In most people, the coronary arteries rest on top of the heart muscle and feed blood down into smaller vessels (e.g. the septal arteries) which then carry blood to 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 fetal stage of development, then a myocardial bridge is formed – a "bridge" of heart muscle over the artery.
Every 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. <1mm and/or short ex. 20mm MB can cause significant symptoms, although this has not been completely proven.[citation needed] MBs can range in length from a few millimetres to 10cm or more.[citation needed]
The overall prevalence of myocardial bridge is at 19%, although the prevalence found at autopsies is much higher (42%). Myocardial bridge is usually a harmless condition, and in many cases bridges don't seem to cause any symptoms. However, some people with myocardial bridges may experience angina, or chest pain.[1][2][3]
Symptoms and signs
While many people have very tiny myocardial bridges that cause no symptoms, others have longer and/or deeper bridges causing significant symptoms, including children. For example, some patients cannot run or exercise at all, others can exercise despite symptoms such as shortness of breath or feelings of tightness in the chest, and still others find improvement of symptoms during exercise. Many competitive athletes have had severe myocardial bridges and unroofing surgery.[4][5]
The symptoms of myocardial bridges differ slightly from patient to patient depending on the length, depth, and location of the bridge. Common symptoms include:[6][7]
Squeezing/tightness/pressure/pain in chest, shoulder, jaw, armpit, neck, and/or down the arm
Inability to exercise, walk, do chores, have to sit/lie down
Feeling like chest is “going to explode”
Feeling of something “clamping down” in the chest
Fainting/passing out (syncope) and/or feeling like one is about to faint
Complications
Myocardial bridges can cause numerous complications – which are often as misunderstood in the medical community as the condition itself. These include:
plaque forming just before (proximal to) the myocardial bridge
Note that studies have shown that plaque does not form inside myocardial bridges, yet there is virtually always plaque just before the myocardial bridge in adults.
Some common triggers of myocardial bridge symptoms are:
anything that raises the heart rate, even positive events
low-oxygen environments ex. hot humid weather, high altitude
sitting/lying/doing nothing for long periods
Notably, high heart rate or tachycardia greatly increases ischemia (low oxygen to the heart) caused by myocardial bridges. Studies[8] have shown that this is because the compressed artery reopens only very slowly each heartbeat and thus stays in a state of semi-compression for most or all of the diastolic period. Thus as the heart rate increases, the time the artery has to reopen (diastolic period) decreases dramatically – to the point that with very high heart rates, the artery never fully reopens and blood flow is constantly reduced.
Diagnosis
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.[9]
IVUScardiac 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.[10][11] 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.[12]
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.,[13][14] 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."[13]
As much of the science of testing for MBs is relatively new, patients frequently go undiagnosed. Stanford's center for myocardial bridges has offered second opinion services from a distance for some ten years, including to numerous international patients.[citation needed]
Notably, 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]
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:[8]
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.
—Chiara Ripa, MD, et al.
A 2017 article in Stanford Medical Center's official blog Scope explains the hardships people with MB face, including the dismissal of their symptoms and obstacles in their lives as a result of the lack of MB education amongst cardiologists:[15]
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 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 depressed.
—Dr. Ingela Schnittger, MD.
Treatment
Myotomy, commonly known as unroofing surgery, is the first-line surgical treatment for myocardial bridges.[6][16] It is the only treatment that actually removes the myocardial bridge itself, releasing the artery from compression. Unroofing surgery today is done via open heart (sternum), thoracotomy (through the ribs), and also using robot-assisted surgery (through tiny keyholes in the chest). Full open heart surgery is usually reserved for very large myocardial bridges and/or specific situations that make thoracotomy difficult. By far, Stanford University has done more unroofing surgeries than any other hospital in the world, with over 200 unroofings completed since starting a decade ago. In 2019, University of Chicago surgeon Dr. Husam Balkhy emerged as a provider of robotic-assisted unroofing surgery, with some patients being possible candidates for this route.[17]
If done properly, unroofing removes the entire band of muscle affecting the artery, restoring more blood flow. Stanford University Medical Center's 2016 study by Pargaonkar et al.[18] showed that unroofing surgery “significantly improves anginal symptoms” and improves “all five dimensions of the SAQ” i.e. Seattle Angina Questionnaire. Some residual symptoms caused by complications from a lifetime of living with a myocardial bridge may continue after unroofing surgery such as endothelial dysfunction, vasospasm, plaque, narrowed artery. However, these often improve slowly over a year or more once the myocardial bridge is gone.[citation needed]
A few cases have occurred in various hospitals in which patients have not been completely unroofed, leaving segments of the MB, resulting in lingering symptoms.[citation needed]
A critical point is that the endothelial dysfunction and vasospasms caused by myocardial bridges cannot start to heal until unroofing surgery is done, because the MB continues to squeeze on the artery, damaging the artery lining.[citation needed]
Bypass surgery is not the first line treatment for myocardial bridges for two main reasons:[6]
Competitive flow problem – blood can flow the wrong way, such as continuing to flow down the original artery instead of the new artery that has been grafted on.
