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Article* "Development of the European Network in Orphan Cardiovascular Diseases" „Rozszerzenie Europejskiej Sieci Współpracy ds Sierocych Chorób Kardiologicznych” Title: Myocardial bridge – diagnosis and treatment in a congenital anomaly. Author: Jakub Podolec MD, PhD Affiliation: Interventional Cardiology Department, Cardiology Institute, Collegium Medicum, Jagiellonian University at the John Paul II Hospital, Krakow, Poland Introduction Myocardial bridge (MB) is a congenital anomaly which presents as a cardiac muscle stretched over a part of an epicardial artery. At the time of systole it may compress a segment of a coronary artery and result in its narrowing [1, 2]. The angiographic findings show the incidence of MB at the level of 1.5 to 16% [3], but the data from autopsy studies highlights much more common incidence, even in 80% of cases [2, 5]. The separate group includes patients with HOCM and after heart transplantation, who have higher incidence of MB at multiple sites [2]. In patients with MB during each systole, reduction in blood flow might be observed [7]. Although, the coronary blood flow is maximal during diastole, for many years there was a hypothesis that this is a normal, anatomical variation [6]. The most frequently affected coronary artery is the left anterior descending (LAD in 70% of autopsy cases) and is mostly located in the mid segment of the vessel. The patients may present asymptomatic for many year. If the symptoms appear they might be atypical or present with angina, which most often do not correlate with the length or depth of the MB. Rare symptoms and complications include: myocardial ischemia, myocardial infarction, paroxysmal AV block, syncope, ventricular tachycardia and SCD. The most severe clinical presentations usually appear during tachycardia, as a result of shortening of the diastole than systole period [2]. John Paul II Hospital in Kraków Jagiellonian University, Institute of Cardiology 80 Prądnicka Str., 31-202 Kraków; tel. +48 (12) 614 33 99; 614 34 88; fax. +48 (12) 614 34 88 e-mail: [email protected] www.crcd.eu Diagnostic methods MB is often an accidental finding detected during invasive or noninvasive diagnostics. Noninvasive imaging methods including MSCT (which is also very useful in identifying subclinical arteriosclerosis located proximally to the narrowing), stress echocardiography and single photon emission computed tomography are often the first to detect the MB. Invasive angiography techniques include typical visual artery contraction during systole, IVUS with the “half moon“ shape image, intracoronary Doppler and FFR [8]. Treatment methods The Shwarz Classification is a useful tool for grouping patients with MB and may be helpful in choosing the best treatment method for each group. In group A, in which MB is an incidental finding during angiography and no signs of ischemia are present, patients usually do not need any treatment. Patients from group B with evidence of ischemia during exercise stress test or any imaging technique and with signs of ischemia are treated pharmacologically with beta blockers (BB) or calcium channel blockers (CCB). The third group of patients are those with altered intracoronary hemodynamics confirmed in FFR or Coronary Doppler examinations. They are treated also with BB or CCB. In case of patients from group C among whom pharmacological treatment is ineffective, revascularization may be considered [8]. In the treatment of angina beta blockers and nondihydropyridine calcium channel blockers are considered as the first-line therapy. Due to antispasmodic properties and increasing preload, which is intensifying systolic compression of the bridged segment, nitrates are contraindicated [8]. As a part of treatment the modification of risk factors and antiplatelet therapy in patients with atherosclerosis should be indicated [8]. Stent implantation in symptomatic patients, despite of optimal pharmacotherapy can improve peak intracoronary systolic pressure and vessel compression, normalize flow, and decrease symptoms. However, many authors present high incidence of complications including: perforation during stent deployment, stent fracture, in-stent restenosis and stent thrombosis. Therefore, indications for this type of treatment are still limited. Stent implantation in patients with symptomatic myocardial bridges result in high rates of early instent restenosis that may be related to bridge-associated decreased lumen area and compared with PCI with baremetal stents (BMS), PCI with drug-eluting stents (DES) has lower rates of John Paul II Hospital in Kraków Jagiellonian University, Institute of Cardiology 80 Prądnicka Str., 31-202 Kraków; tel. +48 (12) 614 33 99; 614 34 88; fax. +48 (12) 614 34 88 e-mail: [email protected] www.crcd.eu target vessel revascularization (TVR). PCI in selected patients with a myocardial bridge might be considered to treat atherosclerotic plaque located proximal to the bridge as well as the negative remodeling and dynamic obstruction within the bridged