Men suffer from atrial fibrillation as do women. Looking at the numbers10, more men develop the disease; however, women, when they suffer the condition, run a higher risk of complications, including death. Although there is an increasing incidence of the condition as people age, young people, even as young as in their teens, can suffer from it, although this is uncommon.

In coming to a better understanding of atrial fibrillation, it is valuable to understand AF associations. To do this, we must distinguish that associations, the factors that lend weight to the possibilty of atrial fibrillation being present, are not causations, that is the mechanisms that give rise to the actual problem.

Let’s look at this from outside the medical field. We know that speeding and alcohol consumption are significant associations with car accidents. However, we also know that people do drive over the speed limit with high alcohol levels yet do not have an accident. Conversely, we know that people who drive safely can be involved in an accident. This does not mean that driving within the speed limit and not consuming alcohol when driving is a waste of time. It simply alters the risk profile. It means that speed and alcohol are associations with having an accident. If they were causations, then every time someone sped or had consumed alcohol, that person would be involved in a car accident.

To take this a step further, alcohol does not cause the car accident; it does not drive the car, yet it can impair the driver’s reflexes and assessment, and contribute to the driver having an accident. The actual cause of the accident may be approaching a sharp bend too quickly or a car in front stopping suddenly, while multiple associations may be present such as alcohol, speeding, driver inexperience, poor weather. The reverse may also be true. There may be no alcohol, no speeding or any other association, and still an accident occurs.
 
atrial fibrillation associations

Atrial fibrillation associationsare found within the heart structure as well as externally.

within the heart

high blood pressure

the pressure changes caused by high blood pressure stretch the left atrium which, over time, will change the shape of the atrium, increasing the likelihood of it developing an abnormal rhythm. The change of shape is often also associated with

micro scarring

that changes the way the electricity flows through the atrium.
These factors along with

general wear and tear

increase the possibility of the electrical signal within the atria being deranged;

problems with the valves

also affect the pressures within the heart, again impacting the atrium’s
structure and subsequently its function, while

abnormality of the myocardium,
cardiac failure (including congenital heart problems)
can be similarly implicated.

outside the heart

obesity
particularly when it leads to

obstructive sleep apnoea

a condition in which the respiratory system is obstructed at night while the sufferer snores, producing low levels of oxygen within the bloodstream. This triggers a very brisk response from the sympathetic autonomic nervous11 system that can increase blood pressure and can drive scarring and inflammation within the heart;

diabetes

long-term diabetes seems to impact the heart, possibly with by-products of diabetic metabolism ending up within the structure and the fibres of the myocardium, again affecting how the atria work;

chronic renal disease

nearly 20 percent of people with poor kidney function will develop atrial fibrillation, caused by elevated blood pressure, inflammation and a general propensity to scarring and change within the heart;

external toxins such as alcohol

regular consumption of too much alcohol has a strong association with the development of AF. A boozy night out, followed by bad sleep and a lot of snoring can trigger enough stimulation of the heart to kick off an episode of atrial fibrillation. Not uncommonly, people will present on Monday morning with a ‘Saturday night arrhythmia’ from just that!

thyroid problems

elevated abnormal levels of thyroid hormone can mimic the autonomic

nervous system and contribute to development of atrial fibrillation;

infections and inflammation

pancreatitis is known to lead to atrial fibrillation, as is severe pneumonia or a severe infection of any sort, as the body responds to extra adrenaline created by the extra nervous activity occurring within it. It appears that anything within the body that increases the sympathetic autonomic nervous system can trigger an episode;

emotional stress
it is not uncommon to see patients who, for various reasons, have had a significant emotional incident which they have, literally, felt in their heart, with their heart jumping and fluttering. That emotional stressor has been the precipitant for atrial fibrillation to occur in that individual;

surgery
any surgery can act as a stressor on the heart; however, very commonly any surgery on the heart itself, in which the atria are actually handled during the process, markedly increases the risk of the development of AF;
 
pulmonary
importantly, after surgery or extended immobilisation, deep vein thrombosis can form in the legs. If these clots break off and flow back to the heart, they can pass through the right side of the heart and straight into the lungs. This is called a Pulmonary (pertaining to the lungs) thromboEmbolism (a blood clot that moves through the bloodstream), PE, and can be life threatening. It can also be a trigger for atrial fibrillation. So, a post-operative patient who develops AF needs PE considered as a matter of priority;

genetic predisposition
there are certain families for whom a genetic link can have a significant up- regulation of the likelihood of someone within that family developing the condition, and interestingly,

endurance training
it is accepted that exercise in general is very good for a person’s health and that normal levels of moderate exercise, several times a week, will lower the risk of heart-related illness and, in fact, lower the risk of atrial fibrillation.

However, endurance athletes who undergo long, protracted training sessions for ultra events have been shown to run a higher risk of developing atrial fibrillation over time.

This is related to endurance activity leading to prolonged, increased cardiac output and subsequent increased size of the cardiac chambers as an adaptation. Neurologically, the heart responds with a tendency towards the parasympathetic nervous system12 which seems to lower the threshold for the development of atrial fibrillation.
So, quite surprisingly, the last group of people impacted by atrial fibrillation are highly (perhaps, over) trained athletes.
 
what can be done about it?

Advancing age will lower a person’s threshold to the development of atrial fibrillation, regardless of any other considerations. As age cannot be avoided, it is something that we can do little about. However, issues such as blood pressure, weight, good sleep, intake of alcohol and emotional stress are all controllable. Being aware of problems that can be associated with atrial fibrillation is a really important first step towards avoidance or management of the condition.

CASE STUDY – KAREN
post-operative

Karen was a 75-year-old woman when I first met her. She was generally fit, well and active. She had had surgery for a colorectal problem. In the post-operative period, she developed AF. I was called and over the phone I recommended some digoxin to slow the heart rate down and also some metoprolol to slow down the heart rate with the potential of reverting the atrial fibrillation back into sinus rhythm.

Before I saw her several hours later, clinically, she had returned to sinus rhythm. On speaking with her, it became clear that she had had episodes of palpitation in the past. I was comfortable in letting her go home on some regular metoprolol, hopefully to keep heroutoftrouble.Ialsoputheronlow-doseaspirinbecauseshehadjusthadsurgery and I didn’t want the risk of bleeding after the surgical procedure. I looked to review her in my rooms several weeks after her surgery and at that stage I also hoped to review her echocardiogram and Holter monitor testing.

The results of the echocardiogram showed that she had a dilated left atrium. This suggested that there was a reasonable chance she would have future recurrences of atrial fibrillation. That supported her reports of having had palpitations before the documented post-operative episode. The Holter monitor, which recorded the electrical activity of her heart over 24 hours, showed multiple episodes of short bursts of atrial ectopy, or extra beats arising from the atria. These can be a trigger for atrial fibrillation and for Karen they were occurring while she was on metoprolol. I was happy to keep her on metoprolol to try to dampen down the likelihood of the occurrence of palpitation.

She reported feeling really well and tolerated the metoprolol without issue. However, I thought there was a reasonable chance that, as time progressed, her AF threshold would reduce and, therefore, her likelihood of recurrence would increase. So, I swapped the aspirin to a NOAC to keep the blood thin. Karen was happy and she was well. We planned to touch base in six months to ensure that everything was travelling smoothly. So, Karen’s post-operative atrial fibrillation was managed in the longer term on a beta- blocker (metoprolol) and anticoagulation, with regular follow-up planned.