Abstract One night 2 years ago, I was on ward duty when a 60-year-old male patient was urgently admitted to our department by the emergency physician. The emergency physician described that the patient had sudden chest pain with profuse sweating 30 min earlier and was given sublingual nitroglycerin tablets, which relieved the chest pain after about 10 min. Blood pressure was measured at 70/40 mmHg during the onset of chest pain, and the electrocardiogram showed that the ST segment in leads II, III and aVF was elevated arch-backwards and formed a unidirectional curve with the T wave, while the ST segment in leads I and aVL was shifted downwards and the T wave was inverted, and the ST segment in leads V1 to V6 was shifted downwards. After receiving the patient, he was immediately given cardiac monitoring and oxygenation. Blood pressure was measured at 120/80 mmHg, and the ECG was traced again, and the ST segments in all leads returned to baseline levels. Preliminary diagnosis: coronary artery disease, unstable angina, variant angina. Treatment plan Bed rest was ordered, and nitrates were given intravenously. After 10 min of infusion, the patient again showed symptoms of chest pain, monitored blood pressure of 70/50 mmHg, and ECG monitoring showed ST-segment arch-back elevation in leads II, III and aVF. Immediately afterwards, the patient had convulsions and loss of consciousness, and ECG monitoring showed ventricular fibrillation, and emergency asynchronous electrical cardioversion was given once immediately, which was successful. After the patient woke up, the ECG monitor showed that the elevated ST segment of the leads returned to the baseline level. The next day, blood cardiac enzymes and troponin were checked in normal range, and there was no significant ST-T change in all leads of the ECG on recheck. Then he added diltiazem 30 mg orally 3 times a day, and was treated with potassium, magnesium and regular fluids for consolidation, and was discharged after 7 days of improvement. The concept of coronary artery spasm and pathogenic factors Coronary artery spasm (CAS) refers to the occurrence of transient constriction of the subepicardial artery, causing partial or complete blockage of the vessel, which can cause variant angina, unstable angina, acute myocardial infarction (AMI), and sudden death. Among them, variant angina is related to smoking, alcoholism, emotional excitement, type A personality, coronary angiography is mostly normal, mostly seen in young people, and more common in women; other cases of coronary artery spasm, such as unstable angina, acute myocardial infarction (AMI), sudden death, etc., are mostly related to hyperlipidemia, coronary atherosclerosis, coronary angiography vessels have certain narrowing, seen in all ages, mostly in the elderly. It is more common in elderly people. The clinical manifestations of coronary artery spasm depend on the above diseases corresponding to coronary artery disease, for example, variant angina, the main symptom is chest tightness and chest pain at rest, which can be accompanied by sweating, mostly paroxysmal; patients with myocardial infarction with coronary artery spasm, the main manifestations are unrelieved chest pain, sweating, anxiety, etc.; in the case of patients with unstable angina , it is manifested as chest pain and chest tightness aggravated by paroxysms at rest or during exertion. The chest pain and sweating that occurs in the resting state of the patient presented in this article belongs to this type of variant angina pectoris. ECG manifestations of coronary artery spasm Coronary artery spasm is manifested by ST-segment depression or T-wave inversion in the localized leads if the vessel is partially blocked, or by ST-segment arch-back elevation in the localized leads if the vessel is completely blocked, which is similar to the ECG manifestations of acute myocardial infarction. These ECG manifestations are often temporary and improve or disappear with treatment. Therefore, in case of complete vasospastic blockage, although temporary, it can cause various arrhythmias that can occur just like myocardial infarction, such as ventricular tachycardia, ventricular fibrillation, atrioventricular block, etc., which are life-threatening. In this case, during the onset of symptoms in the patient, the ST segment in leads II, III, and aVF was elevated arch-back upward, the ST segment in leads I and aVL was shifted downward and the T wave was inverted, and the ST segment in leads V1 to V6 was shifted downward, and the cool-view myocardial infarction graph basically identified complete vascular occlusion after coronary artery spasm in the right coronary artery, and ST segment shift downward in the corresponding leads suggested incomplete occlusion in other vascular spasms or the presence of stenosis. The presence of ventricular fibrillation in the patient is highly suggestive of complete vessel occlusion after coronary artery spasm, similar to the state of myocardial infarction, and requires high attention. Serum marker presentation Serum markers of myocardial damage, such as CK-MB and troponin, can be elevated, normal, or mildly elevated, depending primarily on the degree of myocardial damage. Community referral recommendations for clinical manifestations Community physicians encountering patients with recurrent episodes of coronary heart disease chest pain, especially those who also have episodes at rest, are advised to promptly refer them to the hospital under close observation. In particular, patients with episodes of chest pain and sweating in the resting state are high-risk patients and prone to sudden death. Such cases require good referral conditions, such as, well-equipped emergency vehicles with monitors and defibrillators, etc., so that in case of accidents, resuscitation can be performed at any time and anywhere; patients who are far from higher hospitals and do not have referral conditions, if they have acute myocardial infarction caused by coronary artery spasm, they should be In case of acute myocardial infarction caused by coronary artery spasm, timely pharmacological thrombolysis should be performed in the local hospital, and drugs such as nitrates and calcium channel blockers should be applied to rescue the patient. General treatment Bed rest and oxygen intake. Calcium channel blockers are the main drugs for the treatment of coronary artery spasm, among which non-dihydropyridine diltiazem is preferred, and the addition of nitrates has a synergistic effect. Oral beta-blockers, on the other hand, can aggravate the condition and should be used with caution. Acute myocardial infarction and hypokalemia are called the “sudden death twin demons”. Patients with severe acute coronary syndrome (including cases caused by coronary artery spasm) have severe chest pain and irritability at the onset, which cause the body to enter a stressful state, and plasma catecholamine levels increase significantly, activating sodium/potassium ATPase and prompting sodium/potassium exchange. This leads to increased secretion of renin, angiotensin, and aldosterone, which increases potassium excretion and leads to hypokalemia or relative potassium deficiency. It is important to note that even if the blood potassium decreases mildly by 0.5 to 0.1 mmol/L compared to the original level, even though it has not yet fallen to the low limit of laboratory normality (3.5 mmol/L), the decrease in blood potassium has actually reached more than 20% to 30%, and this rapid onset of relative hypokalemia is clinically important in patients with acute myocardial infarction, coronary artery spasm and other severe acute coronary syndromes. It is still possible to promote hypokalemia-associated malignant arrhythmias in acute myocardial infarction. Therefore, acute hypokalemia and relative hypokalemia in the early phase of acute myocardial infarction should also be given high priority. Clinical practice has demonstrated that in patients with critical cardiovascular disease, the blood potassium should be maintained at >4.5 mmol/L and blood magnesium at >1.0 mmol/L in the vulnerable myocardial state, and malignant arrhythmias are less likely to occur in this condition. In this case, the patient was safely discharged after 7 days after the above mentioned treatment.