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.[6]
However, papers by Ekeke et al., 2015 [19] have shown bypass surgery is helpful as an addition to supplement unroofing surgery, but only when there is significant plaque just before (proximal to) the myocardial bridge or anatomic anomalies increase the risk of recurrence of such plaque. A 2013 Russian study by Bockeria et al.[20] concludes that this competitive flow problem is much more likely to occur if the LIMA artery is used for the graft rather than the SVG, so the SVG is recommended.
Stents 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.[6]
In many other countries, including a number of highly developed countries such as the UK, Australia, New Zealand, Ireland and Sweden, unroofing surgery for myocardial bridges remains unavailable, and in some, the condition remains unrecognized as a medical problem.[citation needed]
Prevalence
The true prevalence of MBs is still largely unknown, as studies have made vastly different assessments. As a 2017 Stanford paper[6] points out:
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 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 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.
—Ian S. Rogers, MD, MPH, et al.
History
According to Stanford University Medical Center, MBs are often misunderstood by doctors, who may have been taught that the condition is always benign.[6] 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:
Normally, only 15% of coronaryblood 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 intravascularultrasonographic studies demonstrated that vessel compression during systole is followed by the delay in the increase in luminal diameter during diastole, thus affecting the predominant phase of coronaryperfusion, 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.”[21]
In other words, while the myocardial bridge itself only compresses the artery while the heart squeezes (systolic period), which is only 15% of the time in the heartbeat cycle, in fact, the artery stays compressed long after the heart relaxes. This is because arteries are sturdy and pliable, so after being compressed they are very slow to reopen, remaining in some level of semi-compression for most if not all of the diastolic period i.e. the other 85% of the heartbeat cycle (hence the critical need for dFFR testing in diagnosing myocardial bridges).[citation needed] Thus the coronary artery is fully open to allow normal blood flow for only a small percentage of each heartbeat cycle.[citation needed] This problem is further exacerbated by tachycardia, which can bring the duration of normal blood flow to zero, as explained below. Dr. Ingela Schnittger, head of the Myocardial Bridge Research Center at Stanford, has appeared on BBC Radio to explain this.[citation needed]
Coronary artery disease (CAD), also called coronary heart disease (CHD), ischemic heart disease (IHD), myocardial ischemia, or simply heart disease, involves the reduction of blood flow to the cardiac muscle due to build-up of atherosclerotic plaque in the arteries of the heart. It is the most common of the cardiovascular diseases. Types include stable angina, unstable angina, and myocardial infarction.
Angina, also known as angina pectoris, is chest pain or pressure, usually caused by insufficient blood flow to the heart muscle (myocardium). It is most commonly a symptom of coronary artery disease.
Coronary artery bypass surgery, also known as coronary artery bypass graft, is a surgical procedure to treat coronary artery disease (CAD), the buildup of plaques in the arteries of the heart. It can relieve chest pain caused by CAD, slow the progression of CAD, and increase life expectancy. It aims to bypass narrowings in heart arteries by using arteries or veins harvested from other parts of the body, thus restoring adequate blood supply to the previously ischemic heart.
Microvascular angina (MVA), previously known as cardiac syndrome X, also known as coronary microvascular dysfunction(CMD) or microvascular coronary disease is a type of angina (chest pain) with signs associated with decreased blood flow to heart tissue but with normal coronary arteries.
Interventional cardiology is a branch of cardiology that deals specifically with the catheter based treatment of structural heart diseases. Andreas Gruentzig is considered the father of interventional cardiology after the development of angioplasty by interventional radiologist Charles Dotter.
Cardiac catheterization is the insertion of a catheter into a chamber or vessel of the heart. This is done both for diagnostic and interventional purposes.
Acute coronary syndrome (ACS) is a syndrome due to decreased blood flow in the coronary arteries such that part of the heart muscle is unable to function properly or dies. The most common symptom is centrally located pressure-like chest pain, often radiating to the left shoulder or angle of the jaw, and associated with nausea and sweating. Many people with acute coronary syndromes present with symptoms other than chest pain, particularly women, older people, and people with diabetes mellitus.
Variant angina, also known as Prinzmetal angina,vasospastic angina, angina inversa, coronary vessel spasm, or coronary artery vasospasm, is a syndrome typically consisting of angina. Variant angina differs from stable angina in that it commonly occurs in individuals who are at rest or even asleep, whereas stable angina is generally triggered by exertion or intense exercise. Variant angina is caused by vasospasm, a narrowing of the coronary arteries due to contraction of the heart's smooth muscle tissue in the vessel walls. In comparison, stable angina is caused by the permanent occlusion of these vessels by atherosclerosis, which is the buildup of fatty plaque and hardening of the arteries.
Unstable angina is a type of angina pectoris that is irregular or more easily provoked. It is classified as a type of acute coronary syndrome.
The intra-aortic balloon pump (IABP) is a mechanical device that increases myocardial oxygen perfusion and indirectly increases cardiac output through afterload reduction. It consists of a cylindrical polyurethane balloon that sits in the aorta, approximately 2 centimeters (0.79 in) from the left subclavian artery. The balloon inflates and deflates via counter pulsation, meaning it actively deflates in systole and inflates in diastole. Systolic deflation decreases afterload through a vacuum effect and indirectly increases forward flow from the heart. Diastolic inflation increases blood flow to the coronary arteries via retrograde flow. These actions combine to decrease myocardial oxygen demand and increase myocardial oxygen supply.
