Dr. Paul Collinson

My name is Professor Paul Collinson. I'm a consultant chemical pathologist, which is a clinical chemist or clinical biochemist. I'm also a physician in that I work in the Department of Cardiology, where I look after the preventive cardiology services for this hospital. That means that I have the chance to both provide lab services and use them. A myocardial infarction occurs when an artery is blocked.

This occurs typically due to the rupture or erosion of an atherosclerotic plaque and so, we get a blood clot which develops on top of it, blocking the artery. Occasionally, it's due to a clot coming from somewhere else and occasionally, due to something like a dissection of coronary artery. The problem that we had in the past was that the tests which we used to detect damaged heart muscle were not specific to the heart.

They could be confused if there was damage to muscle coming from elsewhere, such as the skeletal muscles. And therefore, we didn't always know whether this was a heart attack or not. Troponin is found only in the heart or specifically, cardiac troponin is found only in the heart. Therefore, if we can detect a rise in troponin, we know that heart damage has occurred, which may be a myocardial infarction.

The reason that we have developed tests with increasing sensitivity is because when the troponin testing was first introduced, it was not a very sensitive test. And most importantly, the analytical imprecision was very poor down at the low end of the range.

So, in order to make sure that we could produce accurate reproducible results, the sensitivity of the tests has been progressively improved, and this has had fringe benefits in other directions, noticeably that we can move the time threshold when we can make a diagnosis progressively further forward. We graduated to the measurement of high-sensitivity troponin about five years ago now.

Previously, we'd been using what's called a contemporary sensitive troponin from Siemens, the Siemens Ultra Assay. This was in fact very good and its performance, in fact, is very close to high-sensitivity. We went over to high-sensitivity because we wanted to have the advantages of being able to make very rapid and early diagnosis and to have very good assay precision at the lower end of the range.

When we transitioned to high-sensitivity, obviously, there are challenges when you go in this direction, because the fact that you are able to measure troponin down to very, very low levels, the lovely analogy is you can measure a sugar cube in Loch Ness, means that any cause of heart damage, be it myocardial infarction, or be it prosaic, like being stabbed in the heart will cause troponin release.

Therefore the greatest challenge for us was to persuade clinicians that elevated troponin does not equate to this is an acute myocardial infarction, but this is myocardial injury and to get them to distinguish between acute myocardial injury, on one hand, chronic myocardial injury on the other. And secondly, that's that acute myocardial injury might not necessarily always be an acute myocardial infarction, but due to a whole range of other conditions, such as myocarditis, trauma, which could cause the troponin to rise.

The problem there is getting people back to their clinical roots and remembering that they are clinicians and not just interpreters of numbers. If you're going to implement a new high-sensitivity troponin assay, the important thing to make sure is that you understand the assay itself. So, obviously, go to meetings, as part of the International Federation of Clinical Chemists Working Group, which I'm on.

We've produced some educational materials to help you in that regard. The other thing to do is to try and make contact with somebody who's already had experience with this assay and learn from their mistakes because they will all have made mistakes and ideally get them to mentor you. Having done all that, the most important thing is to get together a team involving both you and the emergency department and the cardiologists, get everybody together, and then it's all a question of education, education, education.

So, what's the future hold for high-sensitivity troponin? Well, first of all, we can move our times of diagnosis forward. We've already changed our algorithms now. So then instead of waiting six hours, we have the ability to discharge patients immediately on presenting to hospital if their troponin levels are very low and they have other low clinical risk factors.

We've reduced the time now to a zero and three-hour algorithm. We're currently exploring whether we could go to a zero and one-hour algorithm, though this requires a little bit more thought and care. And so, in terms of speed of diagnosis for acute cardiac injury, I think we're pretty much on top of where we're going to go. The area which I think is most interesting though is the potential that troponin has for chronic disease management, something obviously dear to my own heart, because it's quite clear that troponin levels now that we can measure them at a very low level, will predict what happens to you in the medium-term 5 to 10 years.

Therefore, the challenge for the future I think is going to be to use this interesting information and develop treatments by which we can monitor by measuring cardiac troponin that will mean that people don't have heart attacks at all.