I am regularly asked, “why have I got atrial fibrillation?”. There are also often discussions and comments about this online, people are particularly curious about what scientific studies are looking into the causes of atrial fibrillation. To take the latter issue first, in 2018 alone there were 1,000 articles published about the topic. This shows that there is great interest among cardiologists and researchers to find relevant connections – but also that there is a long way to go before we have a more complete understanding of these.
Finding relevant content is difficult
Atrial fibrillation is – like many other diseases – what we call “multifactorial”. This means that there are many different reasons that can contribute to getting the problem. And, since atrial fibrillation is often periodic, there are also many different reasons why it is triggered. I myself argue that there are people who have a certain “vulnerability” in relation to developing atrial fibrillation. This vulnerability can be due to many factors, both known and unknown. Once you have acquired this “vulnerability”, then there are various – again known and unknown – factors that can trigger episodes in the “vulnerable”.
Does genetics play a role?
We know of families where there are disturbances in genes that help to regulate normal heart rhythm function. In these families, about half will have the “sick” gene and half will not. In those who have the “sick” gene, many will get atrial fibrillation – but not all. We also see that atrial fibrillation in these families often occurs already at a young age – sometimes all the way down to the teenage years.
There is thus no doubt that genetics alone can cause atrial fibrillation. However, it is very rare that we see such a clear connection between genetics and atrial fibrillation. Probably far less than 1% of all those who have atrial fibrillation have one – or a few – nuisances that explain their problem. And not even in these rare individuals is there a 100% coincidence between the incidence of genetics and the development of atrial fibrillation.
Presumably, there are other families where gene variations occur in several genes, which – together – give an increased risk of atrial fibrillation. Here, unfortunately, we, as researchers, begin to be on thin ice. We know, on the one hand, that there is a genetic variation that matters. However, on the other hand, not exactly what genes are – and how they play together. Furthermore, these complex relationships are likely to differ from family to family.
This complicated context combined with limited knowledge means that genetics does not play a major role in determining the cause of atrial fibrillation. In the vast majority of cases we cannot come to sensible conclusions regarding the inherited risks for developing atrial fibrillation.
Other risk factors for developing or triggering atrial fibrillation
I have previously written about age, high blood pressure, other heart disease for example a sick heart valve, obesity, sleep apnea, alcohol, stress and sports. The common thread here is that these are all risk factors.
Sometimes your risk doubles if you have one of these factors. Sometimes, as in the case of high blood pressure, we see a 4-5 times increase in the risk of atrial fibrillation. On the other hand, there are people with high blood pressure who do not go on to develop atrial fibrillation. Thus we can infer that blood pressure merely increases the risk of developing atrial fibrillation, as opposed to guaranteeing its development. The same applies to obesity, sleep apnea, stress and sports, where the connection with the risk of atrial fibrillation is weaker.
Common to all of these is that they are precisely risk factors. That is, presence increases the risk of atrial fibrillation. On the other hand, there are even more people with e.g. high blood pressure that does not get the flicker. High blood pressure thus increases the risk, but is not a sufficient factor for everyone with high blood pressure to also get atrial fibrillation. The same applies – to an even greater extent – to obesity, sleep apnea, stress and sports, where the connection with the risk of atrial fibrillation is weaker.
We know that about 25% of us – during our lifetime – get atrial fibrillation. We also know that being overweight is a risk factor for atrial fibrillation. Let us imagine that we have eradicated obesity, so that no one weighs too much anymore. Then it might mean that instead of 25%, 24% will get atrial fibrillation over the course of a lifetime. Maybe a little less – but not much.
Additionally, although we know that increasing age is associated with significantly increased risk of atrial fibrillation, and is probably one of the strongest risk factors, there are still significantly more 80-year-olds without atrial fibrillation than with.
We also know that atrial fibrillation itself can cause changes in the heart that cause even more episodes to occur, or that atrial fibrillation bites hard and becomes chronic.
These complex relationships are a large part of the reason why it is usually impossible to point to the single factor which, in the specific person, has been the cause of atrial fibrillation. I often find it quite frustrating when you have been burdened with atrial fibrillation – that even if you try and want to, you can not find any unambiguous connection that can explain why you have the problem.
On the other hand, it does not change the fact that it is important to do something about the risk factors that may be present. You unfortunately need to accept that while you can’t solve the problem, you can make it less pronounced and improve the outcome of your treatment by mitigating risk factors.
While we struggle to understand the cause of atrial fibrillation, we are in fact quite good at treating both atrial fibrillation, and the potential underlying causes. Additionally we are also aware that it is essential to treat both atrial fibrillation, and the underlying risk factors early in the process. This helps to prevent the condition from becoming chronic. This is also why it is important for you to take a proactive approach, and seek medical help early if you feel that something is wrong.
We know of this complex relationship between cause, effect and treatment from other common diseases such as, for example, atherosclerosis. Here are also examples of rare genetic defects that alone are sufficient to get atherosclerosis. However, the vast majority of cases of atherosclerosis are due to a complex interplay of internal and external factors. For atherosclerotic diseases, we have, since the 1980s, had an increased focus on both prevention and treatment. This has meant that the risk of dying from e.g. a blood clot in the heart has more than halved since 1990. It is a very significant effect and it gives, in my eyes, reason for further optimism in relation to atrial fibrillation.
So, even though we do not know all the factors, and their interactions with each other, there is “light at the end of the tunnel”. It is useful to do something about the risk factors in order to prevent the issue from worsening. It is certainly also essential to treat atrial fibrillation with medication, ablation and other measures.