As we routinely look to anticoagulate patients to reduce the risk of clot formation in the heart and a subsequent stroke, this makes anticoagulation a really important component of our management. Yet ...

what if we are dealing with a patient
who is elderly, frail and liable to fall?

This is a complicated issue which I have covered to some degree with the HAS-BLED score, the score which assists with attempting to determine the risk of bleeding. However, in general terms, the clinician, with the patient, in an open and frank discussion, will need to try to ascertain the patient’s ability to deal with anticoagulation, including the patient’s risk of falling, hitting his/her head and bleeding. We need to be very specific, engaging the patient in a discussion about how the patient believes he/she will cope with those risks on a daily basis. In general, the doctor will wish to see the patient on blood thinning because, as I say to my own patients, “It is easier to deal with a bleed than a stroke” (the exception of course being a bleed in the brain, but this is less likely).

I’ve had elderly patients who remain active and are not frail. I had one patient who regularly went into the bush where he used a chainsaw. He had been a logger all his life and that was not going to change. So, we took this into account when deciding on his care: the man being 80+ years of age, in the bush with a chainsaw and other sharp pieces of equipment, and a long, long way from help. He still went on anticoagulation, but not before a detailed discussion which led him to understand the pros and cons of his situation.
 
So, a case of the elderly and/or the frail, who are likely to fall, may well be when the clinician and the patient need to discuss what would work best, perhaps reducing doses, perhaps using alternate agents and certainly weighing the risk-benefit.

who has need of a stent in a narrowed artery?

Narrowed arteries and atrial fibrillation can be common bed fellows.

The incidence of both can increase with age, and some of the risk factors, such as hypertension, are also common. So, it is no surprise that sometimes a patient with atrial fibrillation also has a narrowed artery that needs to be opened.

One way is to open the artery by using a stent. A stent is a fine metal scaffold that is inserted into a narrowing in an artery and then is expanded to keep the artery open.

It is a great technology when used in the right situation and it is a terrific technique to enable the blood to flow more freely again. There is a catch, though, and the catch is that the metal of the stent is seen as a foreign material by the platelets.

When platelets encounter foreign material, they interpret that as a cut in a blood vessel and go to work forming a clot to heal it. Problem! We don’t want a clot in an artery as the clot will block it. Bad news!

In regular situations, the way to overcome the clotting is to give the patient drugs that prevent the platelets from clumping. Such drugs are called antiplatelet agents. Aspirin is the most well-known.

However, and importantly, in the setting of stenting, two antiplatelet agents or Dual AntiPlatelet Therapy (DAPT) are needed to prevent clot formation.

Most often patients will remain on DAPT for a minimum of three months to a maximum of 12 months. During this time, as DAPT is preventing clot formation, the inner layer of the blood vessel grows over the metal struts of the stent, thus preventing the platelets from interacting with the metal.

This process starts immediately. By one month the process will have produced reasonable coverage, by three months, a pretty good coverage and by 12 months the stent, generally, will be completely covered.

What if the patient has atrial fibrillation and is already on an anticoagulant? Does the patient then take a blood thinner and two antiplatelet agents?

Think about the high risk of a bleeding complication that scenario may carry: medication to block the coagulation cascade and two medications blocking platelet function.

This situation needs to be dealt with using caution and care.

Remember, antiplatelet agents are not effective for the clot forming in the left atrial appendage, while anticoagulants are not effective for clots forming on stents. So, a patient in AF with a new stent needs DAPT and anticoagulation to protect the stent and reduce the risk of AF-clot formation.

Generally, the objective is to minimise any risk of a clot forming in the stent, while offsetting that against the risk of the patient having a problematic bleed.

As the highest risk of stent thrombosis is in the first 30 days, patients will be on two antiplatelet agents as well their regular anticoagulant.

Depending on the complexity of the stent and other patient-specific issues, this triple therapy will be stopped after the first 30 days or continued for about three months when one antiplatelet will be stopped. One antiplatelet and the anticoagulant will be used until month 12.
At 12 months, generally, the antiplatelet agent will be stopped and the anticoagulant continued long-term.

Guidelines related to these decisions are available and your cardiologist will be the most up to date with current practice should you be in this situation.
 
who has cardiac failure?

