Angina pectoris is a clinical syndrome with episodes of chest pain or chest discomfort caused by acute and temporary ischemia and hypoxia of the myocardium due to insufficient blood supply to the coronary arteries. According to the pathogenesis of angina and the proportion of coronary artery atherosclerosis plaque blockage and coronary artery spasm, angina is divided into stable angina, unstable angina and variant angina. The direct cause of angina is insufficient myocardial blood supply, which is mainly seen in coronary heart disease, but sometimes other types of heart disease can also cause angina, and coronary slow flow is one of them. Slow coronary flow (SCF) was discovered and described by Tambe et al. in 1972 and is not uncommon in patients without coronary stenosis, with detection rates ranging from 7% to 23.7% on coronary angiography. The main clinical manifestation is chest discomfort or angina, which usually lasts for a long time. To date it has not been possible to classify it into any of the angina types such as stable angina, unstable angina, variant angina, or cardiac X syndrome. Laboratory tests and coronary angiography show no cardiovascular disease or coronary risk factors or cardiac bridges present, but significant slowing of blood flow at the ends of multiple vessels is seen. The mechanism of SCF is unclear, and Tambe et al. suggest that it may be related to abnormalities in the function of small vessels in the coronary arteries. One study found abnormal platelet function and imbalance of vasoactive substance levels in patients with SCF. A small sample study found significantly higher levels of blood inflammatory factors in patients with coronary slow flow, suggesting that inflammatory mechanisms may be involved in the development and progression of SCF. In terms of treatment, a uniform and effective approach is lacking, and traditional anti-anginal and vasodilator drugs are ineffective. This may be related to SCF-specific small vessel involvement: the lack of enzymes necessary for the conversion of nitrates into effective metabolites in small vessels, so nitrate drugs are less effective; and the lack of L-type voltage-gated calcium channels on microvessels, so traditional L-type calcium antagonists are not effective in SCF. Currently, the following drugs are used for the treatment of coronary slow flow phenomenon: 1. Calcium channel blockers, mainly T-type calcium channel blockers, such as mibefradil, act on T-type calcium channels on microvessels to improve the microvascular diastolic function of coronary arteries. Recently, Qian Juying et al. reported that intracoronary injection of verapamil can also improve the blood flow condition. 2.Dipyridamole, which has good dilating effect on small vessel wall with lumen diameter less than 200μm, and reduces the uptake and degradation of adenosine by endothelial cells and erythrocytes, thus it is effective for SCF. 3.Statin drugs. 4.3rd generation beta-blocker, nebivolol. 5.Intracoronary nitroglycerin injection is also effective in improving blood flow, but weaker than intracoronary verapamil injection, and neither has restored coronary blood flow to normal levels in patients. Extracorporeal counterpulsation can also be used to treat SCF, which is performed by wrapping a special balloon sleeve around the extremities (or both lower extremities) and buttocks of the body, using the R wave of ECG as the trigger signal. causing the aortic systolic pressure to fall.