Percutaneous coronary intervention (PCI) is one of the main tools for reperfusion treatment of acute coronary syndromes (Acs). PCI can significantly improve the prognosis of patients with acute coronary syndromes, prolong their life span and improve their quality of life. In the past three decades, PCI has gone through the PTCA era, BMS era and DES era. Currently, PCI technology in the drug-eluting stent (DES) era is an important option for the treatment of coronary artery disease and is widely used in clinical practice. Especially with the continuous development of interventional devices, interventional techniques, perioperative medications, the deepening understanding of pathophysiological mechanisms of different types of coronary heart disease, and the wide application of evidence-based medicine in the field of interventional cardiology, the progress of PCI indications Percutaneous coronary intervention (PCI) is the most important option for the treatment of acute PCI can significantly improve the prognosis of patients with acute coronary syndromes, prolong their life expectancy and improve their quality of life. In the past three decades, PCI has gone through the PTCA era, BMS era and DES era. Currently, PCI technology in the drug-eluting stent (DES) era is an important option for the treatment of coronary artery disease and is widely used in clinical practice. Especially with the continuous development of interventional devices, interventional techniques and perioperative medications, the deepening understanding of pathophysiological mechanisms of different types of coronary heart disease, and the wide application of evidence-based medicine in the field of interventional cardiology, the progress of PCI indications has shown a trend of continuous broadening and refinement, which has increased the status of PCI technology in the overall strategy of coronary heart disease treatment. In recent years, the AHA/ACC/SCAI guidelines for PCI have been continuously updated. The guidelines have repeatedly reaffirmed the importance of PCI in the management of coronary artery disease and have emphasized the need for scientific and rational evaluation of the benefit/risk ratio of PCI. Patients at high risk, including those with anatomically suitable multi-branch lesions (especially those with good cardiac function and non-diabetic patients) should be aggressively intervened in the early stages. PCI remains an effective treatment for patients who have been thrombolized after myocardial infarction or who have not undergone thrombolysis, such as those with recurrent myocardial infarction, severe myocardial ischemia, developing cardiac insufficiency, or unstable electrocardiographic activity. Numerous clinical study data encourage clinical practitioners to apply PCI to more challenging coronary cases, such as chronic total occlusive lesions, multi-vessel lesions, unprotected left main lesions, and coronary bifurcation lesions. As the scope of DES continues to expand and the number of patients treated with DES increases, there is a growing realization that current DES is far from perfect. The occurrence of events such as vascular remodeling, intimal hyperplasia, inflammatory response, reperfusion injury, and coronary spasm has led to thrombosis, in-stent restenosis, slow flow or no reflow in some patients after PCI (flow r11MI class II). How to further improve the PCI treatment protocol to make it a powerful weapon to conquer coronary artery disease? This has led to an eager and widespread interest in exploring the application of a clinical pathway (CP) for the management of CAD patients treated with interventions. This is done by developing a holistic therapeutic care model that follows an orderly and time-sensitive standardized therapeutic care process for the continuation of patient care after PCI. In particular, it is important that patients receive standardized therapeutic care according to this model after successful PCI in order to control quality and shorten recovery time. So, what should we do after PCI to further reduce the incidence of these cardiovascular events? Recurrent myocardial ischemia after PCI and secondary prevention of coronary events after PCI remains one of the most important issues in the prevention and treatment of cardiovascular disease in the world today, and recurrent myocardial ischemia after PCI may be the result of restenosis or the progression of a new lesion. Clinically, typical restenosis occurs around 3 months after PCI, with occasional rapidly progressive restenosis occurring around 1 month. Angina that occurs after 12 months after PCI is more likely to be the result of progression of an existing lesion or the development of a new lesion rather than restenosis. However, our recent study found that restenosis also occurs after 6 months after drug stenting, which is called the Catch-up phenomenon of stent restenosis. It is important to note that approximately 10% of patients present with asymptomatic restenosis after PCI. Therefore, it is important to apply flexible screening methods for the postoperative out-of-hospital management of this population. As recommended by the American College of Cardiology (ACC)/American Heart Association (AHA) guidelines, routine loading tests combined with non-invasive myocardial imaging should be performed 3-6 months after PCI in patients at high risk (left ventricular insufficiency, multiple