Abstract
Objective
Left anterior descending Myocardial Bridge (LADMB) is considered a benign condition and actually becomes a forgotten cause of serious cardiac events. This study was conducted to estimate the prevalence of LADMB and its association to atherosclerosis.
Methods
An observational retrospective study was conducted on patients referred for coronary angiography between June 2012 and June 2020. Coronary angiography database was revisedand studied population was divided into 2 groups: LADMB group versus Non-LADMB group.
Results
LADMB was detected in 510 patients out of 35813 included in the study resulting in a prevalence at 1.42%. The mean age was 66.5 years. Male gender was more common than female (70vs30%). The prevalence of significant atherosclerotic LAD disease was more than two times higher in the non-LADMB group compared to the LADMB group. Statistical analysis revealed a significant negative association between LADMB and atherosclerosis (p < 0.001). A significant greater rate of MINOCA cases was observed in acute coronary syndrome LADMB patients.
Conclusions
LADMB is an inborn anatomic variation associated to atherosclerotic risk reduction in LAD. Physicians must be aware about the potential complications and pay attention to those classified at high risk for cardiovascular events.
Keywords: Myocardial bridge, Left anterior descending coronary artery, Atherosclerosis, MINOCA
1. Introduction
Because myocardial bridge (MB) is usually benign, silent and incidentally discovered; it currently becomes a forgotten cause of hot topics in cardiovascular field like myocardial infarction and non-obstructive coronary artery disease (MINOCA). Firstly, described at autopsy by Reyman in 1737, MB is an anatomical congenital variant characterized by an intra-myocardial pathway of an epicardial coronary artery.1 Until now, there are no available standard of care regardless that MB is a very old angiographic feature recognized by Portsmann in 1960.2
Previous studies have been attributed a wide spectrum of clinical presentation to MB such as acute coronary syndromes (ACS) including myocardial infarction,3 silent ischemia,4 arrhythmias3 and sudden death.5 The location, depth and length of MB on top of the degree of systolic compression were the determinant factors for clinical relevance.6 Since angiography, the pathophysiological consequences and ischemia-inducing mechanisms of MB become more understood in parallel to the evolution of diagnostic imaging modalities like IVUS (intravascular ultrasound) and OCT (optical coherence tomography) whereas the therapeutic options remain limited.
The reported rates of MB with angiographic documented systolic compression varies between 0.5 and 12% and the middle part of left anterior descending (LAD) coronary artery is most commonly involved.7 Usually, the Schwarz classification is used to guide the management of MB that was mainly based on beta blockers, calcium channel blockers and surgical intervention for refractory cases.8 This study was conducted on one of the largest populations in the literature in order to estimate a recent prevalence of angiographic Left Anterior Descending Myocardial Bridge (LADMB) with systolic compression, its clinical presentation and its association to cardiovascular risk factors and coronary atherosclerosis. (Fig. 1).
Fig. 1.
Left coronary angiogram with myocardial bridge. Left coronary angiogram showing non-significant coronary artery disease and LADMB (a) with severe systolic compression (b). LADMB: Left anterior descending myocardial bridge.
2. Materials and methods
2.1. Study design and population
An observational retrospective single center study was conducted on all patients referred to coronary angiography in our interventional cardiology department between June 2012 and June 2020. Then, the studied population was divided into 2 groups: those with angiographic left anterior descending myocardial bridge and systolic narrowing versus others.
2.2. Data collection and end points
Data concerning the clinical indication for coronary angiography, cardiovascular risk factors (systemic hypertension, diabetes mellitus, dyslipidemia, smoking, familial history of coronary artery disease, body mass index, creatinine clearance), presence of previous significant cardiovascular disease, baseline characteristics (sex and age) and coronary angiography results were collected from the Hemolia® database. The study has been conducted according to the principles outlined in the Declaration of Helsinki and approved by the local ethics committee. In this study, we primarily aim to estimate the prevalence of angiographic LADMB and the related potential clinical presentation. The secondary end point is to investigate the correlation between LADMB and atherosclerotic coronary artery disease. A significant atherosclerotic left anterior descending coronary artery disease was visually assessed by 50% and more lumen diameter reduction on coronary angiogram.