In medicine, collateralization, also vessel collateralization and blood vessel collateralization, is the growth of a blood vessel or several blood vessels that serve the same end organ or vascular bed as another blood vessel that cannot adequately supply that end organ or vascular bed sufficiently.
Transmyocardial laser revascularization (TMR) is a procedure used to treat inoperable heart disease in people with persistent angina that is not relieved by any other revascularization method.
Coronary vasospasm refers to when a coronary artery suddenly undergoes either complete or sub-total temporary occlusion.
Coronary artery anomalies are variations of the coronary circulation, affecting <1% of the general population. Symptoms include chest pain, shortness of breath and syncope, although cardiac arrest may be the first clinical presentation. Several varieties are identified, with a different potential to cause sudden cardiac death.
The following outline is provided as an overview of and topical guide to cardiology, the branch of medicine dealing with disorders of the human heart. The field includes medical diagnosis and treatment of congenital heart defects, coronary artery disease, heart failure, valvular heart disease and electrophysiology. Physicians who specialize in cardiology are called cardiologists.
Coronary ischemia, myocardial ischemia, or cardiac ischemia, is a medical term for abnormally reduced blood flow in the coronary circulation through the coronary arteries. Coronary ischemia is linked to heart disease, and heart attacks. Coronary arteries deliver oxygen-rich blood to the heart muscle. Reduced blood flow to the heart associated with coronary ischemia can result in inadequate oxygen supply to the heart muscle. When oxygen supply to the heart is unable to keep up with oxygen demand from the muscle, the result is the characteristic symptoms of coronary ischemia, the most common of which is chest pain. Chest pain due to coronary ischemia commonly radiates to the arm or neck. Certain individuals such as women, diabetics, and the elderly may present with more varied symptoms. If blood flow through the coronary arteries is stopped completely, cardiac muscle cells may die, known as a myocardial infarction, or heart attack.
A myocardial infarction (MI), commonly known as a heart attack, occurs when blood flow decreases or stops in one of the coronary arteries of the heart, causing infarction to the heart muscle. The most common symptom is retrosternal chest pain or discomfort that classically radiates to the left shoulder, arm, or jaw. The pain may occasionally feel like heartburn.
Coronary steal is a phenomenon where an alteration of circulation patterns leads to a reduction in the blood flow directed to the coronary circulation. It is caused when there is narrowing of the coronary arteries and a coronary vasodilator is used – "stealing" blood away from those parts of the heart.
Spontaneous coronary artery dissection (SCAD) is an uncommon but potentially lethal condition in which one of the coronary arteries that supply the heart, spontaneously develops a blood collection, or hematoma, within the artery wall due to a tear in the wall. SCAD is one of the arterial dissections that can occur.
Reperfusion therapy is a medical treatment to restore blood flow, either through or around, blocked arteries, typically after a heart attack. Reperfusion therapy includes drugs and surgery. The drugs are thrombolytics and fibrinolytics used in a process called thrombolysis. Surgeries performed may be minimally-invasive endovascular procedures such as a percutaneous coronary intervention (PCI), which involves coronary angioplasty. The angioplasty uses the insertion of a balloon and/or stents to open up the artery. Other surgeries performed are the more invasive bypass surgeries that graft arteries around blockages.
1 2 Alexandre A, Vieira P, Dias-Frias A, Pereira A, Campinas A, Sá-Couto D, Brochado B, Sá I, Silveira J, Torres S. Myocardial Bridging Leading to Cardiac Collapse in a Marathon Runner. Journal of Cardiovascular Development and Disease. 2022; 9(7):200. https://doi.org/10.3390/jcdd9070200
1 2 3 4 5 6 7 Rogers, Ian S.; Tremmel, Jennifer A.; Schnittger, Ingela (September 2017). "Myocardial bridges: Overview of diagnosis and management". Congenital Heart Disease. 12 (5): 619–623. doi:10.1111/chd.12499. PMID28675696.
↑ Fractional flow reserve with dobutamine challenge and coronary microvascular endothelial dysfunction in symptomatic myocardial bridging. Yoshino et al., 2014. Circulation Journal.
1 2 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
↑ 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
↑ Robotic totally endoscopic off-pump unroofing of left anterior descending coronary artery myocardial bridge: A report of two cases. Mirzai, Patel, Balkhy. June 18, 2019. Journal of Cardiac Surgery. doi:10.1111/jocs.14094
↑ Pargaonkar et al. Effect of Surgical Unroofing of a Myocardial Bridge on Exercise Induced QT interval Dispersion and Anginal Symptoms in Patients with Angina in the Absence of Obstructive Coronary Artery Disease. Journal of the American College of Cardiology
↑ "Myocardial bridging over the left anterior descending: Myotomy, bypass, or both?" Ekeke et al. 2015. Journal of Thoracic Cardiovascular Surgery.
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