vascular lesions, proximal left anterior descending lesions, history of sudden death, diabetes mellitus, hazardous occupations and suboptimal PCI results). For review of patients after coronary stenting, coronary CT angiography (CTA) is able to assess some degree of restenosis for thicker stents, but restenosis within most metallic stents is limited on CT. There is a lack of results from such large clinical studies on whether strategies established to guide treatment based on CTA stent follow-up are consistent with treatment strategies based on coronary angiographic findings. Drug therapy remains the most basic and important treatment for coronary artery disease, not only to relieve symptoms but also to reduce mortality and prolong patients’ lives by altering the course of coronary artery disease. Therefore, even after coronary revascularization therapy, it is important to adhere to the optimal pharmacological treatment for symptom relief and improved survival. To date, four classes of drugs have been shown to reduce the incidence of cardiovascular events in patients after PCI, including aspirin, statin lipid-lowering agents, ACE inhibitors (ACEI), and B. receptor blockers. Overall, the reduction in event risk in patients after PCI was similar for all four drug classes, with a 25% to 30% reduction in risk, respectively, while the combination of the four drugs resulted in an even greater benefit, with a 70% reduction in overall cardiovascular event risk. ① The role of platelet activation in coronary heart pain is unquestionable. In contrast, PCI treatment disrupts the integrity of the vascular endothelium, leading to exposure of the subendothelial matrix, triggering platelet adhesion and aggregation, followed by the formation of platelet-rich thrombi, while activation of the coagulation system increases the size of the formed thrombus, resulting in lumen occlusion. The implantation of intracoronary stents can also activate platelets and increase the incidence of acute, subacute and late thrombosis, the occurrence of which is uncommon but often causes MI and sudden death. Therefore, dual antiplatelet therapy is considered the standard of care after PCI and is recommended for more than 1 year. The American College of Chest Physicians (ACCP) recently published the 2008 Antithrombotic and Thrombolytic Guidelines recommending 4 weeks of clopidogrel after bare stent placement and 1 year after drug-eluting stents if there are no bleeding complications. Triple antithrombotic therapy is recommended for patients undergoing stenting with an indication for vitamin K rejection. ② Statin therapy after PCI is well known. The mechanism of benefit is related to its effects on platelet aggregation, antithrombotic, endothelial function, anti-inflammatory and plaque stabilization. Therefore, statin therapy in post-PCI patients should avoid the misconception that it should be discontinued after the lipids are “normalized”. ③A large body of evidence-based medical evidence confirms that ACEI therapy is effective in improving long-term prognosis, delaying the progression of heart failure, and reducing cardiovascular morbidity and mortality in all patients at high risk of coronary heart disease. Therefore, the new ACC/AHA guidelines for the treatment of chronic stable angina recommend that all patients with coronary artery disease, including those after PCI, should receive ACEI therapy, thus extending the indication for ACEI in coronary artery disease from patients after MI to all patients with coronary artery disease. ④ There is sufficient evidence for ß-blockers in the secondary prevention of coronary artery disease to reduce the incidence of all-cause versus cardiac death, recurrent nonfatal MI, and sudden death. At direct PCI, ß-blocker application has the benefit of reducing malignant arrhythmias and periprocedural cardiac enzyme and marker release and improving left ventricular function at follow-up. It is currently believed that ß-blockers are recommended to improve prognosis after PCI in all patients with coronary artery disease diagnosed with MI, acute coronary syndrome, or left ventricular insufficiency, if not contraindicated. Although PCI can recanalize completely blocked or highly stenosed coronary arteries and restore the function of the myocardium that is still alive but functionally impaired, it cannot resolve the stenosis, blockage and extensive atherosclerosis of the microvessels, which means that PCI does not necessarily lead to complete revascularization in patients with coronary artery disease, it is only one part of the treatment and does not cure coronary artery disease. Since coronary atherosclerosis is a diffuse lesion, interventional treatment only deals with vessels with more than 70% diameter stenosis, not with mild to moderate lesions, and patients still have the possibility of re-occurrence of angina pectoris and myocardial infarction; secondly, there is a certain recurrence rate of successful interventional treatment, and vessels that have been unblocked still have the possibility of re-stenosis. Therefore, timely coronary angiography review after intervention is necessary, especially for patients with combined diabetes, multiple coronary lesions and adventitia, to assess the efficacy and guide future treatment strategies. Many pharmacologic treatments can improve heart failure symptoms and delay patient life, but have limited effect