2.3. Statistical analysis
Quantitative data were summarized as means and standard deviations whereas qualitative data were summarized as count and percentage. Bivariate associations between continuous and categorical variables were studied with Student t-test while bivariate associations between categorical variables were studied with Chi square test. Then, variables found significantly associated with LADMB were introduced into multivariate logistic regression analysis investigating the association of LADMB and LAD atherosclerosis. A p value < 0.05 was considered significant. All statistical analysis was carried out using SPSS version 20.
3. Results
A total of 35813 patients were included in this observational descriptive study. LADMB were observed in 1.42% (510/35813) of cases. The mean age of studied population was 66.5 ± 13.4 years. Out of 35813, 30% (10728) were females and 70% (25085) were males. The indication for coronary angiography referral was ACS (cardiac arrest, unstable angina, STEMI, and NSTEMI) in 33.6% (12037/35813), stable angina or atypical chest pain with silent ischemia in 27.2% (9740/35813), arrhythmia in 2.7% (965/35813), newly diagnosed or decompensated heart failure in 14.2% (5079/35813) and others (pre-surgical or valvular heart disease work-up) in 22.3% (7991/35813). A significant angiographic atherosclerotic disease reducing ≥50% the lumen of LAD was detected in 46.7% of the whole population (16724/35813). Regarding the prevalence of cardiovascular risk factors among the studied population: 50.5% had systemic hypertension, 24.3% had diabetes mellitus, 38.3% had dyslipidemia, 22.2% were smokers, 61.4% were overweight (BMI ≥25) and 45.6% had chronic kidney disease (CrCl <60 ml/min) (Table 1).
Table 1.
Patients demographic data and bivariate association test between 2 groups.
| Whole population N = 35813 (%) |
LAD MB Yes(N = 510) No(N = 35303) |
P-value | ||
|---|---|---|---|---|
| Mean age | 66.5 ± 13.4 | 66.3 ± 13.6 | 66.5 ± 13.4 | 0.8 |
| Sex | 0.9 | |||
| Male | 25085(70) | 357(60) | 24728(70) | |
| Female | 10728(30) | 153(30) | 10575(30) | |
| LAD disease | 16724(46.7) | 114(22.4) | 16610(47) | <0.001 |
| Clinical situation | ||||
| ACS | 12037(33.6) | 175(34.3) | 11862(33.6) | |
| Angina | 9740(27.2) | 168(32.9) | 9572(27.1) | |
| Arrhythmias | 965(2.7) | 16(3.1) | 949(2.7) | |
| Heart failure | 5079(14.2) | 26(5.1) | 5053(14.3) | |
| Asymptomatic | 7991(22.3) | 125(24.5) | 7866(22.3) | |
| Main CVRF | ||||
| Diabetes mellitus | 8718(24.3) | 58(11.4) | 8660(24.5) | <0.001 |
| Systemic hypertension | 18098(50.5) | 202(39.6) | 17896(50.7) | 0.02 |
| Dyslipidemia | 13714(38.3) | 171(33.5) | 13543(38.3) | 0.41 |
| Smoking | 7963(22.2) | 121(23.7) | 7842(22.2) | 0.0003 |
| BMI ≥ 25 | 21988(61.4) | 273(53.5) | 21715(61.5) | <0.001 |
| CKD | 13892(45.6) | 159(36) | 13733(45.7) | <0.001 |
∗LADMB: Left anterior descending myocardial bridge. ACS: acute coronary syndrome. LAD: left anterior descending coronary artery. CVRF: cardiovascular risk factors. BMI: body mass index. CKD: chronic kidney disease.
