What is myocardial bridge?

Coronary artery myocardial bridge is a congenital coronary artery malformation. Under normal circumstances, the coronary artery runs on the epicardial surface. If a section of the coronary artery penetrates into the cardiac muscle layer, this section of the myocardium is called a myocardial bridge, and the covered coronary artery is called a parietal coronary artery or a tunnel artery.

Myocardial bridge was originally considered to be a benign variation that did not require interventional treatment. However, with the progress of clinical research, some scholars believe that myocardial bridge may cause a series of cardiovascular events. Therefore, the diagnosis and treatment of myocardial bridge has received increasing attention from clinical physicians in recent years.

Due to differences in research and examination methods, the detection rate of myocardial bridges varies greatly, and the detection rate of myocardial bridges in autopsy is approximately 33%-42%.

Myocardial bridges can be single or multiple, mostly located in the proximal and middle segments of the left anterior descending artery. Myocardial bridges are divided into superficial (thickness ≤ 2 mm) and deep (thickness > 2 mm) according to the depth of the wall coronary artery. The superficial type runs in the interventricular groove and is covered by a thin layer of connective tissue, nerves, fat and other tissues before reaching the apex. It is more common, accounting for about 75%; the deep type runs in the interventricular septum close to the right ventricle, covered by myocardial fibers, and can compress the wall coronary artery below, thereby causing hemodynamic damage.

Clinical manifestations of myocardial bridge:

Superficial myocardial bridges generally have no obvious clinical symptoms. Deep myocardial bridges may cause myocardial ischemia, angina pectoris, arrhythmia, acute coronary syndrome, etc. due to their compression, which may lead to cardiogenic shock or even sudden death.

Common diagnostic methods for myocardial bridge:

1. Coronary computed tomography angiography (CCTA): The most commonly used method, which can clearly show the positional relationship between the wall coronary artery and the myocardial bridge, the thickness and length of the myocardial bridge, the degree of systolic compression, and whether there are atherosclerotic plaques.

2. Coronary angiography (CAG): It is the gold standard for diagnosing myocardial bridges. Its characteristic manifestation is "systolic compression-induced stenosis", also known as "milking phenomenon", that is, the wall coronary artery is significantly narrowed during systole, and the stenosis disappears during diastole. Since the detection rate of ordinary CAG for myocardial bridges is not high, it is sometimes combined with injection of vasodilators (such as nitroglycerin) in clinical practice to induce or enhance this characteristic manifestation.

3. Coronary intravascular ultrasound (IVUS): The characteristic manifestation is the appearance of a half-moon-shaped echo-free area between the epicardium and the external elastic membrane of the blood vessel, which exists throughout the cardiac cycle and is called the "half-moon sign". It is highly specific. Compared with CAG, IVUS has a higher sensitivity in diagnosing myocardial bridges. IVUS can also evaluate the length, depth, lumen size, lumen compression, wall condition, and the presence of atherosclerotic plaques in myocardial bridges.

4. Optical coherence tomography (OCT): It is manifested as a spindle-shaped, uneven low-signal area with clear boundaries in the epicardium. OCT has high resolution and can observe finer structures of plaques, but has poor penetration and cannot clearly display the outer structure and compression degree of the lumen.

Treatment of myocardial bridge:

1. Preferred drug treatment: Commonly used beta-blockers and non-dihydropyridine calcium channel blockers. Beta-blockers are preferred, which can reduce myocardial contractility by slowing down the heart rate, reduce the pressure on the wall of the coronary arteries during cardiac contraction, and relieve patient symptoms. Commonly used drugs include bisoprolol, metoprolol, atenolol, etc. For patients who have contraindications to the use of beta-blockers, non-dihydropyridine calcium channel blockers such as diltiazem and verapamil can be used, which can also relieve the patient's ischemic symptoms. Ivabradine can be used as a second-line medication for patients with myocardial bridges, mainly for patients who cannot use beta-blockers and non-dihydropyridine calcium channel blockers. Be careful to avoid the use of nitrates.

2. Percutaneous coronary intervention: It is not recommended as a routine treatment. Although coronary stent implantation can relieve the compression of the myocardial bridge on the wall coronary artery and restore the heart's blood flow reserve in the short term, many related studies have shown that the rate of stent restenosis and revascularization after stent implantation is high, and there is a long-term risk of coronary artery perforation, stent fracture or stent thrombosis, so special caution should be taken when choosing stent implantation for treatment.

3. Surgical treatment: mainly for patients with poor drug treatment effects, frequent angina attacks and severe symptoms. It includes: myocardial bridge incision and release and coronary artery bypass grafting. Myocardial bridge incision and release is suitable for patients with short and superficial myocardial bridges. Coronary artery bypass grafting is recommended for patients with length > 2.5 cm and depth > 0.5 mm.

References:

[1] Zu Yanan, Zhang Mingyu. Research progress of coronary myocardial bridge[J]. Journal of Cardiovascular Rehabilitation Medicine, 2023, 32(3): 254-258. DOI: 10.3969/j.issn.1008-0074.2023.03.09.

[2] Expert group of the Chinese Society of Research Hospitals on the diagnosis and treatment of coronary myocardial bridge. Expert consensus on the diagnosis and treatment of coronary myocardial bridge[J]. Chinese Research Hospitals, 2022, 9(5): 1-8. DOI: 10.19450/j.cnki.jcrh.2022.05.001.