on established stenoses and atherosclerosis. Therefore, PCI and pharmacological treatment of patients with coronary artery disease still have limitations. Extracorporeal counterpulsation has undergone more than 20 years of exploration and practice, and is an effective treatment measure and supplement to the current conventional treatment after PCI for coronary artery disease. The main mechanisms of EECP for coronary artery disease are: on the one hand, (i) EECP can significantly increase aortic diastolic pressure, improve coronary perfusion, increase the pressure gradient between myocardial ischemic and non-ischemic zones, facilitate the formation and opening of pre-existing vascular anastomotic branches, establish collateral circulation, and thus improve the perfusion zone of myocardial ischemia. (ii) Due to sequential inflation of the balloon, the arteries in the lower extremities and buttocks are squeezed. In the pre-systolic phase of the heart, the balloon rapidly deflates and the peripheral resistance sharply decreases, reducing cardiac afterload, decreasing myocardial oxygen consumption and improving cardiac function. ③EECP also increases the output per beat, improves cardiac index, decreases systemic vascular resistance, and opens and promotes collateral circulation. On the other hand, (1) the dual pulsatile blood flow (systolic and diastolic pressurization waves) generated during EECP both increases blood perfusion to tissues and organs and raises blood flow shear stress. The increase of blood flow shear stress can significantly increase the level of nitric oxide (NO) and vasodilator factors such as prostacyclin (PGI2), decrease vasoconstrictor factors such as endothelin-1 (ET-1) and thromboxane A2 (TXA2), increase the ratio of NO/ET-1 and PGI2/TXA, and regulate cytokines related to endothelial protection, improve vascular endothelial function and vascular EECP can improve vascular endothelial function and vascular tension, and can promote vascular endothelial cell synthesis. EECP can increase the levels of VEGF, HGF, bFGF and MCP-1, which can affect endothelial division, proliferation and migration in myocardial tissues, thus promoting vascular neovascularization, increasing the opening and formation of collateral circulation, increasing local blood flow and improving myocardial perfusion, (ii) EECP can significantly increase myocardial blood flow, improve myocardial perfusion, and increase exercise tolerance. (3) EECP significantly increases tissue-type fibrinogen activator (t-PA), decreases fibrinogen activator inhibitor (PAI), increases t-PA/PAI, regulates platelet function, maintains the balance between coagulation and fibrinolytic state, and inhibits coronary thrombosis. Thus, the effect of EECP is not only in the hemodynamic effect itself, but also in the promotion of the expression and benign regulation of a series of related genes in the vascular endothelium by increasing the blood flow shear stress, which can protect the vascular endothelium, promote the structural and functional repair of damaged vascular endothelial cells, improve the vascular endothelial function, and inhibit the occurrence and development of atherosclerosis. At the same time, early rehabilitation exercises after interventional treatment will bring more and more benefits to patients. According to the recommendations of the American College of Sports Medicine, for patients with simple lesions, there is no need to strictly limit the amount of post-intervention exercise, and some patients may be able to return to daily non-manual work with simple rehabilitation exercises. For patients with complex lesions or untreated complications, such as premature beats, heart failure, and residual intravascular lesions, attention should be paid to gradually increasing the amount of exercise from a low load, with the aim of improving cardiac function, gradually increasing the speed and distance, and increasing the intensity and duration of exercise to prepare for return to work and society. Systematic rehabilitation training helps to improve the ischemic myocardium, increase the exercise endurance of patients, and help to delay or stop the development of coronary atherosclerosis, and together with psychotherapy and diet therapy, alleviate various adverse symptoms caused by negative emotions such as anxiety and depression, so that patients can return to society, family life and work, and to prevent the recurrence of cardiac events, encourage patients to make lifestyle changes. changes. In summary, in modern PCI treatment of coronary artery disease, we should pay attention not only to the procedure itself, but also to the scientific and orderly management after PCI, and effectively translate the evidence-based medical evidence into clinical treatment plans in order to further improve the coronary artery disease treatment measures. The use of individualized principles of scientific and standardized selection of systemic therapies can help patients recover and improve the quality of life after PCI for coronary artery disease. At the same time, the improvement of drug delivery technology, the selection of better drugs, the application of fully biodegradable stents, especially the deeper understanding of marrow stem cells (MSCs) research and the continuous exploration of myocardial perforation technology will make the treatment plan of coronary heart disease more effective.