Joe, patient, Hobart

When diagnosed, I was unaware that I had atrial fibrillation. I had been aware of ‘something’ but thought it was due to tension and pressure of work.
After being referred by my GP, we discovered that I was close to having a heart attack. This was something of a surprise as when I was younger, I had been fit, ate a healthy diet and there was no family history of heart problems.

After discovering the presence of atrial fibrillation, I soon began recognising the signs of an episode. Mostly, it occurred in the early hours of the morning when I was asleep. It would wake me up. I would feel uncomfortable, with a tightness in my neck, my chest pounding and sometimes with an ache in my arm. My brain felt as if it were scrambled; it was hard to think logically. When such an episode occurred, I would ensure I was warm and sit in a chair next to the phone until it passed. It was quite scary and at times I thought it might be the end.

I have had an ablation which worked for a time.

I also tried different medications and concentrations. Now the condition has settled down (except when I forget to take my medication). Even so, I often wonder when it will come back.

In the meantime, I am so thankful that with patience and trying different approaches. I am currently in a good position.

According to the European Society of Cardiology guidelines for the management of atrial fibrillation (2016), there have been major advancements in treatment and management strategies for atrial fibrillation in the past 20 years. As you have already read, oral anticoagulants and, in particular, more recently NOACs, have markedly reduced the incidence of stroke and mortality in atrial fibrillation patients. Other improvements, such as in rate control and rhythm control, have improved related symptoms. However, although they may have improved symptoms and cardiac function, reduction in long-term morbidity or mortality has not improved to the same extent.

The guidelines say that in contemporary, well-controlled and randomised clinical trials, the annual average stroke rate is about 1.5 percent and the annualised death rate is about three percent in anticoagulated atrial fibrillation patients. A minority of these deaths is related to stroke, while sudden cardiac death and death from progressive heart failure are more frequent.

Furthermore, atrial fibrillation is also associated with high rates of hospitalisation, commonly for management, but is often also linked to heart failure, myocardial infarction and treatment-associated complications.

Current figures for Australia, in terms of both prevalence and cost, are not available. Among the most recent publicly available are figures from a June 2010 report by Price Waterhouse Cooper25. This estimated that the annual costs to the Australian economy resulting from atrial fibrillation in 2008-09 were at least $1.25 billion per annum through medical costs, costs of long term care for those with a disability and lost productive output. By way of comparison, the cost per person with atrial fibrillation was more than double the estimated per person cost in relation to obesity and higher than the per person cost of cardiovascular disease or osteoarthritis.

Relying on international evidence to derive prevalence estimates for Australia, the report estimated that, in 2008-09, 240,000 people or 1.1 percent of the population suffered from atrial fibrillation, with more than half the sufferers aged over 75 years. It estimated that an extra 6300 people suffered a stroke for the first time as a result of atrial fibrillation and that there were 45,600 hospital separations for atrial fibrillation, more than for stroke or heart failure.

A 2011 Deloitte Access Economics report, Off beat: atrial fibrillation and the cost of preventable strokes, uses an atrial fibrillation prevalence rate of seven percent for people in Australia aged 50 years or older.

It estimated that nearly 62,000 strokes would occur in Australia in 2011, including 45,873 first-ever strokes. Nearly one-third (14,364 of the 45,873 strokes) would occur in people with atrial fibrillation and three-quarters (10,709 strokes) could be specifically attributed to patients’ atrial fibrillation rather than other clinical factors.

 This is a serious condition with significant human and economic cost.

Although the figures quoted here might not be as recent as one would like, consensus in Australia and around the world says that both atrial fibrillation prevalence and cost are on a significantly rising trajectory.

If there is one thing that by now must be patently obvious, it is this. Atrial fibrillation comes in many guises and one treatment or management plan does not fit all. There is a compelling responsibility for individualising care that addresses not only patient treatment but the day-to-day management implications of living with atrial fibrillation.

CASE STUDY – LISA
pregnancy

Lisa was an otherwise well, slim and normotensive26 39-year-old mother of an 18-month daughter when she came to see me. Lisa and her husband were looking to have a second child as soon as possible as she was aware her biological time clock was ticking along. The problem was that Lisa had recently developed intermittent runs of atrial fibrillation which were escalating. There were some stresses at home and there were some stresses at work, and I’m not convinced these weren’t contributing. However, there was no family history of atrial fibrillation, nor was there a history of alcohol.

At the time of reviewing Lisa, she was severely affected by the recurrence of atrial fibrillation almost every other day. It was interrupting her sleep; it was interrupting activities of daily living and was causing her a deal of panic and distress. An echocardiogram showed that she had normal heart structure and function. That, with a normal thyroid blood test, meant there was no clear-cut indicator as to why she had developed atrial fibrillation. Yet, she had.

