Myocardial bridge
A myocardial bridge (MB) is a congenital heart defect in which one of the coronary arteries tunnels through the heart muscle itself (myocardium). In normal patients, the coronary arteries rest on top of the heart muscle and feed blood down into smaller vessels (ex. septal 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 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 constricts the artery, reducing blood flow to the heart. This defect is present from birth. It is important to note that even a very thin ex. < 1 mm and/or short ex. 20 mm MB can cause significant symptoms. MBs can range from a few mm in length to 10 cm or more. The overall prevalence of myocardial bridge is 19%, although its prevalence found by autopsy is much higher (42%). 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. The symptoms of myocardial bridges differ slightly from patient to patient depending on the length, depth, and location of the bridge. Common symptoms include: Complications. Myocardial bridges can cause numerous complications - which are often as misunderstood in the medical community as the condition itself. These  include: 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: Notably, high heart rate or tachycardia greatly increases ischemia (low oxygen to the heart) caused by myocardial bridges. Studies such as Ripa et al., 2007 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. 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. Notably, EKG is not a reliable or conclusive diagnostic tool  for diagnosing MBs. Some symptomatic MB patients show normal EKG results and others abnormal. 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 by Ripa et al.: "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." In a 2017 article in Stanford Medical  Center's official blog Scope, Dr. Ingela Schnittger stated: "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." Treatment. Myotomy, commonly known as unroofing surgery, is the first-line surgical treatment for myocardial bridges. 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. 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. 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. 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. 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. Bypass surgery is not the first line treatment for myocardial bridges  for two main reasons: Notably, many myocardial bridge patients have had bypass surgery only to later need unroofing surgery after the bypass proved unsuccessful. However, papers by Ekeke et al., 2015 and others 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. 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. Unroofing surgery has been performed in the United States, Belgium, Spain, Italy, England, China, Russia, United Arab Emirates among other countries. Hospitals that have performed unroofing surgery include: In many other countries, including a number of highly developed countries such as the UK, Australia, New Zealand, Ireland, Sweden, and Singapore, unroofing surgery for myocardial bridges remains unavailable, and in some, the condition remains unrecognized as  a medical problem. Prevalence. The true prevalence of MBs is still largely unknown, as studies have made vastly different assessments. As a 2017 Stanford paper by Rogers, et al. points out: History. According to Stanford University Medical Center, MBs are often misunderstood by doctors, who may have been taught that the condition is always benign. 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: 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). Thus the coronary artery is fully open to allow normal blood flow for only a small percentage of each heartbeat cycle. This problem is further exacerbated by tachycardia (high heart rate), 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.