segment [9-14]. No randomized controlled trials comparing optimal medical therapy with interventional treatment including PCI with DES and surgical treatment are available. Therefore, medical therapy appears to be superior to PCI. Ischemia-guided revascularization using DES may be considered in carefully qualified symptomatic patients refractory to maximal medical therapy and who are not optimal surgical candidates. Surgical intervention involves either supraarterial myotomy or CABG. Although both myotomy and CABG are reasonable initial choices, it is unclear which procedure is superior. The intervention might be considered in patients with coronary narrowing of more than 75% on angiography, or evidence of myocardial ischemia or infarction [3]. CABG is favored over myotomy in cases of extensive (>25 mm) or deep (>5 mm) myocardial bridges (the risk of myotomy can be considerable) or when the bridged coronary segment fails to decompress completely in diastole (myotomy is unlikely to correct the persistent diastolic compression) [3]. These limited data suggest that surgical therapy, either myotomy or CABG, appears safe and effective in symp- tomatic patients with myocardial bridging refractory to medical therapy. Conclusions Long-term prognosis for patients with isolated MB is good. The main treatment should be pharmacotherapy. Revascularization should be reserved only for symptomatic patients refractory to medical therapy and who are not considered as surgical candidates. It appears that it can also be considered in group of patients with plaque proximal to the bridge. References: 1. Portsman W., Iwing J. Die intramurale Koronarie im Angiogramm. Fortschr. Rontgenst. 1960; 92: 129. 2. Mohlenkamp S, Hort W, Ge J, Erbel R. Update on myocardial bridging. Circulation John Paul II Hospital in Kraków Jagiellonian University, Institute of Cardiology 80 Prądnicka Str., 31-202 Kraków; tel. +48 (12) 614 33 99; 614 34 88; fax. +48 (12) 614 34 88 e-mail: [email protected] www.crcd.eu 2002;106:2616–22. 3. Wu Qy, Xu ZH. Surgical treatment of myocardial bridging, report of 31 cases. Chin Med J(Engl) 2007; 120; 1689-93 4. Hill SF, Sheppard MN. Non-atherosclerotic coronary artery disease associated with sudden cardiac death. Heart 2010;96:1119 – 25 5. Bourassa MG, Butnaru A, Lesperance J, Tardif JC. Symptomatic myocardial bridges: overview of ischemic mechanisms and current diagnostic and treatment strategies. J Am Coll Cardiol 2003;41:351 6. De Giorgio F, Grassi VM, Polacco M, Pascali VL, d'Aloja E, Arena V. Myocardial bridging and sudden cardiac death: is the actual classification exhaustive? Int J Cardiol. 2014 Apr 1;172(3):e383-4. 7. Priori SG, Aliot E, Blomstrom-Lundqvist C, et al. Task Force on sudden cardiac death of the European Society of Cardiology. Eur Heart J 2001;22:1374 – 4508. 8. Corban MT, Hung OY, Eshtehardi P et al. Myocardial bridging: contemporary understanding of pathophysiology with implications for diagnostic and therapeutic strategies. J Am Coll Cardiol. 2014 Jun 10;63(22):2346-55. 9. Ernst A, Bulum J, Separovic Hanzevacki J, Lovric Bencic M, Strozzi M. Five-year angiographic and clinical follow-up of patients with drug-eluting stent implantation for symptomatic myocardial bridging in absence of coronary atherosclerotic disease. J Invasive Cardiol 2013;25:586–92. 10. Tandar A, Whisenant BK, Michaels AD. Stent fracture following stenting of a myocardial bridge: report of two cases. Catheter Car- diovasc Interv 2008;71:191–6. 11. Haager PK, Schwarz ER, vom Dahl J, Klues HG, Reffelmann T, Hanrath P. Long term angiographic and clinical follow up in patients with stent implantation for symptomatic myocardial bridging. Heart 2000;84:403–8. 12. Kursaklioglu H, Barcin C, Iyisoy A, Kose S, Amasyali B, Isik E. Angiographic restenosis after myocardial bridge stenting. Jpn Heart J 2004;45:581–9. John Paul II Hospital in Kraków Jagiellonian University, Institute of Cardiology 80 Prądnicka Str., 31-202 Kraków; tel. +48 (12) 614 33 99; 614 34 88; fax. +48 (12) 614 34 88 e-mail: [email protected] www.crcd.eu 13. Kunamneni PB, Rajdev S, Krishnan P, et al. Outcome of intracoronary stenting after failed maximal medical therapy in patients with symp- tomatic myocardial bridge. Catheter Cardiovasc Interv 2008;71: 185–90. 14. Tsujita K, Maehara A, Mintz GS, et al. Impact of myocardial bridge on clinical outcome after coronary stent placement. Am J Cardiol 2009; 103:1344–8. [* The article should be written in English] Please type your text. (2-3 pages, font- TimesNewRoman 12, interline- 1,5) In case of a Case Report please follow the instruction: Background, Case presentation, Discussion, Reference. In case of a non- case report article please follow the instruction: Background, Literature Review, Discussion, Summary. ……………………………………….. Author’s signature** [** Signing the article will mean an agreement for its publication] John Paul II Hospital in Kraków Jagiellonian University, Institute of Cardiology 80 Prądnicka Str., 31-202 Kraków; tel. +48 (12) 614 33 99; 614 34 88; fax. +48 (12) 614 34 88 e-mail: [email protected] www.crcd.eu