Taking the group with LADMB from the whole studied population (510/35813), the mean of age was 66.3 ± 13.6 years and 30% were females. A significant angiographic atherosclerotic LAD lesion was identified in 22.4% (114/510) of the LADMB group and this proportion was two times higher in the non LADMB group (47% or 16610/35303). Moreover, 24.5% (125/510) of LADMB were incidentally discovered without related clinical relevance while 3.1% (16/510) may were related to arrhythmia, 5.1% (26/510) to heart failure, 32.9% (168/510) to angina and 34.3% (175/510) to ACS which were respectively the clinical indication to undergo for coronary angiography. Out of those presenting for ACS, 44% (77/175) were diagnosed with MINOCA whereas a significant coronary artery disease was detected in others (56%). Regarding cardiovascular risk factors: systemic hypertension (39.7 vs. 50.7%), diabetes mellitus (11.4 vs. 24.5%), dyslipidemia (33.5 vs. 38.3%), overweight (53.5 vs. 61.5%) and chronic kidney disease (36 vs. 45.7%) were less common in the LADMB group compared to others except for smokers (23.7 vs. 22.2%) (Table 1).
The first statistical analysis studying the bivariate association between the presence of LADMB and cardiovascular risk factors, demographic characteristics and LAD atherosclerotic disease showed a significant negative association with diabetes mellitus (p < 0.001), dyslipidemia (0.02), systemic hypertension (p < 0.001), body mass index (p < 0.0003), chronic kidney disease (p < 0.001) and LAD atherosclerosis (p < 0.001) while no significant association was observed with age (p = 0.8), sex (p = 0.9), and smoking (p = 0.41) (Table 1). Furthermore, a significant difference between the two groups (LAD-MB vs No LAD-MB) in terms of distribution of MINOCA was observed which was more common in LAD-MB group (44% vs 19%; p < 0.001) (Fig. 2). Then, a multivariate logistic regression investigating the association between LAD atherosclerosis and LADMB adjusted on the previous statistically significant variables confirmed the significant inverse relationship (OR = 0.39 95% CI [0.30; 0.49]) (Table 2).
Fig. 2.
Prevalence of MINOCA in acute coronary syndrome patients. Prevalence of MINOCA in acute coronary syndrome patients stratified by groups (LADMB vs. No LADMB). Black boxes (significant CAD); Grey boxes (MINOCA); P < 0.001 LADMB: Left anterior descending myocardial bridge. CAD: coronary artery disease. MINOCA: Myocardial infarction and non-obstructive coronary artery disease.
Table 2.
Multivariate logistic regression investigating the association between LADMB and atherosclerotic LAD adjusted on previously significant variables.
| Variables | P -value | O.R | 95% CI |
|---|---|---|---|
| LAD atherosclerosis | <0.001 | 0.39 | [0.30; 0.49] |
| Diabetes mellitus | <0.001 | 0.47 | [0.35; 0.64] |
| Dyslipidemia | 0.67 | 1.04 | [0.86; 1.25] |
| Systemic hypertension | 0.058 | 0.81 | [0.65; 1.07] |
| BMI | 0.02 | 0.79 | [0.65; 0.97] |
| CKD | <0.001 | 0.65 | [0.51; 0.81] |
∗LADMB: left anterior descending myocardial bridge. LAD: left anterior descending. BMI: body mass index. CKD: chronic kidney disease.
