Except for 18 patiens who received off-pump CABG,the mean CPB time was 53.5 ± 19.8 minutes and mean cross-clamp time 24.0 ± 10.1 minutes..None of the patients in this study died during hospitalization and follow-up; only one patient had a myocardial infarction in the fifth year after the operation, and no major adverse cardiac events (MACEs) occurred in the remaining patients. In the baseline data of the two groups, the proportion of males in the operation group was higher than that in the non-operation group (75% vs. 51.3%, p = 0.017). The average age of patients in the operation group was higher than that in the non-operation group (60.95 ± 8.437 vs 53.15 ± 10.274, p = 0.001). The proportion of patients with severe angina pectoris and who received regular drug treatment was higher in the operation group than in the non-operation group, (66.1% vs. 43.6%, p = 0.030) and (73.2% vs. 41%, p = 0.02), respectively. The proportion of S-T segment changes was higher in the operation group than in the non-operation group (50% vs. 23.1%, p = 0.08). There were no significant differences in the other preoperative data (P > 0.05) (Table 1).
From the follow-up results in this study, there were no deaths during hospitalization or after surgery in the operation and non-operation groups.12 patients (18.8%) in the operation group had S-T segment changes on ECG one week after operation. There was no significant difference in the incidence of the S-T segment between the two groups 3 years after discharge or in the left ventricular ejection fraction between the two groups. The postoperative symptom improvement rate was higher in the operation group than in the non-operation group (82.1% vs. 48.7%, p = 0.001), while the reintervention rate after discharge was lower in the operation group than that in the non-operation group (14.3% vs. 35.9%, p = 0.027). The postoperative left ventricular diameter was smaller in the operation group than in the non-operation group (79 vs. 95, p = 0.001). The symptom improvement rate of patients in the operation group is higher than that in the non-operation group (82.1% vs 48.7%, p = 0.001) (Table 2).
The patients in the CABG group were divided into the bridging vessel patency group (graft patency, n = 27) and restenosis group (graft stenosis, n = 29) according to whether the bridging vessels were patent. In the baseline data of the two groups, the average age of patients in the restenosis group was higher than that in the bridge patency group (63.8 ± 7.7 vs 57.9 ± 8.2, p = 0.008). The different postoperative antiplatelet strategies suggested that the proportion of aspirin antibodies in the restenosis group was higher than that in the patency group (72.4% vs. 40.7%, p = 0.031). No significant differences were observed in the other data (Table 3). Univariate risk analysis revealed that the age of the surgical patients (p = 0.016, OR = 1.099, 95%CI = 1.018–1.187) and different postoperative antiplatelet drug strategies (p = 0.004, OR = 0.187, 95%CI = 0.059–0.594) were risk factors for graft restenosis in patients undergoing CABG. Multivariate risk analysis suggested that different postoperative antiplatelet drug strategies (p = 0.014, OR = 0.224, 95%CI = 0.068–0.736) were independent risk factors for restenosis after CABG in patients with myocardial bridge, suggesting that the aspirin + tigrel / clopidogrel dual antiplatelet prescription as a protective factor was 1.224 times lower than aspirin alone in preventing platelet bridging restenosis ( Table 4).
The 10-year follow-up results of the two groups by Kaplan-Meier analysis showed that the patency rate of bridging vessels in the DAPT group was higher than that in the ASA group (59.3% vs. 40.7%, p = 0.0093). Additionally, 43.4% of the patients in the ASA group developed bridging vascular restenosis in the fourth year, and 52.1% of the patients in the DAPT group still had bridging vascular restenosis in the sixth year (Table 5 and Fig. 2).
Comment
MBs can be seen in any epicardial artery, but most MBs (70–98%) involve the left anterior descending branch. Currently, the most popular and effective examination method is coronary angiography, which determines the existence of MBs by identifying “milking signs”. The reported incidence of MBs is 1.5–16%, and the detection rate can increase to 40% after intracoronary injection of nitroglycerin 3–5. Although MBs are considered benign, with the gradual deepening of the understanding of MBs, a series of complications caused by MBs have been widely recognized. In recent years, some researchers have considered MBs to be an independent risk factor for coronary atherosclerosis 6. It has been reported that vasospasm caused by MBs may not only be the cause of myocardial ischemia and ventricular fibrillation and cardiac arrest but also lead to myocardial fibrosis, contractile band necrosis, and increased vascular density, which is closely related to myocardial insufficiency, angina pectoris, acute myocardial infarction and malignant arrhythmia 7,8. Biomechanical changes caused by MBs are also the basis of its complications, such as plaque vulnerability, thrombosis, and vasospasm. Prolonged contraction of the MBs caused by delayed ventricular relaxation may damage early congested diastolic blood flow and local coronary artery spasm, which lasts to diastole because the relaxation time of arterial vascular smooth muscle is later than that of diastole, especially tachycardia. This further worsens coronary perfusion, resulting in diastolic blood flow damage with two secondary pathophysiological consequences, which were related to heart rate and the severity and duration of epicardial artery compression 9. A recent study has shown that MBs may increase the risk of atherosclerosis in the proximal LAD of MBs, especially in patients with cardiovascular disease risk factors, including age, male sex, smoking, diabetes, hypertension, hyperlipidemia, and a family history of cardiovascular disease 10. In summary, MBs may lead to significant cardiovascular consequences (MACE, myocardial ischemia), which require continued follow-up and medical intervention.