Cardiac failure brings to light another group of patients in whom AF has been shown to worsen prognosis.

If possible, we like to see patients in cardiac failure brought back to normal sinus rhythm as they have better outcomes. This is the case whether it is cardiac failure due to a poor functioning ventricle or cardiac failure in which the ventricle appears to contract ‘normally’.
A relatively recent trial called CASTLE-AF21 showed certain patients definitely did better if they could be maintained in sinus rhythm. Of course, in AF they also run a much higher risk of stroke.

So, if the patient is also affected with cardiac failure, the clinician will try to keep the patient in sinus rhythm, understanding that if there is any chance of the person being in atrial fibrillation, the person really does need to be anticoagulated to reduce the very high risk of stroke complications.

who has severe renal failure?

Renal failure is one of the situations where atrial fibrillation can be more prevalent. As patients with renal failure have a greater risk of bleeding, we need to be very careful.

Chronic end stage renal failure patients in atrial fibrillation are most likely to be managed with warfarin. This needs regular monitoring and levels can fluctuate depending on external variants.

We know also that NOACs generally need at least some renal function to be cleared from the body. If they accumulate, complications may arise. The NOACs are not ideal, then, for the patient with advanced renal failure. There are clear guidelines available to help doctors know the cut off points for renal function that are acceptable for prescription of the NOACs.

However, in cases where mild or moderate renal failure is present, there is very good data to support the use of NOACs as an alternative to warfarin, as long as the renal function is sufficient to allow adequate clearance of those drugs from the patient’s system, and so remain safe.

who has other complications?
CASE STUDY – BETTY
complication: AV malformations

I have a patient, Betty, who developed atrial fibrillation in her late 70s. That’s not uncommon but the difficulty in Betty’s situation was that I had been monitoring her for the previous 10 years, or maybe more, for a leaky mitral valve which had required surgical repair. As a mitral valve leaks, blood regurgitates into the left atrium leading to left atrial stretch. This had happened over the years before her surgery. Until the development of her atrial fibrillation, it had not been a significant problem. We were tracking the functioning of the valve and she had been on a low dose of aspirin in relation to her valve repair, blood pressure and some known coronary irregularities.

The other concern with Betty, however, was that she had a very difficult condition to sort out: bleeding from her small bowel. It is called an ArterioVenous malformation or an AV malformation. This is a vessel abnormality which can bleed, unpredictably, spontaneously and significantly. Betty had had these AV malformations over a number of years.

So, here is a patient
•    on low-dose aspirin for mitral valve repair, hypertension on treatment and minor coronary artery irregularities on treatment;
•    with a history of mitral regurgitation which is going to drive atrial fibrillation because of left atrial stretch, and
•    who also has a condition that leads to unpredictable bleeding. Tricky!

With her development of atrial fibrillation, we took a considerable time trying to use medications to keep her in sinus rhythm. This worked initially.
 
However, her atrial fibrillation progressed, albeit intermittently, to a point where we needed to look at reducing her risk of stroke.
I elected to use a NOAC and specifically one known to have a reversal agent, or antidote, readily available. This means that if she presents at the local hospital with a significant bleed from her AV malformation, there is a reversal agent available that could stop that bleeding almost immediately.

Betty carries the risk of a stroke but there is also a real risk of her bleeding from her gut. Both are catastrophic. I’m running her on a low dose of NOAC and, to-date, all is going well for her.

Tom is in his mid-to-late 70s. He had atrial fibrillation and he was appropriately managed on warfarin in the pre-NOAC era.

Unfortunately, the INR, or coagulation, caused by the warfarin increased and Tom had a cerebral bleed; his blood was thin enough that it bled into his brain. This caused a substantial stroke. He remained in atrial fibrillation but, for a time, the doctors caring for him did not want to give him an anticoagulant again because of the history of bleeding into his brain.

When I saw him several years after the haemorrhagic stroke, I said that his ongoing risk was probably greater from the formation of a clot within his heart and subsequent stroke than another haemorrhagic stroke. This risk could be reduced if we used one of the newer NOACs which would have a better anticoagulant control and without the fluctuations that can be associated with warfarin. So, Tom started on a dose of one of the NOACs.