4. Discussion
This study is interested in angiographic MB confined to the LAD coronary artery and showed a prevalence of angiographic LADMB at 1.42%. The global prevalence of angiographic MB reported in literature varies widely from 0.5 to 12%, but all previously published studies showed that LAD is the most involved coronary artery.9, 10, 11, 12, 13, 14, 15 A recent published study by Çay et al performed on 25982 patients revealed an angiographic LADMB prevalence at 1.17%.16 Indeed, it is worthy to mention that the prevalence of MB differs with the used diagnostic modalities. For example, it was estimated at 80% with autopsy series17 and at 22.5% with CT-scan based studies.18 Until now, the clinical significance of MB is debated and it is traditionally considered as benign inherited abnormality. In this study, one-quarter of LADMB was detected incidentally while performing coronary angiography for pre-operative work-up (extra-cardiac surgery, valvular heart disease, aortic or peripheral vascular disease). Otherwise, the three-quarter were diagnosed in symptomatic patients presenting respectively for acute coronary syndromes, chest pain (typical or atypical angina), acute/chronic heart failure and arrhythmias. The causal relationship between LADMB and clinical presentation could not be investigated view the retrospective observational study type limited to coronary angiography database. Instead, the study findings emphasize on a potential role that could be attributed to MB in MINOCA cases. The mechanical compression or systolic milking effect of MB is the main mechanism predisposing to an adjacent plaque rupture3 or spontaneous coronary dissection19 resulting in acute coronary syndromes. Also, vascular compression enhances myocardial ischemia causing angina especially when systolic compression lead to a more than 50% reduction in vascular lumen.20 Moreover, MB segment had a predilection for coronary spasm21 and Kim et al showed a hyper-reactivity to vasoconstrictive agents in the tunneled segments.22
In this study, the percentage of significant LAD atherosclerotic disease is more than two times higher in the non-LADMB group compared to LADMB group. In fact, a part of this difference could be due to the lower prevalence of cardiovascular risk factors in the LADMB group. However, this study showed a significant negative correlation between the presence of LADMB and the coexistence of atherosclerotic LAD coronary artery disease. The protective role of MB against atherosclerosis was explained by the prominent biomechanical forces and the increased wall shear stress in the tunneled segment.6 This protective role was documented at histological level by Risse et al23 via showing a thinner intima in the bridged segment and Ishii et al24 by showing an absence of synthetic-type smooth muscle cells that promote collagen and elastic fibers production enhancing the progression of atherosclerosis. In addition, Masuda et al documented an alteration in the expression of endothelin-1 and other vasoactive agents that participate in the pathogenesis of atherosclerosis in patients with MB.25 Instead, few published data suggest that a mid-LADMB contributes in the pathogenesis of atherosclerosis especially in the proximal adjacent coronary segment. For example, Nakaura et al26 reported a positive correlation with mid-LADMB and atherosclerosis irrespective to atherosclerotic plaque localization, while Hong et al27 reported a higher prevalence of coronary stenosis located proximally to the MB. In fact, we conventionally agree with the anti-atherosclerotic role of MB in the bridging segment whereas the proximal pro-atherogenic effect remains controversial and depending on the coexisting cardiovascular risk factors.6,27
Lastly, the management of MB is not well standardized. Both invasive and non-invasive strategies are reported with no available data from randomized clinical trials defining the optimal therapeutic approach.28 Pharmacological management including beta-blockers29 and non-dihydropyridine calcium-channel blockers were frequently used as first line therapy for symptomatic MB while the invasive strategies like percutaneous coronary intervention and surgical approach are recommended for refractory unresponsive cases.30 In general, using beta-blockers are preferred over calcium channel blockers despite the absence of head to head comparison studies.31 Indeed, the resulting beneficial symptomatic outcomes were explained by the mechanisms of action of these substances that reduce myocardial contractility and subsequently the burden of compression on the tunneled coronary segment, diminish the hemodynamic disturbances triggered by MB and decrease the heart rate prolonging the diastolic filling period.29 Data from previous studies supported the symptomatic improvement associated with the use of beta-blockers especially for esmolol29 and nebivolol29, 30, 31, 32 in cases of MB whereas no benefits regarding morbidity and mortality have been documented.33 In parallel, the results from using percutaneous coronary stenting as a therapeutic approach for recalcitrant MB cases are controversial. Regardless the improvement of symptoms and hemodynamic abnormalities noted by numerous studies after performing percutaneous coronary intervention,34 multiple deleterious outcomes such as stent fracture,35 stent thrombosis36 and in-stent restenosis37 were commonly observed constituting a limitation for stent implantation in MB condition. In opposition, coronary artery bypass graft (CABG) and myotomy (unroofing) are the preferred therapeutic approach for MB cases refractory to medical therapy. We preferentially proceed with surgical unroofing which relieve the myocardial ischemia via correcting the anatomic abnormality and improving blood flow31 while CABG is preferred for extensive MB (>25 mm), deep MB (>5 mm), persistent diastolic compression and coexisting significant coronary artery disease.38, 39, 40
The limitation of this study is the retrospective nature. Only the written reports were reviewed while coronary angiograms weren’t. Some physicians may miss to note the presence of myocardial bridge which subsequently leads to an underestimation to the prevalence of LADMB. Indeed, it is worthy to mention that reports on Hemolia® database could not be validated by operators if the required parameters had not completed leading to attenuate the potential missing values.
