gathering information

Once atrial fibrillation is confirmed on the electrical trace, there is much more information to be gathered. What is going on within the patient’s life and within the patient’s heart that we can tie to atrial fibrillation?

It is easy to see if the patient is over-weight. We also want to assess the individual for diabetes, alcohol intake, sleep, blood pressure, thyroid function, stress and then we want to know about the structure of the heart, the function of the valves and the pressures within the heart and the lungs.

Importantly, we need to know the size of the atria. The bigger the atria, the greater the risk that the condition will recur. If the atria are normal size and the structure is normal, there is a good chance that the patient’s heart can be returned to normal rhythm.

An echocardiogram (echo, sound; cardio, heart; gram, picture) or ultrasound of the heart will not only give a good appreciation of the size of the atria, but also the size of the ventricles and how well they are working. If there are conditions such as cardiac failure, features of longstanding hypertension or anything that could be wrong with the muscle, these are important factors to add to management strategy decisions for the individual.

The echo will also look at the valves in the heart. The aortic valve, the mitral valve, the pulmonary valve and the tricuspid valve are all important to our understanding of the patient’s atrial fibrillation.

Particularly significant is the mitral valve, the valve between the left atrium and the left ventricle. If this valve is affected, for example narrowed or leaking excessively, then back pressure is directed immediately into the left atrium. This is significant when making management strategy decisions.

If the mitral valve is narrowed, thus slowing flow through the atrium, this is referred to as ‘valvular’ atrial fibrillation and is associated with a greater risk of a clot forming in the left atrial appendage. It is also a factor in treatment selection, which will be discussed later.

The ultrasound also looks at pressures within the heart. Are pressures elevated or are they normal? We look at pressures within the lungs too, also measured using ultrasound, as this gives an idea of the health of the remainder of the vascular system, including pulmonary vascular function.

In addition to confirming the diagnosis electrically and seeing the structure of, and function within, the heart, blood tests are also important at this stage. A thyroid function blood test is done routinely as it is known that increased thyroid hormone levels can be associated with initiating atrial fibrillation. Blood tests also allow us to determine if other problems are present. These could be sepsis, or inflammation, or illnesses such as anaemia which are known to be associations of atrial fibrillation.

considerations

Once atrial fibrillation has been diagnosed and the relevant associated information for the patient has been gathered, there are three areas of focus for AF management: heart rate, risk of stroke and if the patient should be returned to normal rhythm.

heart rate

Because of the chaotic beat within the atria, the heart is racing, often as fast as 150 and sometimes over 200 bpm, irregularly. This is very distressing to the person. At this rate, the heart doesn’t work or fill properly so the speed needs to be slowed.

risk of stroke

Risk of stroke is of concern because, when the atria are not contracting properly, blood can pool, particularly in the left atrial appendage. Where it pools, a clot can form. Should this happen, the clot can find its way to the brain, leading to a catastrophic outcome, a stroke. To lower this risk, the blood needs to be ‘thinned’. As part of the management strategy, especially around anticoagulant therapy, we utilise the CHA₂DS₂-VASc score, a clinical predictor for estimating the risk of stroke in patients with AF. Then, to determine the risk of complications from bleeding, another score, HAS-BLED, is used. (For further information, please refer to pages 80 and 81.)

returning the heart to sinus rhythm

A number of factors come into play in the decision of whether or not an attempt should be made to bring the person’s heart back to normal, or sinus, rhythm.

understanding risk-benefit

Before elaborating on various treatments that are available, it is important to understand the concept of risk-and-benefit in relation to therapy. There is no medication available that has zero risk, so it is essential that patients be clear about what any risk might be. However, risk needs to be put into the context of the benefit, and benefit generally needs to be considered in the light of two different components: the symptomatic benefit (improving the way the patient feels) and the prognostic benefit (improving the long-term outcome).
 
In the case of symptomatic intervention for atrial fibrillation, if the patient’s heart rate can be reduced, it will improve that patient’s symptoms. So, the risk of the heart rate medication is weighed against the improved symptoms and better quality of life for the individual.

As the therapy is implemented, checks are done to ensure there really is a benefit. If we have improved the symptoms without unacceptable drug side-effects, then the benefit outweighs the risk for that individual and it’s a reasonable intervention.

An example of a prognostic intervention for atrial fibrillation would be to give the person an anticoagulant to reduce the risk of stroke. This carries the risk of increased bleeding. It is also likely that thinning the blood doesn’t make patients feel any better; they may even feel worse if they have problems with the medication.

So, ironically, patients may go for years thinking the prognostic medication has not done anything. Yet, the fact they have managed for so long probably means that the medication has worked very well and has been beneficial to them. “But I don’t feel any different” is exactly the long-term goal for which we are aiming.

