“Coronary artery myocardial bridge”, which is a longer segment of coronary artery travels within the muscle of the ventricular wall, narrowing the lumen of that segment of the vessel after the lumen is squeezed during cardiac systole. The total detection rate is 5.4% to 85.7%. Generally, systolic coronary artery stenosis is less than 75% and is not clinically symptomatic with insignificant ECG changes. If the stenosis is greater than 75%, it should undergo surgical treatment, i.e. myocardial release surgery. At the proximal end of the myocardial bridge, coronary atherosclerosis is likely to develop due to blood turbulence. Both coronary angiography and multi-row spiral CT can clearly show the myocardial bridge and thus clarify the diagnosis. Coronary angiography is characterized by the blockage or even complete disappearance of blood flow in a section of the coronary artery during the systolic phase of the heart, and the reduction or complete return to normal in the diastolic phase. According to the degree of stenosis in the systolic coronary artery after compression, there are three grades: grade I with stenosis <50%, which is often asymptomatic; grade II with stenosis 50%-75%, which may have symptoms of myocardial ischemia and angina; grade III with stenosis >75%, which mostly has symptoms of angina and even myocardial infarction and sudden death. Electrocardiogram is often inaccurate for the diagnosis of coronary artery myocardial bridge, some patients can be completely normal, and some can have mild T-wave changes. Multi-row spiral CT shows myocardial tissue overlying the coronary arteries, but cannot determine the degree of vascular compression. Asymptomatic myocardial bridges generally do not require treatment. Patients with symptomatic myocardial bridges are preferred to be treated with medication, and those who fail to do so after medication can be treated surgically or with stent implantation. According to the classification of myocardial bridges: Grade I does not require special treatment. The pharmacological mechanism is to reduce the myocardial contraction and the compression of the wall coronary artery in the myocardial bridge segment, and to slow down the heart rate to reduce the number and total time of narrowing of the wall coronary artery by compression. Class III generally advocates surgery, which can be performed in two ways: first, myocardial release; second, coronary artery bypass surgery. It should also be noted that coronary myocardial bridges rarely require coronary stenting because they rarely have fixed stenoses and have a high recurrence rate after stenting. Treatment of myocardial bridges with placement of coronary stents has been attempted, but a high rate of postoperative restenosis (in excess of 50%) was found, as well as the aggressive intraoperative complication of coronary artery rupture. Therefore, the overall preference is for non-interventional treatment. Beta-blockers such as metoprolol and bisoprolol can improve cardiac blood supply by decreasing cardiac contractility and slowing heart rate. Calcium blockers, especially non-dihydropyridine calcium blockers such as verapamil and diltiazem, can eliminate coronary spasm, but also prolong the diastolic time frame of the cardiac cycle and reduce the degree of ischemia, and are the main effective drugs for the treatment of myocardial bridges; antiplatelet agents are used in the treatment of myocardial bridges with unstable angina or acute heart attacks. In particular, nitrates can aggravate the systolic stenosis of coronary arteries caused by myocardial bridges and should be avoided as much as possible. Nitrate drugs can reduce cardiac preload, increase myocardial contractility and aggravate the compression of wall coronary arteries by myocardial bridges, so nitrate drugs are not recommended for patients with myocardial bridges. Nitrate drugs include nitroglycerin, cardiac pain relief, and Xinkang.