In conclusion, this study conducted on one of the largest populations in literature estimates the prevalence of LADMB at 1.42% which was closer to previous published data. Myocardial bridge which is an inborn congenital abnormality may result in life-threatening complications. Physicians must be aware about the potential consequences and the available therapeutic strategies. Future prospective studies targeting MB pathophysiological pathway, ischemia mechanisms, clinical significance and atherosclerotic pathogenesis are required in order to select high risk patients, establish an appropriate direct therapy and prevent the cardiovascular events. Key messages:
It is well known that myocardial bridge is a common silent inborn coronary abnormality. This study provides an up-to-date review about the angiographic prevalence of LAD-MB (Left anterior descending myocardial bridge) and the potential corresponding clinical relevance. This study shows a negative association between the presence of LAD-MB and development of significant atherosclerotic disease. Furthermore, we introduce the hypothesis of correlation between myocardial bridge and MINOCA (myocardial infarction with no obstructive coronary artery) in order to put into question a probable contributing role of MB to this clinical entity which could be the purpose for future studies.
Funding
This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.
Declaration of competing interest
The authors declare that there are no conflicts of interest.
References
- 1.Reyman H. Disertatio de vasiscordispropriis. Med DissUniv Gottingen. 1737;7:1–32. [Google Scholar]
- 2.Portsmann W, Iwig J. Intramural coronary vessels in the angiogram. FortschrGebRontgenstrNuklearmed1960;92:129-132. [PubMed]
- 3.Ishikawa Y., Akasaka Y., Suzuki K. Anatomic properties of myocardial bridge predisposing to myocardial infarction. Circulation. 2009;120:376–383. doi: 10.1161/CIRCULATIONAHA.108.820720. [DOI] [PubMed] [Google Scholar]
- 4.Tauth J., Sullebarger T. Myocardial infarction associated with myocardial bridging: case history and review of the literature. Cathet Cardiovasc Diagn. 1997;40:364–367. doi: 10.1002/(sici)1097-0304(199704)40:4<364::aid-ccd9>3.0.co;2-7. [DOI] [PubMed] [Google Scholar]
- 5.Desseigne P, Tabib A, Loire R. Myocardial bridging on the left anterior descending coronary artery and sudden death. A propos of 19 cases with autopsy. Arch Mal Coeur Vaiss1991;84:511-516. [PubMed]
- 6.Alegria J.R., Hermann J., Holmes D.R. Myocardial bridging. Eur Heart J. 2005;26:1159–1168. doi: 10.1093/eurheartj/ehi203. [DOI] [PubMed] [Google Scholar]
- 7.Soran O., Pamir G., Erol C. The incidence and significance of myocardial bridge in a prospectively defined population of patients undergoing coronary angiography for chest pain. Tokai J Exp Clin Med. 2000;25:57–60. [PubMed] [Google Scholar]
- 8.Corban M T, Hung O Y, Eshtehardi P, et al. Myocardial bridging: contemporary understanding of pathophysiology with implications for diagnostic and therapeutic strategies. J Am Coll Cardiol;63:2346-2355. [DOI] [PMC free article] [PubMed]
