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AzuriteWind (talk | contribs) Moved the authors of quotes to the quotes themselves, added more links, removed a disambiguation, and rewrote some parts of the text. I've also removed the disambiguation template as I feel that all them have been fixed, but feel free to re-add it if needed (with justification). |
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{{More medical citations needed|date=December 2020}}
{{Cleanup rewrite|date=June 2024}}{{Infobox medical condition (new)
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In most people, the coronary arteries rest on top of the [[Cardiac muscle|heart muscle]] and feed [[blood]] down into smaller [[Blood vessel|vessels]] (ex. septal [[Artery|arteries]]) which then take blood into the heart muscle itself (i.e. populate throughout the myocardium). However, if a band of muscle forms around one of the coronary arteries during the [[Fetus|fetal]] stage of development, then a myocardial bridge is formed – a "bridge" of heart muscle over the artery.
Each time the heart squeezes to pump blood, the band of muscle exerts pressure and it is very rarely constricts the artery, reducing blood flow to the heart. Even a very thin ex. <1 [[Millimetre|mm]] and/or short ex. 20 mm MB can cause significant symptoms, though this has not been completely proven.{{Citation needed|date=June 2024}} MBs can range from a few mm in length to 10 [[Centimeter|cm]] or more.{{Citation needed|date=June 2024}}
The overall prevalence of myocardial bridge is at 19%, although its prevalence found by autopsy is much higher (42%). A myocardial bridge is a usually harmless condition, and in many cases bridges don't seem to cause symptoms. However, some people with myocardial bridges can experience [[angina]], or [[chest pain]].<ref>{{Cite journal |last1=Hostiuc |first1=Sorin |last2=Negoi |first2=Ionuț |last3=Rusu |first3=Mugurel C. |last4=Hostiuc |first4=Mihaela |date=2017-10-16 |title=Myocardial Bridging: A Meta-Analysis of Prevalence |url=https://onlinelibrary.wiley.com/doi/abs/10.1111/1556-4029.13665 |journal=Journal of Forensic Sciences |volume=63 |issue=4 |pages=1176–1185 |doi=10.1111/1556-4029.13665 |pmid=29044562 |s2cid=2494037 |issn=0022-1198}}</ref><ref>https://stanfordhealthcare.org/medical-conditions/blood-heart-circulation/myocardial-bridging.html</ref><ref> https://my.clevelandclinic.org/health/diseases/myocardial-bridge</ref>
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There are three key tests currently used to diagnose myocardial bridges by [[Stanford University]]: CT scan, cardiac catheterization, and stress ultrasound.
# [[CT scan]] – on which the myocardial bridge often appears as a compressed or squashed area of the artery in which, notably, the fatty areas surrounding the artery (shown in black on CT scans) disappear, since the artery is tunneling through muscle not fat in this area. CTs often allow an assessment of an approximate length and depth of the myocardial bridge, but compression cannot be assessed accurately from a CT scan.<ref name="pmid28690285">{{cite journal | vauthors = Forsdahl SH, Rogers IS, Schnittger I, Tanaka S, Kimura T, Pargaonkar VS, Chan FP, Fleischmann D, Tremmel JA, Becker HC | title = Myocardial Bridges on Coronary Computed Tomography Angiography - Correlation With Intravascular Ultrasound and Fractional Flow Reserve | journal = Circ J | volume = 81 | issue = 12 | pages = 1894–1900 | date = November 2017 | pmid = 28690285 | doi = 10.1253/circj.CJ-17-0284 | doi-access = free }}</ref>
# [[Intravascular ultrasound|IVUS]] [[cardiac catheterization]] including dFFR measured during [[dobutamine]] challenge – from which readings of dFFR and percentage compression as well as measurements of the approximate length and depth (shown as the halo or echolucent band) of the MB are taken. It is critical to note that in order to be meaningful in diagnosing a myocardial bridge, it is critical to measure dFFR i.e. the diastolic period, not mean FFR. This is because, contrary to a common misconception, myocardial bridges cause compression of the artery during diastole as well as systole, as explained above. This has been shown in multiple studies.