Several years later, thankfully, there have been no troubles. We have reduced the risk of a thromboembolic stroke, or a clot from the heart going to the brain, and there have been no further haemorrhagic strokes or ‘bleeds’.
 
complication: pre-excitation syndrome

Another difficult situation I would like to discuss is a condition called a pre-excitation syndrome.

In a normal heartbeat the electrical signals from the atria pass through the AV node into the ventricles. In a few patients, there is a connection directly between the top of the heart and the bottom of the heart which is a muscular band or bridge. This is in addition to the AV node. Now, as we know, the importance of the AV node is that it slows down electrical activity from the top of the heart to the bottom of the heart; it acts as a capacitor.

In a normal heart, when the patient goes into atrial fibrillation not all the chaotic electrical activity is transmitted to the lower part of the heart because the AV node slows down some of the chaos; it protects the ventricles. In the setting of this extra pathway, there is no slowing down the electrical activity; there is no filter; there is no capacitor.

In a patient with this direct connection between the atrium and the ventricle, a setting called pre- excitation, the chaotic electrical activity of atrial fibrillation is transmitted directly down that muscular band to the ventricle. This could lead to a very fast heartbeat or, at worst, ventricular fibrillation which means death.

A pre-excitation syndrome is also called Wolf-Parkinson-White Syndrome named after the people who first described it.

A pre-excitation pathway is a very difficult thing to deal with in the setting of acute atrial fibrillation.

In the short term, one wants to stabilise the atria as best as possible.

Most drugs used in AF management slow down the AV node, the normal conduction pathway. Those drugs are contraindicated if a patient has atrial fibrillation and a pre-excitation syndrome because the normal pathway is slowed down but the abnormal pathway is preferentially advantaged. So, drugs such as digoxin, metoprolol and calcium channel blockers often cannot be used in that setting.

If an agent is selected, it is a bridging strategy. In that situation, an agent such as amiodarone might be appropriate.

My experience is that the safest treatment, however, is to immediately use electrical current to revert the patient. More often than not, the person’s condition is quite unstable.

The longer-term objective is to have this patient considered for destruction of the abnormal pathway using electrophysiological ablation techniques, a process of tissue injury similar to that used in an EP ablation of AF. That patient may also be considered for an atrial fibrillation ablation at the same time. While the individual is having the abnormal pre-excitation connection ablated, it is a great opportunity to isolate the pulmonary veins to reduce future occurance of atrial fibrillation.

CASE STUDY – BOB
complications: lifestyle challenges, hypertropic cardiomyopathy

We met in 2003. Bob was 42 years old and weighed 140 kg. He suffered from obstructive sleep apnoea and was intermittently using a Continuous Positive Airways Pressure (CPAP) machine which forces air into the lungs during sleep to keep the oxygen levels up. His blood pressure was 160 to 170 over 90 (elevated).

He came to see me because of an abnormal ECG which we evaluated with stress testing. We found no problems with the way his heart worked but certainly there were changes on the ECG that were not within the normal range.

At the time, I talked to him about the value of trying to reduce his weight. Over the following year he dropped approximately 25 kg in weight and felt better for it.

A visit in 2004 was the last time I saw him until 2012.

By 2012, he had developed atrial fibrillation. Given that blood pressure, obstructive sleep apnoea and weight are all significant contributors to the condition, it was no surprise. Initially, the atrial fibrillation was relatively well-controlled on medication and he was having episodes intermittently. He still had the same changes on his ECG, which we describe as deep T wave inversion. Basically, it was a change in the way the heart re-polarised and it didn’t look normal. I was concerned about that.

Between 2003 and 2012, available technology had changed, so I ordered a cardiac CT scan which allowed us to have a really thorough look at the arteries of the heart. The advantage of a CT scan is that it also gives us very clear imaging of the chambers of the heart which we can then slice in 90° planes or orthogonal views. This just means we can get great views of the heart and can literally pick it up and move it around as we want, using our sophisticated work stations with their high-end graphics.

By doing this I was able to clearly demonstrate a couple of really important findings. Firstly, that Bob had a considerable build-up of plaque in his arteries. Secondly, I also made the diagnosis of a condition called hypertrophic cardiomyopathy (hyper, increased; trophic, growth; cardio, pertaining to the heart; myopathy, a muscle condition or an increase growth of heart muscle problem). Hypertrophic cardiomyopathy is a thickening of the wall of the main pumping chamber of the heart, a thickening of the wall of the left ventricle. As it has a strong genetic link, it is important to screen in families.
 
