Normally, the coronary artery travels in the fatty tissue on the epicardial surface, but sometimes a segment of it travels in the myocardial fibers and comes superficially to the surface of the myocardium. It is covered by myocardial fibers shaped like a bridge. This bundle of myocardial fibers covering the coronary arteries on the surface of the heart is called a myocardial bridge, and the coronary artery underneath the myocardial bridge is called a wall coronary artery.
Myocardial bridges and wall coronary arteries are variations of the normal congenital anatomy of the coronary arteries. It is often found in the left anterior descending branch of the coronary artery (including the first diagonal branch) and occasionally in the right coronary artery. The detection rate of myocardial bridges varies from 0.4% to 9.7% during coronary angiography and from 5.4% to 85.7% during autopsy.
I. Pathophysiological effects of myocardial bridges on coronary artery blood supply
Previously, myocardial bridges were considered to be normal benign anatomical variants of the coronary arteries, which do not cause the occurrence of cardiac events. The basis includes.
1. myocardial bridges are congenital anatomical abnormalities that are present at birth, but those with clinical symptoms are often over 30 years of age.
2. the incidence of cardiac events is significantly lower than that in anatomy
3. maximum compression stenosis of the wall coronary arteries by myocardial bridges occurs only during systole, and only a small amount of antegrade flow is present in the coronary arteries at this time in the physiological state
4. There is no reliable evidence that wall coronary artery stenosis found during coronary angiography is clearly related to clinical myocardial ischemia.
It is now believed that myocardial bridges are benign anatomical variants that do not cause cardiac events in most patients, but can lead to pathophysiological changes with varying degrees of coronary ischemia under certain circumstances.
1. Reduced coronary blood flow.
Myocardial bridges severely compress wall coronary arteries during systole, resulting in delayed diastole, decreased blood flow, and reduced coronary flow reserve. The minimum and maximum cross-sectional areas of normal coronary arteries occur in the systolic and diastolic phases of the heart, respectively. In contrast, the minimum cross-sectional area of wall coronary arteries involved in myocardial bridges appears from end-systole to early diastole, and the maximum cross-sectional area does not appear until mid-diastole, i.e., the compression of wall coronary arteries by myocardial bridges continues until early and mid-diastole. Especially when the heart rate is fast or during exercise, the diastolic period is shortened, myocardial oxygen consumption increases, and myocardial perfusion is insufficient.
2. Wall coronary artery proximal atherosclerosis.
Ultrasound and pathology confirm that there are often atherosclerotic lesions in the proximal wall coronary arteries, while the wall coronary arteries themselves do not appear. This may be related to the higher shear pressure in the wall of the wall coronary artery and the lower shear pressure in the proximal vessels.
3. Coronary artery spasm.
Repeated compression of the wall coronary artery by the myocardial bridge leads to coronary artery endothelial dysfunction and induces coronary artery spasm.
4, arrhythmia.
Atrioventricular node ischemia causing AV block. Myocardial bridges (mostly with connective tissue) may act as components of the folding loop, leading to premature beats and tachycardia.
5. Heart failure.
Due to long-term myocardial ischemia.
II. Clinical manifestations
Most myocardial bridges do not cause clinical symptoms, and the symptoms that appear are mainly manifested as
1, angina pectoris, acute myocardial infarction
Due to the compression of myocardial bridges during systole, wall coronary artery stenosis, local coronary artery spasm, proximal coronary artery sclerosis, decreased coronary blood flow reserve, thrombosis, all of which can lead to reduced coronary blood flow below the myocardial bridge, myocardial ischemia, angina pectoris, and even acute myocardial infarction. Beijing has reported a case of acute extensive anterior wall myocardial infarction due to proximal myocardial bridge of the left anterior descending branch of the coronary artery in a 21-year-old male student.
2.Atrioventricular conduction block
When the myocardial bridge involves the coronary artery supplying the atrioventricular node, it causes atrioventricular node ischemia and atrioventricular conduction block of different degrees.
3.Heart failure
In 1999, Roul et al. reported a case of recurrent acute left heart failure in a patient with myocardial bridge, whose symptoms were rapidly relieved after surgical release of myocardial bridge compression, and no heart failure occurred for more than one year after follow-up.
4.Sudden death
Ventricular fibrillation and sudden death due to acute severe myocardial ischemia. Some autopsies confirmed that in some patients with sudden cardiogenic death, no abnormality was found except for myocardial bridges, which were considered to be the cause of sudden death.
Third, the diagnosis method
1.Coronary angiography
Coronary angiography does not show myocardial bridges per se, but can show that wall coronary arteries become narrowed, blurred, indistinct, or even completely non-visible in systole, while the diameter of the segment is normal in diastole. This change is different from the fixed narrowing during the cardiac cycle caused by coronary atherosclerosis, which is called “systolic stenosis”. This is due to compression of the wall coronary artery by the myocardial bridge during systole, but the compression is removed during diastole. This “systolic stenosis” during coronary angiography is currently used as a basis for diagnosing myocardial bridges.
