The results of the 2002 survey on the current smoking situation in China showed that there were 350 million smokers and 900 million passive smokers in China, making it the world’s largest area of tobacco consumption and tobacco harm. Even after nearly eight years of publicity on the harms of smoking, the 2010 Global Adult Tobacco Survey results show that after 2002, China’s smoking situation, quit rate and exposure to secondhand smoke did not significantly improve. The 2011 China Tobacco Control Report 350 million smokers and 740 million people with secondhand smoke. Epidemiological studies have found that active smoking increases the risk of coronary heart disease by 80% and passive smoking similarly increases the occurrence of coronary heart disease by 30%, smoking increases the occurrence of myocardial infarction and fatal coronary heart disease, and the INTERHEART study found that the risk of non-fatal myocardial infarction was 2.95 times higher in smokers than in non-smokers. Studies have shown that smoking is an independent risk factor for coronary heart disease and an independent predictor of new damage formation in the coronary arteries. Tobacco smoke contains more than 4,000 chemicals and 250 toxic and harmful substances, of which more than 60 are carcinogenic, and nicotine is the main addictive substance. Secondhand smoke has higher concentrations of many carcinogenic and toxic chemicals than the smoke inhaled by the smoker himself. Nicotine, carbon monoxide, oxygen free radicals, polycyclic aromatic hydrocarbons, and butadiene in tobacco smoke are directly associated with damage to the cardiovascular system. Smoking causes oxidative modifications of lipid components, inflammation, and vascular dysfunction that can be involved in the overall process of atherosclerosis. In the initiation phase, smoking leads to decreased nitric oxide production and reduced bioactivity, causing reduced endothelial diastolic function; monocytes are involved, triggering inflammation; smoking promotes oxidative modification of LDL cholesterol and lowers HDL cholesterol. In the progressive phase, smoking causes sustained endothelial function impairment, vascular inflammation, smooth muscle cell proliferation and production of fibers, and foam cell formation. During the complication phase, smoking further exacerbates inflammation, lipid core enlargement, promotes unstable plaque formation and rupture, and leakage of material from unstable plaques into the vascular lumen, causing acute thrombosis. Thus, smoking can be involved in the development and progression of acute coronary syndromes. One study found that in patients who underwent percutaneous coronary revascularization followed for 16 years, the risk of Q-wave myocardial infarction was 2.08 times higher in current smokers than in nonsmokers (95% CI 1.16 to 3.72). In patients who underwent percutaneous coronary revascularization or coronary artery bypass grafting for acute myocardial infarction, smoking increased the rate of restenosis and recurrent ischemic events. It was found that the dose-effect relationship between the degree of smoking and the effect on endothelial function was not linear, and that the effect on endothelial function was similar between small amounts of smoking and heavy smoking, the latter possibly related to the presence of saturating effects of biochemical and cellular processes of toxic substances during smoking. Therefore, complete cessation of smoking is part of a comprehensive treatment for patients with acute coronary syndromes who smoke. Tobacco dependence is a slow-form addictive disease, and treatment of tobacco dependence requires a gradual, four-step approach. The first step is to ask: through questioning, the patient’s smoking history is understood and a nicotine dependence score is performed, along with an understanding of the patient’s cessation status and willingness to quit. The second step is to introduce: through guidance, help the patient to correctly position himself or herself and fully understand that tobacco dependence is a disease; inform the patient of the dangers of smoking, that smoking is an independent risk factor for cardiovascular disease as important as hypertension, hyperlipidemia and diabetes, and that it is associated with a variety of diseases such as cardiovascular disease; in the comprehensive treatment of acute coronary syndrome, smoking cessation is one of them, and gradually guide the patient to establish the determination to quit smoking The first step is to introduce the current means and progress of smoking cessation treatment, including pharmacological treatment, and establish the patient’s confidence to quit smoking. The third step is to make a plan to quit smoking with the patient. The fourth step is to visit, through follow-up visits, to understand the quitting situation, withdrawal symptoms and adverse drug reactions, and to strengthen smoking cessation education, insist on quitting and prevent relapse. Tobacco dependence is a chronic addictive disease, and tobacco dependence includes both physical and psychological dependence. Therefore, in patients with acute coronary syndrome, adequate health education should be provided to patients, especially for patients who only have smoking as the only cardiovascular risk factor, including the correlation between smoking and the occurrence, development, and prognosis of their current disease, and patients and their families can be shown information on the effects of their coronary angiograms, etc., so as to reason with them and move them to firm up their determination to quit smoking, and make their families become the patients’ The patient’s family can become the supervisor of the patient’s smoking cessation. The degree of dependence on tobacco is similar to that of the drug cocaine, and the withdrawal process is difficult, and withdrawal symptoms can occur, mainly in the form of irritability, irritability, anxiety, depression, inattention, insomnia, reduced heart rate, increased appetite, irritability, depression, etc., which can cause extreme distress to the quitter and is the most important reason for failure to quit smoking. Nicotine levels in the body usually begin to decline soon after daily nicotine use is stopped, and withdrawal symptoms usually begin within one day of stopping nicotine use, are most intense during the first 14 days, and begin to subside about one month after stopping nicotine use, and may last for up to six months. Literature on the incidence of withdrawal symptoms in different countries indicates that approximately 50% of quitters experience withdrawal symptoms. Dry withdrawal affects the psychosocial state of the patient. An analysis of data from the POMS scale, which scores the pre- and post-withdrawal state of mind of patients with dry withdrawal, showed that the scores of patients with dry withdrawal before withdrawal were similar to those of the general adult population; however, during withdrawal (5 days), the scores of patients increased to levels similar to those of psychiatric outpatients, with clinical manifestations such as anxiety, insomnia, irritability, and difficulty concentrating. This psychiatric abnormality is related to the abnormal secretion of hormones, ACTH, cortisol and prolactin levels. Mental stress and abnormal hormone secretion are important risk factors for the development of acute cardiovascular events. Therefore, it is important to assess the withdrawal symptoms during smoking cessation in patients with cardiovascular disease and to provide timely interventions. During the patient’s hospitalization, the patient can temporarily quit smoking by will due to the smoke-free environment of the ward, supervision by medical staff, and the influence of the disease itself. After discharge, when the environment changes, especially when they are in a smoking place, the chances of relapse are very high and the success rate of quitting smoking is unlikely. Therefore, in order to successfully quit smoking, some patients will require pharmacological intervention. Of course, patients should be informed that medications are not only for quitting, but also to help alleviate withdrawal symptoms due to inability to smoke, ease through the difficult period of quitting, avoid fluctuations in heart rate and blood pressure, and help in the treatment of current disease to achieve permanent cessation. For example, there was a patient with acute inferior wall and orthoposterior wall myocardial infarction who had smoked for more than 30 years, about 40 cigarettes per day, with a heavy nicotine dependence score, and after educating the patient about smoking cessation, the patient chose to quit dry, and on the third day of dry cessation, withdrawal symptoms appeared, and the patient agreed to a pharmacological cessation intervention, and after a week, he did not feel anything even when he saw others smoking, and at a follow-up of 3 months, no withdrawal symptoms appeared, and he did not return to smoking.