The treatment strategy for myocardial bridge remains controversial. Schwarz et al. 11 proposed that β-blockers have negative chronotropic and inotropic effects, making them one of the first choices for MBs drug therapy. MBs drug therapy focuses on alleviating the potential triggers of aggravating MBs and hemodynamic disorders such as hypertension, myocardial hypertrophy, increased heart rate, and abnormal coronary artery contraction. Calcium channel blockers can reduce myocardial ischemia caused by coronary spasms. Vasodilators, such as nitroglycerin and isosorbide dinitrate, may aggravate the reversal of blood flow from the proximal coronary segment to MBs, resulting in local coronary systolic compression, tachycardia, and proximal vasodilation. However, drug therapy does not fundamentally address the environment of MBs. With increasing age, the prolonged contraction of MBs caused by delayed ventricular relaxation may affect early diastolic blood flow filling, thus shortening the diastolic perfusion time. At the same time, it also leads to locally related coronary spasm, which lasts to the diastolic phase, and finally leads to subendocardial ischemia and interventricular septal ischemia, which is caused by intramural blood theft or branching blood theft. Therefore, the symptoms of angina pectoris in patients without coronary revascularization are usually difficult to reduce with drug treatment, and the frequency of angina pectoris gradually increases with age. Long-term ischemia of the endocardium and interventricular septum in patients will further lead to left ventricular relaxation, followed by an increase in left ventricular volume, and finally require further treatment. The main reason for choosing surgery instead of coronary stents is that there are many complications associated with the latter, such as intraoperative perforation, stent rupture, in-stent restenosis, and thrombosis, and the results of long-term follow-up are not ideal 12–14. MBs increase the incidence of stent restenosis after interventional therapy for proximal atherosclerotic lesions. According to follow-up, interventional therapy had a higher incidence of MACEs in patients with left anterior descending artery MBs with significant proximal stenosis, and the presence of MBs was significantly correlated with MACEs 15. Therefore, the results of this study suggest that if there are symptoms of angina pectoris, changes in the S-T segment of the ECG, and the effect of regular drug treatment is poor, surgical treatment should opted for as soon as possible.
Surgical unroofing and CABG have both advantages and disadvantages. Early complications of surgical myotomy include cardiac perforation, ventricular aneurysm formation, and postoperative bleeding. These complications are often serious and endanger the lives of patients. It is generally believed that when depth more than 5 mm or longer than 25 mm, CABG is better than unroofing 16. In this study, the follow-up results of patients in the operation and non-operation groups showed that the improvement rate of angina pectoris in the operation group was significantly higher than that in the non-operation group. The reintervention rate of patients undergoing operation was significantly lower than that in the non-operation group.
Some researchers believe that the target vessels need to be ligated to avoid competitive blood flow 17. In this study, the coronary artery with the myocardial bridge was not ligated or clipped in the CABG operation, and the primary consideration was to reduce perioperative coronary artery injury, bleeding, ventricular perforation, and other serious complications. It can be found from previous literature that although there is a risk of bridging vessel occlusion caused by competitive blood flow inhibition, no severe stenosis or occlusion of bridging vessels was found during an average follow-up of 35 months 18,19. However, the target vessels in patients with MBs are difficult to block spontaneously. During our follow-up, we found that in some patients with stenosis and occlusion of the bridging vessels, there was no obvious stenosis of the target vessels during ventricular diastole, which meant that competitive blood flow existed for a long time. Therefore, it was found that 50% of the patients had bridge stenosis or occlusion during follow-up. However, what is interesting is that although these patients had serious stenosis or occlusion of the bridging vessels, their subjective clinical symptoms, namely angina pectoris, were significantly better than those before the operation. Current research results cannot explain this phenomenon well.
From the follow-up results of ASA versus DAPT in this study, it can be suggested that although there has been competitive blood flow inhibition in patients with MBs after CABG, which leads to bridging vascular stenosis, dual antiplatelet therapy remains an effective antiplatelet strategy to prevent bridging vascular stenosis. Bridging vessel restenosis may not affect the survival outcome of patients after surgery. The authors believe that CABG surgery delayed the negative effect of MBs on the left ventricular myocardium to some extent, and the left ventricular volume did not continue to increase and tended to return to normal volume in the presence of the bridge. Owing to the short follow-up time, no changes in the left ventricular myocardium were observed after stenosis and occlusion of the bridging vessels. The authors speculated that if the follow-up time continues to be prolonged, cardiac function changes and ECG changes may occur later in patients with patency of bridging vessels than in patients with bridging vessel stenosis.
This study has some limitations. First, it was a single-center retrospective study, and the data may be biased due to the small sample size; thus, prospective, multicenter studies are needed to confirm our conclusions. Second, we did not compare the outcomes of surgical unroofing and CABG because the number of unroofing surgeries was little.
This study suggests that surgical treatment can be performed safely and effectively in patients with chest pain and isolated LAD coronary artery myocardial bridging.However,patients should be aware of the potential for recurrent chest pain, and continued medical therapy was important.
Figure 1.Among 124 patients with the diagnosis of myocardial bridging,103 with isolated MB received surgical or medical treatment after applying the specified inclusion and exclusion criteria.
Figure 2. The 10-year follow-up results of the two groups by Kaplan-Meier analysis. The patency rate of bridging vessels in the DAPT group was higher than that in the DAPT group (59.3% vs. 40.7%, p = 0.0093). Additionally, 43.4% of the patients in the ASA group developed bridging vascular restenosis in the fourth year, and 52.1% of the patients in the DAPT group still had bridging vascular restenosis in the sixth year.