I commenced her on a beta-blocker, metoprolol, and she responded well. However, for a woman who wanted to become pregnant, nurture a child through that pregnancy and then breastfeed the new baby, being on a beta-blocker, or any agent for that matter, was not desirable. I thought Lisa presented a situation in which it was paramount to try to control the atrial fibrillation as best as possible without medication, for the sake of a healthy pregnancy and the safe delivery of a child.

So,  I  discussed  the  situation  with an electrophysiological colleague. I considered Lisa was a good candidate for electrophysiological ablation for her atrial fibrillation at the earliest opportunity. If successful, this could control the atrial fibrillation without therapy and allow a pregnancy, delivery and the early life of her new child to proceed without Lisa being on any drugs. My colleague agreed and was very helpful. We started medication for thinning the blood and we booked Lisa in for the procedure as soon as was feasible.

She had that done in six weeks. All went well. When I saw Lisa several weeks later, we stopped medications to see how she would react. I followed her up again in eight weeks with a clinical assessment. Up-to-date Holter monitoring showed no abnormality. The EP ablation had controlled her rhythm, she was feeling much better and looking forward to extending her family.

questions for daily living

For people who have atrial fibrillation, day-to-day living is often based
around questions relating to very common issues, such as:

What effect does caffeine have in relation to AF?

Caffeine is a stimulant. It is also my preferred drug of addiction during the day. It commonly pops up in news articles as either ‘good’ or ‘bad’ for you. Probably, on balance, several cups a day will keep the world turning and is not a bad thing for your health. Over stimulation of the autonomic nervous system, however, can precipitate an event of atrial fibrillation.

I have patients who are clearly sensitive to caffeine and report the same. They cut back or avoid caffeine to help control their condition. Other patients don’t seem as sensitive and continue to enjoy a cup or two a day without issues. It is case-by-case and individuals need to see how they respond. It is certainly a conversation to be had with your doctor.

Energy drinks with high levels of caffeine are probably best avoided.

Can I exercise safely?

Atrial fibrillation, of itself, is not a reason not to exercise. It is worth, however, noting a few things.

Firstly, when patients ask if they can exercise, they are really asking if they are going to have a heart attack, a lay term for a blocked artery.
Atrial fibrillation and blocked arteries are two different processes affecting the electrical system and the fuel lines, respectively. Although they are not linked directly, they can occur in the same individual. Both are common and the risk of each increases with the age of the person. Speak with your doctor.

Secondly, if you are in atrial fibrillation, is the heart rate well controlled? If it isn’t, then exercising will only make the heart rate even higher and make exercise difficult.

Although, in general terms, we like to see our patients exercising, your best course of action is to check with your doctor to ensure that he or she is happy with your rate-controlling medications and the possibility of you exercising.
 
What if I need to have surgery?

In the past, if a patient on warfarin for atrial fibrillation needed to undergo a planned or an elective surgical procedure, then there was much fuss about managing the warfarin dosage around the time of surgery. Invariably, we would stop the warfarin about five days prior to the procedure and then put the patient on a ‘bridging anticoagulation’ regime that used injections of the blood thinner heparin, morning and night, until the day of the surgery.

This complexity is no longer necessary.

Recent research indicates, that in simple surgeries and where the AF is uncomplicated, it is safe to stop the warfarin before and restart it after the procedure. This is also the case with the newer NOAC agents. Missing these drugs for three full days prior to the procedure and for a few days after will suffice.

If the situation is more complicated, like a metallic valve replacement, a previous stent or by-pass grafting, cardiac failure, a complicated surgery, previous stroke or very large left atrium, then a plan needs to be put in place. Involve your cardiologist and ensure the plan is based on your risk of stroke and the risk of bleeding associated with your surgery. I like to see my patients who are in this situation so that I can ensure that nothing is missed and so that I can document that the patient has a good understanding of the risks and benefits. It can also be a timely catch-up and review.

Can I stop the medications if I feel well?

Taking tablets when feeling well is a real frustration for many patients.

However, remember, that in the context of atrial fibrillation, the medications will be keeping you in normal rhythm or controlling your heart rate, or reducing your risk of stroke. So, if you are feeling well, the medications are probably doing their job.

My strong recommendation is that if you have been put on medication, it is for a specific and good reason. Before unilaterally altering your management plan, it is best to speak with your treating doctor.