- 9.Rossi L., Dander B., Nidasio G.P. Myocardial bridges and ischemic heart disease. Eur Heart J. 1980;1:239–245. doi: 10.1093/oxfordjournals.eurheartj.a061125. [DOI] [PubMed] [Google Scholar]
- 10.Noble J, Bourassa M G, Petitclerc R, et al. Myocardial bridging and milking effect of the left anterior descending coronary artery: normal variant or obstruction? Am J Cardiol;37:993-999. [DOI] [PubMed]
- 11.Ishimori T. Myocardial bridges: a new horizon in the evaluation of ischemic heart disease. Cathet Cardiovasc Diagn. 1980;6:355–357. doi: 10.1002/ccd.1810060403. [DOI] [PubMed] [Google Scholar]
- 12.Greenspan M., Iskandrian A.S., Catherwood E. Myocardial bridging of the left anterior descending artery: evaluation using exercise thallium-201 myocardial scintigraphy. Cathet Cardiovasc Diagn. 1980;6:173–180. doi: 10.1002/ccd.1810060207. [DOI] [PubMed] [Google Scholar]
- 13.Kramer J.R., Kitazume H., Proudfit W.L. Clinical significance of isolated coronary bridges: benign and frequent condition involving the left anterior descending artery. Am Heart J. 1982;103:283–288. doi: 10.1016/0002-8703(82)90500-2. [DOI] [PubMed] [Google Scholar]
- 14.Wymore P, Yedlicka J W, Garcia-Medina V, et al. The incidence of myocardial bridges in heart transplants. CardiovascInterventRadiol1989;12:202-206. [DOI] [PubMed]
- 15.Juilliere Y., Berder V., Suty-Selton C. Isolated myocardial bridges with angiographic milking of left anterior descending coronary artery: a long-term follow-up study. Am Heart J. 1995;129:663–665. doi: 10.1016/0002-8703(95)90312-7. [DOI] [PubMed] [Google Scholar]
- 16.Çay S, Ozturk S, Cihan G, et al.Angiographic prevalence of myocardial bridging. Anadolu KardiyolDerg2006;6:9-12. [PubMed]
- 17.Venkateshu K V, Mysorekar V R, Sanikop M B. Myocardial bridges. J Indian Med Assoc;98:691-693. [PubMed]
- 18.Donkol RH, Saad Z. Myocardial bridging analysis by coronary computed tomographic angiography in a Saudi population. World J Cardiol;5:434-441. [DOI] [PMC free article] [PubMed]
- 19.Ge J.B., Huang Z.Y., Liu X.B. Spontaneous coronary dissection associated with myocardial bridge causing acute myocardial infarction. Chin Med J. 2008;121:2450–2453. [PubMed] [Google Scholar]
- 20.Ge J., Jeremias A., Rupp A. New signs characteristic of myocardial bridging demonstrated by intracoronary ultrasound and Doppler. Eur Heart J. 1999;20:1707–1716. doi: 10.1053/euhj.1999.1661. [DOI] [PubMed] [Google Scholar]
- 21.Nam P., Choi B.G., Choi S.Y. The impact of myocardial bridge on coronary artery spasm and long-term clinical outcomes in patients without significant atherosclerotic stenosis. Atherosclerosis. 2018;270:8–12. doi: 10.1016/j.atherosclerosis.2018.01.026. [DOI] [PubMed] [Google Scholar]
- 22.Kim J.W., Seo H.S., Na J.O. Myocardial bridging is related to endothelial dysfunction but not to plaque as assessed by intracoronary ultrasound. Heart. 2018;94:765–769. doi: 10.1136/hrt.2007.115980. [DOI] [PubMed] [Google Scholar]
- 23.Risse M, Weller G. Coronary muscle bridge and its relations to local coronary sclerosis, regional myocardial ischemia and coronary spasm: a morphometric study. Z Kardiol;74:700-705. [PubMed]