<ref>{{cite journal |last1=Tremmel |first1=Jennifer A. |last2=Schnittger |first2=Ingela |title=Myocardial Bridging |journal=Journal of the American College of Cardiology |date=18 November 2014 |volume=64 |issue=20 |pages=2178–2179 |doi=10.1016/j.jacc.2014.07.993 |pmid=25457408 |doi-access=free }}</ref><ref>{{cite journal |last1=Escaned |first1=Javier |last2=Cortés |first2=Jorge |last3=Flores |first3=Alex |last4=Goicolea |first4=Javier |last5=Alfonso |first5=Fernando |last6=Hernández |first6=Rosana |last7=Fernández-Ortiz |first7=Antonio |last8=Sabaté |first8=Manel |last9=Bañuelos |first9=Camino |last10=Macaya |first10=Carlos |title=Importance of diastolic fractional flow reserve and dobutamine challenge in physiologic assessment of myocardial bridging |journal=Journal of the American College of Cardiology |date=July 2003 |volume=42 |issue=2 |pages=226–233 |doi=10.1016/s0735-1097(03)00588-6 |pmid=12875756 |doi-access=free }}</ref> It is also critical that the dobutamine challenge be used, elevating the heart rate, because dFFR decreases significantly at high heart rates as shown by Yoshino et al., 2014.<ref>Fractional flow reserve with dobutamine challenge and coronary microvascular endothelial dysfunction in symptomatic myocardial bridging. Yoshino et al., 2014. Circulation Journal.</ref>
# [[Cardiac stress test|Stress echocardiogram]] (i.e. before and after running on a treadmill) – used to identify evidence of ischemia i.e. a lack of oxygen delivered to the ventricle due to the MB. This test does not visualize the MB itself but rather its effects on the ventricle. Multiple studies have shown that ischemia from MBs is indicated by the appearance "septal buckling" in the stress echocardiogram, as the septum gives out under stress.,<ref name="Stanford Stress Echo Pattern 2013">A Novel Stress Echocardiography Pattern for Myocardial Bridge With Invasive Structural and Hemodynamic Correlation. Lin, Tremmel, Yamada, et al. (J Am Heart Assoc. 2013;2:e000097 {{doi|10.1161/JAHA.113.000097}}</ref><ref>Stress echocardiography pattern: a promising noninvasive test for detection of myocardial bridging with haemodynamic relevance. Mariachiara Siciliano;Federico Migliore;Piergiuseppe Piovesana, 2016. Journal of Cardiovascular Medicine</ref> which a 2013 paper by Lin et al. describes as "a transient focal buckling in the end-systolic to early-diastolic motion of the septum with apical sparing which correlates prospectively with the presence of LAD MB."<ref name ="Stanford Stress Echo Pattern 2013" />
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Notably, [[Electrocardiography|EKG]] is not a reliable or conclusive diagnostic tool for diagnosing MBs. Some symptomatic MB patients show normal EKG results and others abnormal.{{Citation needed|date=June 2024}}
Many doctors have suggested that there is a need for more awareness of MBs among doctors and better testing, including testing of young people as the disease is congenital. According to a 2007 study
{{Quote|text=Clinical suspicion of a myocardial bridge would be warranted in all cases of typical or atypical [[chest pain]] in subjects who have a low probability of [[atherosclerosis]] because they are free from the traditional [[cardiovascular]] risk factors, particularly in the young.|author=Chiara Ripa, MD, et al.}}
{{Quote|text=Many of these patients have these heartbreaking stories to tell. They can’t hold a job, they can’t travel, they can’t take care of their families. Most [[cardiologists]] are completely at a loss. They know myocardial bridges exist, but they have been taught they are benign and never cause problems... When these patients go to the [[Emergency department|ER]], and they go there a lot, all the cardiology tests come back normal. They’re told, 'Here’s a little [[Valium]]. I think you’re [[anxious]].' They get belittled, not taken seriously, and they get really [[Depression (mood)|depressed]].|author=Dr. Ingela Schnittger, MD.}}
==Treatment==
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[[Bypass surgery]] is not the first line treatment for myocardial bridges for two main reasons:<ref name ="Stanford Overview 2017" />
# Competitive flow problem – blood can flow the wrong way,
# Jailed septal arteries still jailed – a jailed artery is a septal artery (a branch off the coronary artery) that lies inside the myocardial bridge and is thus also compressed with each heartbeat. Septal arteries are critical as they carry blood into the heart septum. Bypass surgery alone does not remedy jailed septal arteries, which still do not get blood flow.