CASE STUDY – KEVIN
flexibility and juggling to suit the patient’s need

Kevin is a 79-year-old man (2018) whom I met for the first time about eight years ago when he had an episode of atrial fibrillation. He had had AF previously and I met him in the setting of an intermittent episode.

When I saw him the ultrasound of his heart was pretty normal, which was reassuring, although I did note that he was relatively anxious about the development of atrial fibrillation. It would also be fair to say, and Kevin wouldn’t mind me mentioning it, that he was fairly sensitive to medication and he was very particular in his demeanour, at the more highly-strung end of the spectrum.

I increased his therapy. He was taking 80 mg of sotalol morning and night and I increased that to 120 mg of sotalol morning and night. I started him on warfarin to lower the risk of stroke and I sent him home.

Kevin was fairly stable for the next couple of years. I saw him again in 2014 when, every few months, he was developing short-lived paroxysmal (intermittent) atrial fibrillation. It seemed to coincide with times of stress or tension and it occurred predominantly at night. As he was relatively stable and protected by the anticoagulation, there was little else to do, although I did increase the sotalol to 160 mg morning and night.

In 2016, he was due for major surgery which carried with it a significant risk of bleeding. It was important at the time of the surgery that Kevin did not have any blood thinners in his system. The healing process which was to take several months also needed to be warfarin-free. So, when Kevin came to consult with me beforehand, my feeling was that we should add in another antiarrhythmic agent. I wanted to minimise, as best as possible, his episodes of atrial fibrillation while he was unable to take an anticoagulant. He was already on sotalol 160 mg morning and night. I elected to add in a small dose of flecainide, 50 mg morning and night, and stop the warfarin, as was required for the surgery.

My normal habit is not to combine sotalol, a class III antiarrhythmic agent, with flecainide, a class I antiarrhythmic agent, because of potential proarrhythmic effect, or causing rhythm problems rather than preventing them. However, I was keeping the flecainide level low and there was a very particular reason for doing it, the surgery. I also monitored him very closely with serial ECGs. One of the indicators that can give us a clue about toxicity developing through the use of flecainide is if the QRS complex on the ECG widens. A change in the Q-T interval can suggest sotalol toxicity. Both indicate that there is a change in the way the membrane of the cell depolarises. It is really important that we track these parameters.

Well, I’m pleased to say that when Kevin had the surgery, he didn’t have a miss-beat. He was able to manage on both medications for two to three months without any atrial fibrillation of which he was aware. He was so pleased with the outcome he asked to remain on flecainide with the understanding that the combination of proarrhythmic agents could carry some risk. I was happy to oblige as long as he was happy for me to monitor him very closely.

Again, we checked his echocardiogram which demonstrated he had normal left ventricular function, normal heart structure and previous cardiac scanning had ascertained that he had no coronary artery disease. As his heart was structurally normal, the risks of a proarrhythmic problem were less than for someone who had abnormal function of the heart. We also knew that he had normal renal function, so it was unlikely that there would be an accumulation of antiarrhythmic agents.

Also, instead of reintroducing warfarin, I began him on one of the novel oral anticoagulants, rivaroxaban. This is working very well. He has been stable and happy with ‘his AF’ since.

One of the other aspects we need to look at closely in atrial fibrillation is blood pressure. As I continued to care for Kevin, it became apparent that his blood pressure was elevated and needed better control. Introducing new therapies was not that easy as he continued to be very sensitive to many medications. Calcium channel blockers, a common first-time blood pressure treatment, gave him headaches, while even a low dosage gave him swollen ankles.

After six to nine months of changing and altering his medications, we eventually came up with a very low dosage of the calcium channel blocker, amlodipine, on a daily basis, 2.5 mg per day. We used an agent called telmisartan at half the lowest dose tablet to be taken only on Saturdays, Sundays, Tuesdays and Thursdays. We also added in a medication called spironolactone, one tablet taken on Mondays, Wednesdays and Fridays. Eventually we had his blood pressure perfect. Unfortunately, it lasted only a couple of months when he came back to see me describing the side- effect of tenderness within the breast. This is a recognised side-effect of spironolactone. We swapped it with an agent that was very similar but less likely to have that side-effect in a male, the drug, eplerenone. Again, it was taken on Mondays, Wednesdays and Fridays. His blood pressure at the time of writing was perfect.

With this combination, Kevin was happy in terms of side-effects, while being well controlled in terms of his atrial fibrillation, blood pressure and his risk of stroke.

Why have I told you about Kevin? Sometimes we need to be flexible and patient as we seek to find what works for the individual, and that can take some juggling. As Kevin was cooperative in terms of trying to find what worked for him, we could work through the process in a systematic way. He remains well and very happy with his current care.