 years, concomitant GI symptoms, H. pylori infection, concomitant NSAIDs, glucocorticoids, anticoagulants, etc. Therefore, the above drugs should be avoided during dual antiplatelet therapy. Studies have shown that the protective effect of proton pump inhibitors (PPI) on gastric mucosa is better than that of H2 receptor antagonists, but the antiplatelet effect of clopidogrel can be weakened by drug interactions when certain PPIs are combined with clopidogrel, and the probability of drug interactions with pantoprazole is small and the safety may be higher. Previous history of cerebral hemorrhage, recent history of ischemic stroke, and combination of oral anticoagulants are high-risk factors for intracranial hemorrhage, and other high-risk factors for hemorrhage are also performing other interventional operations and surgical procedures. Therefore, those who require concomitant oral anticoagulants during dual antiplatelet therapy should try to maintain an international normalized ratio (INR) below 2.5, preferably around 2.0. Postpone other interventions and surgical procedures until the end of duplex antiplatelet therapy, or advise the patient to consult a cardiologist if this is not possible. (iii) What should I do if I have bleeding during duplex antiplatelet therapy? Mild bleeding (e.g. skin bleeding, nasal bleeding, urinary tract bleeding, etc.): there is no need to be nervous, and do not discontinue duplex antiplatelet therapy without authorization. It is generally recommended to check the coagulation function and platelets, take appropriate local hemostatic measures, closely observe the development of bleeding signs clinically, and reduce enteric aspirin to 75 mg/d if necessary. The most common site of major bleeding with dual antiplatelet therapy is the gastrointestinal tract, while the most dangerous bleeding site is intracranial bleeding. During long-term antiplatelet therapy, especially during the first 3 months of administration, clinicians and patients should observe and monitor patients for adverse effects such as gastrointestinal discomfort and bleeding, and pay attention to the presence of black stools or unexplained anemia for early detection of bleeding complications. It is recommended that those taking the drug should have their fecal occult blood test rechecked every 1 to 3 months, and once bleeding occurs, blood tests should be performed immediately, and active treatment should be given. If bleeding persists despite aggressive treatment, dual antiplatelet therapy may be discontinued briefly. In principle, one antiplatelet drug should be discontinued first. In clinical practice, enteric aspirin is mostly discontinued first, but theoretically clopidogrel is more damaging to the repair function of gastric mucosa than aspirin, and clopidogrel should be discontinued first. All antiplatelet drugs should be discontinued if bleeding still cannot be stopped, or if hemodynamic abnormalities are caused by hemorrhage, or if intracranial bleeding occurs. It should be noted that if there is no recurrence of bleeding within 3-7 d after discontinuation and hemodynamic stabilization, dual antiplatelet therapy should be restarted as soon as possible. III. Drugs for treatment of existing cardiovascular risk factors The generation and development of coronary heart disease are mostly associated with cardiovascular risk factors such as smoking, hypertension, diabetes mellitus, hyperlipidemia, and obesity. Although the stent is implanted, the above pathological basis of coronary heart disease still exists and is still at work, and the end of interventional treatment is not equal to coronary heart disease being cured. Therefore, in addition to seriously insisting on changing poor lifestyle (including quitting smoking) after stenting, efforts should be made to control hypertension, diabetes and hyperlipidemia up to the standard. For general coronary artery disease patients, blood pressure should be controlled to <140/90 mmHg, and for those with combined chronic kidney disease, blood pressure should be controlled to 130/80 mmHg. Lifestyle changes should be combined with pharmacological treatment, with β-blockers and/or ACEI therapy being the first choice. If necessary, small doses of thiazide diuretics may be used. Patients need to be prevented from having a DBP below 60-70 mmHg while ensuring that blood pressure lowering is achieved. It is recommended that the HbAIC of patients with diabetes combined with coronary artery disease be controlled at 6.5% to 7.0%. Care should be taken to avoid hypoglycemia in patients with advanced age, longer history of diabetes, higher overall cardiovascular risk level, history of severe hypoglycemic events, shorter life expectancy, and coexisting multiple diseases. Patients with coronary artery disease combined with diabetes mellitus who have unsatisfactory glycemic control may consult an endocrinologist. To choose appropriate lipid-lowering drugs, statins are generally required to bring LDL-C down to below 1.82 mmol/L. Those with low basal LDL-C levels can use weaker statins (e.g. pravastatin 40mg/d or simvastatin 20mg/d); those with high basal LDL-C (>3.38mmol/L) should use strong statins (e.g. atorvastatin 20mg/d or rasulvastatin 10mg/d); those with very high basal LDL-C levels (>4.16 mmol/L), a higher dose of statin should be used (e.g., atorvastatin 40 mg/d or rivastigmine 20 mg/d). The use of statins for patients with coronary artery disease is not only useful for lipid lowering, but is the main therapeutic measure to modulate lipids, stabilize plaque, slow down the progression of atherosclerosis, and prolong event-free survival of patients. Statin therapy is a long-term process and should be continued even after the lipid standard is reached and stabilized. The incidence of adverse reactions to long-term statins is low, and liver function and muscle enzymes can be monitored regularly, especially after 1 to 2 months of taking the drug or when symptoms such as muscle pain, weakness, and poor nasal function occur. The common adverse reactions are mainly myalgia or mild elevation of transaminases (less than 3 times the upper limit of normal), which can be closely observed without dose reduction or discontinuation. If the aminotransferase level rises more than 3 times the upper limit of normal, or if it is accompanied by bilirubin, or if it is accompanied by symptoms such as poor health and weakness, or if the creatine kinase level rises more than 5 times the upper limit of normal, the drug should be stopped and closely observed. Fourth, take drugs that can clearly improve the long-term prognosis of patients after coronary heart disease stenting Studies have proved that the drugs that can more clearly improve the long-term prognosis of patients after coronary heart disease interventions are ? receptor blockers and ACEI (or ARB), which can antagonize the excessive activation of endoneuroendocrine, improve myocardial blood supply, prevent myocardial remodeling, and protect cardiac function. The use of ? receptor blockers requires that the resting heart rate be reduced to 55-60 beats/min,? Contraindications to the use of receptor blockers include asthma, symptomatic hypotension or bradycardia, and severe decompensated heart failure. In the absence of contraindications, all patients with STEMI with heart failure (LVEF <0.45), hypertension, diabetes mellitus or chronic kidney disease should be on long-term ACEI. low-risk STEMI patients (i.e., those with normal LVEF, successful bloodway re-entry and satisfactory control of various cardiovascular risk factors) may also be considered for ACEI therapy. The use of ACEI is contraindicated in patients with symptomatic hypotension, severe renal failure (Cr>265μmmol/L), bilateral renal artery stenosis, allergy, etc. V. Do patients still need to apply anti-myocardial ischemic drugs after coronary intervention? Patients who have undergone intervention to achieve complete coronary revascularization and have no symptoms of myocardial ischemia can no longer apply anti-myocardial ischemic drugs such as nitrates. For patients who have undergone coronary intervention but have not achieved complete revascularization (such as residual stenosis in the distal part of the offender vessel or untreated lesions in the non-offender vessel), or who still have myocardial ischemic chest pain, anti-myocardial ischemic drugs should be used, mainly ? receptor blockers, calcium antagonists and nitrates. Finally, it is especially emphasized that patients should go to a hospital with interventional conditions as soon as they have an angina attack after coronary intervention.