So, the risk-benefit has to be weighed against associated conditions such as cardiac failure, hypertension, increasing age, diabetes. Has the patient previously had a stroke? These factors point to the patient being at very high risk. Therefore he or she should derive a good deal of benefit from anticoagulation medication.

However, if the person is prone to tripping, has a history of self-harm with medications or is poor at taking medication, then the risk of using a blood thinning medication, perhaps, is unacceptable.

The bottom line is, is the risk of bleeding outweighed by the reduction in the risk of stroke for this person?

CASE STUDY – FRANCESCA
long-term tweaking

Francesca is a patient I have looked after for more than a decade. She was in her mid-to-late 60s when I first met her.

Francesca had had an episode of atrial fibrillation, somewhat unexpectedly. Her heart appeared structurally normal and she developed her symptoms without any clear-cut precipitant. In the early stages, she started aspirin and tried the beta-blocker, metoprolol. This didn’t do the job and metroprolol was changed to sotalol which works through a slightly different mechanism.

A follow-up at that time included investigation

through the use of a Holter monitor. This showed that she was getting a number of extra beats within the atrium, beats called atrial ectopic beats or atrial ectopics. I find these atrial ectopics can sometimes respond well to calcium channel blockers and so I elected to swap Francesca to a relatively low dose of verapamil. It worked reasonably well. That was 2009.

After several months, she came back with a brief recurrence of palpitation. I added in a small dose of flecainide to her therapy regime. This seemed to do the job for Francesca and I didn’t see her for more than two years. In that time her heart was structurally normal; she was not having atrial fibrillation; she had no other significant risk factors and was being appropriately managed with aspirin, verapamil and flecainide.

She came back in 2011. The recurrence of atrial fibrillation was no surprise as we expect AF to return, eventually. While we don’t have a magic bullet to fix it, we do aim to control it.

In 2011 I gave her some instructions for a ‘pill in a pocket’ approach to deal with the recurrence of her AF and really, that worked pretty well over the next two to three years with only a couple of episodes occurring each year. During that time, she would take some extra flecainide, just to dampen down those episodes which were over within an hour or two. It would be fair to say that Francesca could worry herself into an episode of atrial fibrillation and more often than not, these episodes were associated with stressful events or situations in her life.

In 2013, she came back again. The latest episodes had been short-lived, occurring very infrequently with no more than one episode every few months. I increased the verapamil dosage slightly and we waited to see how things would progress. In the course of the next year, we increased the dosage of both the verapamil and the flecainide, just a little.

The way I describe that, the up-titration or increasing the dose, is a little bit like adding salt to a casserole. You don’t want to pour a whole tub of salt in because you can spoil the dish. You really want to add in just what’s required, no more, no less. And so, bringing patients back and adding in just a little allows us to creep up the dose so that we are meeting the needs of the patient by reducing the recurrence of the arrhythmia, but we are not giving the patient more than is needed.

In 2017, which was the next time Francesca came back, she was having only intermittent, short-lived episodes. However, she was by then nearly 10 years older and I was concerned about the recurrence of atrial fibrillation in someone who would have been at increased risk from atrial fibrillation- induced stroke.

We had the conversation about anticoagulation. Francesca started on one of the new NOAC agents available, rivaroxaban.

While she still has short-lived episodes infrequently, she is really comfortable on her current therapy using verapamil and flecainide and she is tolerating the NOAC without any problems. A Holter monitor follow-up showed she was having less than 0.5 percent of her day in atrial fibrillation. So, the anticoagulant was making her safe and the antiarrhythmics were keeping her symptom-free for the vast majority of the time.

In very recent times she has described a little shortness of breath. A follow- up echocardiogram showed that her pulmonary pressures had snuck up a little bit. This meant her body may have been retaining a little bit too much fluid in the circulation. This was not surprising. As people get older their heart can become stiffer. This stiff heart sends messages to the kidneys that something is ‘just not right’ and this tends to lead to fluid retention. This fluid can build up in the lungs and manifest as shortness of breath. So, we introduced some diuretic therapy13 just to take the fluid off on an as-needed basis. Voila, symptomatic success!

Francesca is now travelling really well. It has been 10 years of atrial fibrillation for her and over that time there have been some changed medications; we’ve up-titrated medications; we’ve given her a ‘pill in the pocket’; we’ve moved from aspirin as a preventative for risk of stroke to an anticoagulant and we are monitoring the flecainide with regular ECGs.

Francesca, who has been a great patient to work with over these years, is happy. She is appropriately covered from a prognostic perspective; she is symptomatically well, and her atrial fibrillation is well-controlled with the risks reduced by the anticoagulant.