The detection rate of myocardial bridges on coronary angiography is much lower than the detection rate on autopsy, probably because myocardial bridges can only be visualized on angiography when they reach a certain thickness. In terms of the projection position, it is generally believed that the left and right anterior oblique positions + head position can show the myocardial bridges more clearly. In addition, the ability of coronary angiography to show myocardial bridges depends mainly on.
(1) the thickness and width of the myocardial bridge.
(2) The anatomic relationship between the myocardial bridge and the wall coronary artery.
(3) The amount of fatty tissue and connective tissue surrounding the wall coronary artery.
(4) Vasodilators (nitroglycerin, sodium nitroprusside) aggravate systolic stenosis, whereas vasoconstrictors (ergometrine, norepinephrine) reduce systolic stenosis.
(5) Atherosclerotic stenosis of the proximal coronary artery of the myocardial bridge reduces the pressure distal to the myocardial bridge, making the systolic stenosis less visible.
2.Intracoronary ultrasound of coronary arteries (IVUC)
Intracavitary coronary ultrasound provides insight into the changes in vessel wall structure and lumen cross-section of wall coronary arteries during the cardiac cycle. ivuc clearly shows the typical characteristic manifestations of wall coronary arteries: compression in systole and delayed dilation in diastole. The reduction in lumen cross-sectional area is mostly eccentric and rarely concentric. The largest lumen of the wall coronary artery appears in mid-diastole and the smallest lumen in systole to early diastole. In contrast, the largest lumen of normal coronary arteries appears in early diastole and the smallest lumen in systole. Atherosclerotic plaques in the proximal coronary arteries of myocardial bridges can also be detected, with a reported detection rate of nearly 80%.
Intracoronary Doppler shows hemodynamic changes: at rest, wall coronary flow is highest in diastole, with a significant increase in mean rate, especially in early diastole where the rate rises to a maximum in a very short period of time and then decreases rapidly; a relatively stable higher flow rate is maintained in mid- to late diastole. As soon as systole begins, the flow rate decreases rapidly again. In severe cases, blood flow is interrupted and may even regurgitate proximally. The diastolic flow rate/systolic flow rate ratio is significantly higher.
3. Intraluminal coronary artery manometry
Early pressure catheters were used, but now 0.014-inch fiberoptic pressure guidewires are used for pressure measurement. It was found that the systolic pressure of the wall coronary artery was significantly higher than that of the proximal coronary artery, while the diastolic pressure was significantly lower than that of the proximal coronary artery. After successful stenting of the wall coronary artery, this abnormal change in pressure between the two disappeared.
4. Other
Electrocardiogram, nuclear imaging. The correlation between myocardial ischemia and the degree of systolic stenosis shown by them is small and of little significance.
IV. Treatment
At present, there is no simple and satisfactory treatment method, and treatment is only considered for those with clinical symptoms.
1.Drug treatment
Those with clinical symptoms, positive exercise test, and systolic stenosis ≥75% on coronary angiography should be treated with drugs first.
(1) β-blockers: reduce the contractility of the myocardium, slow down the heart rate, prolong the diastolic time frame, and improve the hemodynamic abnormalities caused by myocardial bridges. Metoprolol, atenolol, etc.
(2) Calcium antagonists: diltiazem, which has been reported abroad to improve myocardial ischemia in patients with myocardial bridges, and the mechanism may be related to its negative inotropic effect on the myocardium.
(3) Anti-platelet drugs: prevent platelets from aggregating at the proximal atherosclerotic vessels of the wall coronary arteries and forming thrombi. Aspirin, ticlopidine, clopidogrel.
2.Intracoronary intervention (PCI)
In recent years, there are many reports on interventional treatment of myocardial bridges with manifestations of myocardial ischemia, and the recent efficacy is positive. the abnormal hemodynamics of wall coronary arteries are corrected after PCI, the blood flow reserve is normalized, and clinical symptoms are rapidly improved. The complete disappearance of symptoms after stent implantation at the wall coronary artery compressed by myocardial bridges has been reported both at home and abroad, with no recurrence after a follow-up period of 6 months to more than 1 year. In China, there is even a case in which coronary angiography was repeated 1 year after the operation and no restenosis was seen in the stent. However, the number of cases is small. PCI is not an effective treatment for myocardial bridges, but it does not eliminate the pressure difference between the pre-existing wall coronary artery and the stent can cause intimal hyperplasia, resulting in restenosis and poor long-term outcome.
The long-term efficacy of PCI needs to be confirmed by evidence-based medicine through further accumulation of clinical data.
3.Surgical treatment
Surgical treatment is the most used method to treat symptomatic myocardial bridges. One is to remove the myocardial bridge compressed on the wall coronary artery (myocardial release), and the other is coronary artery bypass grafting (CABG). For those with atherosclerosis in the proximal coronary arteries, a combination of both approaches is required. The procedure is more invasive compared to interventional treatment.
The understanding of myocardial bridges is still controversial, but an increasing number of studies have shown that under certain conditions myocardial bridges can cause structural changes in the coronary arteries that are compressed by them, with significant hemodynamic abnormalities, and can lead to varying degrees of cardiac events. Individualization should be emphasized, and further clinical experience is needed regarding the choice of treatment.