Notably, many myocardial bridge patients have had bypass surgery only to later need unroofing surgery after the bypass proved unsuccessful.<ref name ="Stanford Overview 2017" />
However, papers by Ekeke et al., 2015 <ref>"Myocardial bridging over the left anterior descending: Myotomy, bypass, or both?" Ekeke et al. 2015. Journal of Thoracic Cardiovascular Surgery.</ref>
[[Stent]]s are never indicated as a treatment for myocardial bridges because trials have shown they are prone to breaking when the artery is squeezed each heartbeat.<ref name ="Stanford Overview 2017" />
Unroofing surgery has been performed in the [[United States]], [[Belgium]], [[Spain]], [[Italy]], [[England]], [[China]], [[Russia]], [[United Arab Emirates]], and [[Singapore]], among other countries.{{Citation needed|date=June 2024}} Hospitals that have performed unroofing surgery include:
* [[Stanford University Medical Center]] – surgeon Dr. Jack Boyd; team leader Dr. Ingela Schnittger
* [[University of Chicago Medical Center]] – surgeon Dr. Husam Balkhy
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* Hospital de las Cruces, Barakaldo, [[Basque Country (autonomous community)|Basque Country]], [[Spain]] – Dr. Crespo and Dr. Aramendi
* [[Istanbul University]] Hospital – Dr. Ihsan Bakir
* St Francis Hospital and Heart, [[New York City|NYC]] - Dr. Newell Robinson
* [[National University Hospital]], Singapore - Dr. Theodoros Kofidis
In many other countries, including a number of highly [[Developed country|developed countries]] such as the [[United Kingdom|UK]], [[Australia]], [[New Zealand]], [[Republic of Ireland|Ireland]] and [[Sweden]], unroofing surgery for myocardial bridges remains unavailable, and in some, the condition remains unrecognized as a medical problem.{{Citation needed|date=June 2024}}
==Prevalence==
The true prevalence of MBs is still largely unknown, as studies have made vastly different assessments. As a 2017 [[Stanford University|Stanford]] paper
{{quote|Estimations of the prevalence of MBs vary... at least in part as a result of several key variables, including the means of identification (eg, computed tomography (CT), intravascular ultrasound ([[IVUS]]), or autopsy), which vessels are examined, and which definition of a bridge is applied (eg, only a “deep” bridge vs both “superficial” and “deep” bridges). Perhaps the most fundamental variable is whether an MB is even considered. Unlike [[hypertrophic cardiomyopathy]], which will usually be obvious to the [[pathologist]], MBs can be easily obscured by [[epicardial]] and [[Pericardium|pericardial]] fat. As such, autopsy series have estimated the prevalence between 5% and 86%. The largest autopsy report, which included 1056 subjects, found a prevalence of 26%, 88% of which involved the [[Left axis deviation|LAD]]. One population-based study with CT estimated a prevalence of 22.5%. As a result of these studies and others, an estimated prevalence of approximately 25% is generally accepted.|author=Ian S. Rogers, MD, MPH, et al.}}
==History==
According to Stanford University Medical Center, MBs are often misunderstood by [[Doctor (title)|doctors]], who may have been taught that the condition is always benign.<ref name ="Stanford Overview 2017" /> As a result, patients are often denied treatment. But a great deal of science has emerged in the past decade to clarify the condition. In particular, Stanford has published over 15 articles on MBs since 2014. One commonly recurring reason for denial of treatment is the myth that myocardial bridges do not significantly affect blood flow. But this myth has been debunked by Stanford and also Daoud and Wafa 2012 who say:
{{quote|Normally, only 15% of [[Coronary circulation|coronary]] [[blood flow]] occurs during [[systole]] and because myocardial bridging is a systolic event on [[angiography]], its clinical significance and relevance have been questioned. [However] angiographic and [[intravascular]] [[ultrasonographic]] studies demonstrated that vessel compression during systole is followed by the delay in the increase in [[Lumen (anatomy)|luminal]] diameter during diastole, thus affecting the predominant phase of [[coronary]] [[perfusion]], especially during episodes of [[tachycardia]]. These data suggest that angina, acute coronary syndromes, and [[arrhythmias]] in patients with myocardial bridging may be explained by the reduced [[ischemic]] threshold.”<ref>{{cite journal |last1=Daoud |first1=Eid M. |last2=Wafa |first2=Ahmed A. |title=Does isolated myocardial bridge really interfere with coronary blood flow? |journal=The Egyptian Heart Journal |date=June 2013 |volume=65 |issue=2 |pages=65–70 |doi=10.1016/j.ehj.2012.05.003 |doi-access=free }}</ref>
}}
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