Download Myocardial bridge – diagnosis and treatment in a congenital anomaly

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