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The heart is a muscle and any living muscle needs a blood supply. The blood is supplied by arteries that are known as coronary ateries. Usually these arteries sit on the surface of the heart. However sometimes a portion of the artery may run an intramuscular course for a portion of its length. This is termed a myocardial bridge. 

The problem with a bridge is that there is a possibility that this blood vessel can become compressed when the heart contracts because it is within the muscle and therefore one could postulate that if the heart muscle contract, the blood vessel constricts and therefore the heart muscle would be deprived of blood and this could be dangerous. However this does not happen in the vast majority because the coronary arteries actually fill with blood when the heart is relaxing and therefore when the heart contracts there is not a huge impact on the coronary flow. Nevertheless there are many cases in the literature where a myocardial bridge has been reported as being the cause behind symptoms such as angina, heart attacks and even sudden death but this is in a very small number of patients.

The first thing to say is that myocardial bridges are very common. When we study autopsy cases unto 42% of patients had at least as mall amount of myocardial bridging. In terms of other tests, up to 25-30% of patients who have cardiac CTs are identified as having bridges and by the far the commonest location is in the Left anterior descending artery which is the biggest and longest of the 3 coronary arteries

When we look at the heart in detail in patients with myocardial bridges we see 2 interesting things.

  1. At the proximal end of the bridge, before the vessel enters into the muscle, there tends to be a much higher likelihood of atherosclerosis and in the bit of the vessel which is within the muscle and the bit which then comes out of the muscle there is often no atherosclerosis so it is thought that there may be something about the way that the blood flow is altered by this constant systolic compression (milking) that seems to predispose to development of atherosclerosis. If a small bit of that atherosclerotic plaque breaks off then that could provide the mechanism for a heart attack because immediately a blood clot can form at the site of injury and this could then cause a blockage to the whole vessel. It is also thought that the abnormal hamodyanamics at that point can release abnormal biochemical inflammatory mediators which can precipitate spasm of the vessel which can then cause chest discomfort.

How do you diagnose it as the cause of the chest pain? 

As bridges are so common it is not difficult to diagnose them. The bigger challenge is to work out whether they are indeed the cause of the patients symptoms. For this usually an invasive angiogram is necessary firstly to ensure that there is no other disease elsewhere that could be the cause of the patients symptoms. Once a bridge has been identified, a functional test is useful to see whether it truly is causing a reduction in the blood supply to the heart muscle it is meant to be supplying.

This is where a technique called FFR is useful. In this a wire is passed into the heart artery and pressure is measured proximal to the bridge and then distal to the bridge both at rest and after infusion of a medication to stress the heart and subsequently a number is calculated. If the FFR number is very low it indicates that only a very small proportion of the flow proximal to the bridge is getting through suggesting that the bridge is causing significant flow limitation.  The magic number is 0.75

How do you treat it?

There are 3 main approaches:

  1. Medications – such as beta blockers although beta blockers can worsen spasm  
  2. Stents – A stent could be placed within the bridged segment to minimise compression
  3. Surgery – either the stetted segment can be bypassed or actually a procedure called surgical unroofing may be performed which involves cutting through the muscle above the tunnelled blood vessel to release the artery. This is perhaps the technique with the best results and I think there was a small study for Stanford which suggested that it significantly improved quality of life in patients with debilitating symptoms from a myocardial bridge.

So in summary:

  1. Bridges are common and in the vast majority of patients they don’t cause a problem
  2. In a small number of patients, who have debilitating symptoms and no other cause found, a bridge may be the culprit
  3. If after investigation, a bridge is found to be the culprit then it is well worthwhile seeing a surgeon with an interest in this subject to see if they could consider unroofing surgery.

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