- 24.Ishii T, Asuwa N, Masuda S, et al. Atherosclerosis suppression the left anterior descending coronary artery by the presence of a myocardial bridge: an ultrastructural study. ModPathol1991;4:424-431. [PubMed]
- 25.Masuda T, Ishikawa Y, Akasaka Y, et al. The effect of myocardial bridging of the coronary artery on vasoactive agents and atherosclerosis localization. J Pathol;193:408-414. [DOI] [PubMed]
- 26.Nakaura T, Nagayoshi Y, Awai K, et al. Myocardial bridging is associated with coronary atherosclerosis in the segment proximal to the site of bridging. J Cardiol;63:134-139. [DOI] [PubMed]
- 27.Hong H, Wang M S, Liu Q, et al. Angiographically evident atherosclerotic stenosis associated with myocardial bridging and risk factors for the artery stenosis located proximally to myocardial bridging. Anadolu KardiyolDerg2014;14:40-47. [DOI] [PubMed]
- 28.Roger I.S., Tremmel J.A., SchnittgerI Myocardial bridges: overview of diagnosis and management. Congenit Heart Dis. 2017;12:619–623. doi: 10.1111/chd.12499. [DOI] [PubMed] [Google Scholar]
- 29.Schwarz E R, Klues H G, Vom Dahl J, et al. Functional, angiographic and intracoronary Doppler flow characteristics in symptomatic patients with myocardial bridging:effect of short-term intravenous beta-blocker medication. J Am Coll Cardiol;27:1637-1645. [DOI] [PubMed]
- 30.Teragawa H, Oshita C, Ueda T. The myocardial bridge: potential influences on the coronary artery vasculature. Clin Med Insights Cardiol;13:1179546819846493. [DOI] [PMC free article] [PubMed]
- 31.Cutler D, Wallace J M. Myocardial bridging in a young patient with sudden death. ClinCardiol1997;20:581-583. [DOI] [PMC free article] [PubMed]
- 32.Gupta S, Wright H M. Nebivolol: a highly selective beta1-adrenergic receptor blocker that causes vasodilation by increasing nitric oxide. Cardiovasc Ther2008;26:189-202. [DOI] [PubMed]
- 33.Gao Y, VanhoutteP M. Nebivolol: an endothelium-friendly selective B1-adrenoreceptor blocker. J Cardiovasc Pharmacol;59:16-21. [DOI] [PubMed]
- 34.Haager P.K., Schwarz E.R., Vom Dalh J. Long term angiographic and clinical follow up in patients with stent implantation for symptomatic myocardial bridging. Heart. 2000;84:403–408. doi: 10.1136/heart.84.4.403. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 35.Tandar A, Whisenant B K, Michaels A D. Stent fracture following stenting of a myocardial bridge: report of two cases. Cathet Cardiovasc Interv;71:191-196. [DOI] [PubMed]
- 36.Derkacz A., Nowicki P., Protasiewicz M. Multiple percutaneous coronary stent implantation due to myocardial bridging- a case report. Kardiol Pol. 2007;65:684–687. [PubMed] [Google Scholar]
- 37.Tsujita K, Maechara A, Mintz G S, et al. Impact of myocardial bridge on clinical outcome after coronary stent placement. Am J Cardiol;103:1344-1348. [DOI] [PubMed]
- 38.Rogers I.S., Tremmel J.A., SchnittgerI Myocardial bridges: overview of diagnosis and management. Congenit Heart Dis. 2017;12:619–623. doi: 10.1111/chd.12499. [DOI] [PubMed] [Google Scholar]
- 39.Lee M, Chen C H. Myocardial bridging: an up-to-date review. J Invasive Cardiol;27:521-528. [PMC free article] [PubMed]
- 40.Xiao R., Liang G. Progress in surgical treatment of coronary myocardial bridge. SOJ Surgery. 2018;6:1–3. [Google Scholar]