This is not a good thing for the heart.

A thickened muscle may not relax as well as normal muscle and so this condition can lead to increased pressures within the left ventricle. Those pressures are transmitted back into the left atrium with the consequence of stretching or dilating that atrium in the longer term. Remember, a big left atrium is a marker of future atrial fibrillation.

Hypertrophic cardiomyopathy is a significant contributor to the possible development of atrial fibrillation.

So, on top of weight, blood pressure and sleep apnoea, Bob had hypertrophic cardiomyopathy, a stiff heart, contributing to the likelihood of the development of atrial fibrillation.

In 2012, Bob again engaged in weight loss because he had regained most of the weight he had shed previously. He was able to lose about 20 kg.

In 2013, he was in and out of AF and was quite symptomatic with it. Part of the reason was the hypertrophic cardiomyopathy. The benefit of a properly contracting left atrium is that the left ventricle fills better, allowing the heart to work more efficiently. Once you take regular, left atrial contractions away, the heart needs to rely on passive filling or, simply, the flow back to the heart. With thickening of the muscle, the stretch of the left ventricle may not be as good as normal and pressures can build up so that the patient becomes quite symptomatic.

In 2013, there were a number of episodes when we cardioreverted Bob because of his symptoms. Although he successfully embraced weight loss, he was still a big man at well over 100 kg. With that being the case, and wanting to maintain sinus rhythm, principally because of his symptoms, I sent him for electrophysiological assessment and consideration of radiofrequency ablation of atrial fibrillation.

Initially he had good results from this but when the atrial fibrillation came back, we added extra therapies. One of these recommended by the electrophysiologist was the medication, amiodarone. One of the issues with amiodarone is the amount of iodine it contains. That high content of iodine means that it can interact with the thyroid gland. It will affect about 25 percent of patients.
 
After using it for several months, it did start to affect Bob’s thyroid gland. Although amiodarone had been working well in controlling his atrial fibrillation, we had to stop it because of the impact it had on his thyroid function.

Some six months after his first EP ablation, towards the end of 2013, he was still having recurrent atrial fibrillation. The electrophysiologist suggested a repeat EP ablation. This second ablation was more successful than the first. Bob was able to remain symptomatically well-controlled in sinus rhythm for most of the next two years.

In the second half of 2015, however, he re-presented; back to his morbid weight, his blood pressure was still elevated, and he was using the CPAP machine for his obstructive sleep apnoea. His left atrium had dilated gradually over the years, due in large degree to the hypertension but also to the hypertrophic cardiomyopathy. He was also symptomatic again. Although we spoke again about the possibility of repeat electrophysiology ablation, I thought two attempts in the face of his other medical issues were as much as we could offer. As Bob was keen to explore further, he visited the electrophysiologist again, only to receive similar information as I had given him. The electrophysiologist reassured Bob that not much ground would be gained by trying again to retain sinus rhythm for him in the long-term.

We are now several years past 2015. As I have observed in many other people, over the course of a year or so the symptomatic effect of atrial fibrillation, as long as it is well controlled in terms of the heart rate, is often accommodated by the individual. Although it takes a while, the patient generally becomes used to it.

Now, Bob’s heart rate is under control. He is anticoagulated. He is on good blood pressure control. He is on a cholesterol-lowering agent because the CT scan demonstrated significant plaque. We are trying to engage him in lifestyle modification, continuing with weight loss and exercise as much as possible. Symptomatically, he is as good as we can hope for and he even enjoys a round of golf once or twice a week. We’ve also taken the opportunity to screen his family for the condition that led to the thickening of his left ventricle, the hypertrophic cardiomyopathy.

Bob’s is a complicated case and one that represents some of the many challenges associated with atrial fibrillation.

IMPORTANT POINT COMPLICATIONS

•    There can be significant individual complications to take into consideration when managing atrial fibrillation. Each patient needs to be treated in relation to his/her particular circumstances. Rarely is AF treatment ‘off the rack’.