Last week I saw a 76-year-old woman called “Marjorie” for Type 2 diabetes.
Marjorie would describe herself as relatively healthy.
She has had controlled Type 2 diabetes for the last five years and was referred to me for management of her diabetes and obesity. In short, Marjorie wanted my help to lose weight.
During a routine consultation and physical exam I took her blood pressure.
Her pulse was irregular.
An electrocardiogram performed in my office confirmed that Marjorie had atrial fibrillation.
Marjorie is without symptoms: she feels no palpitations, has no chest pain or shortness of breath.
She is among the 350,000 Canadians with atrial fibrillation — the most common heart rhythm disorder.
What is atrial fibrillation?
It occurs, as the name implies, when the atria — the top chambers of the heart — “fibrillate”.
Heart muscle is a pretty amazing tissue.
These cells have the ability to generate electrical impulses all on their own.
The reason our hearts beat in an orderly fashion and don’t just lie there and “jiggle” uncontrollably is due to a highly evolved electrical conduction system and the heart’s own intrinsic pacemaker.
The pacemaker of the heart lies in the right atrium and is called the sinoatrial node (SA node).
At a rate of anywhere between 50-100 beats per minute, it sends out an electrical signal to trigger the atria to contract.
The SA node is part of an elaborate conduction system that involves the atrio-ventricual node, bundle of His and the right and left bundle branches.
All work together like an electrical network to keep the heart beating in a rhythmic and organized fashion.
But for a variety of reasons, this system breaks down and rhythm disturbances happen.
Atrial fibrillation is one such rhythm disturbance.
It typically occurs when the atria are stretched either suddenly or over time for whatever reason, causing an electrical disturbance in the atria.
As a result electrical changes occur in the atria of the heart and it fibrillates.
The heart still pumps blood as usual but the beat of the heart is no longer a rhythmic fashion.
The atria fibrillate and the ventricles pump variably and sometimes too quickly.
Why is it a concern?
There are two things we worry about most in atrial fibrillation; heart rate control and stroke risk.
Atrial fibrillation can cause the heart to beat too quickly. If a patient’s heart rate is too high the heart does not pump properly and it does not fill properly and the heart can indeed fail as a result.
Furthermore, if the atria are fibrillating, blood can pool in the top chambers of the heart and form a blood clot. This of course poses an increased risk of a stroke.
People with atrial fibrillation have a 3-5 fold increase risk of stroke than those without atrial fibrillation. Certain factors can influence a person’s stroke risk.
In fact there are risk-scoring systems known as the CHADS-2 score and CHADS-VASC to help predict a person’s risk of stroke in atrial fibrillation
How do you treat atrial fibrillation?
For decades we’ve used warfarin or aspirin (depending on the patient’s risk score) to help reduce the risk of stroke in atrial fibrillation.
Warfarin is effective. Sure, it is rat poisoning, but as I always tell my patients… They are people and not mice.
And yes, there is a great deal of evidence to show that anticoagulation in the right patient with warfarin dramatically reduces the risk of stroke in atrial fibrillation.
But warfarin has its problems.
Warfarin works to inhibit Vitamin K production in the body.
Certain blood clotting factors are indeed dependent on Vitamin K to function. By inhibiting Vitamin K warfarin works to thin the blood, by rendering certain Vitamin K-dependent factors of blood clotting ineffective.
Blood can’t clot as well and so it thins.
If blood is thinner, it is less likely to form a clot in the atria of a person with atrial fibrillation.
Without a blood clot in your atria, you are at a lower risk of stroke.
Because warfarin is a Vitamin K antagonist, the drug has an individualized dose in every patient.
Not everyone can take the same dose of warfarin for the desired effect.
Blood tests need to be done regularly to ensure that a person’s blood is thin enough and the dose often needs to be adjusted especially if a person changes their medications or even their diet.
A diet rich in Vitamin K (eating green leafy vegetables) for example will alter the effects of warfarin and the dose will need to be adjusted.
Are there alternatives to warfarin?
In October 2010, a new medication was approved for the treatment of atrial fibrillation.
The drug, dabigatran, was in a class of drugs called direct thrombin inhibitors.
This class of medicines works independently of Vitamin K, it does not require constant monitoring, has very little drug-drug interactions and has no interactions with food.
Green leafy vegetables have no effect on their potency.
The safety and efficacy of these agents has been well studied.
Since 2010 two other agents have been approved for the treatment of atrial fibrillation.
Both belong to the class of drugs known as Factor Xa (10a) inhibitors and are Apixaban and Rivoroxaban. Both work independently of Vitamin K, do not require monitoring or dose adjustments.
All three medications have impressive safety data compared to warfarin.
Indeed, a meta-analysis of all agents showed a reduced risk for stroke when compared to warfarin, a reduced risk of intracranial bleeds and major bleeding with the direct thrombin inhibitors and factor Xa inhibitors.
The newer agents did show an increase risk of gastrointestinal bleeds compared to warfarin.
According to a report in the Lancet, “42,411 participants received a new oral anticoagulant and 29,272 participants received warfarin. New oral anticoagulants significantly reduced stroke or systemic embolic events by 19% compared with warfarin, mainly driven by a reduction in hemorrhagic stroke. New oral anticoagulants also significantly reduced all-cause mortality (relative reduction of 10%) and intracranial hemorrhage (relative reduction of 52%), but increased gastrointestinal bleeding (relative increase of 25%).”
The evidence on the safety and efficacy of these agents is strong and reassuring.
These drugs do provide an added benefit to stroke reduction in atrial fibrillation.
So much so that the American Heart Association, the European Heart Association and the Canadian Cardiovascular Society have all included them in their recommendations for the treatment of non-valvular atrial fibrillation for stroke prevention.
Make no mistake, no drug is without risk.
These are powerful blood thinners and of course the risk involved in their use is bleeding.
But a good clinician must weight the risk of any treatment over the benefit and present the facts to a patient.
As for me?
I should state my biased up front: I’m an early adopter.
Early adopters in medicine are those physicians who, once a therapy is approved for use, are early to try said therapy in an appropriate patient population.
As an early adopter I make sure I review the science and safety data. I study the available trials and evidence in order to ensure that my prescribing practices will be appropriate, effective and safe.
Early adopters have an advantage of having early experience with the use of new medications and therapies because they use them early and have firsthand experience.
Early adopters don’t have the advantage of waiting to see where a new therapy will fit into the medical landscape after a few years in everyday practice.
As an early adopter, I am able to have first hand experience with new therapies in my practice. I believe my patients benefit from this.
The more experience I have with a therapy, the more first hand knowledge I have.
When these drugs were first approved for use over three-and-a-half years ago I used them. I reviewed the science and felt they were appropriate for many of my patients with atrial fibrillation.
Furthermore, they had been approved for use by Health Canada. I was not throwing caution into the wind or experimenting with people’s lives. But, I was an early adopter.
Some of my colleagues are late adopters.
They wait to see what their colleague’s experiences are with agents before using a drug.
They are comfortable with using “tried and true” therapies that they have used forever. I’m not faulting them: there is something to be said for this method of practice.
I would argue that the “new” anticoagulants indeed make some physicians uncomfortable.
If a patient bleeds on these blood thinners, there is no way to reverse them other than giving the patient plasma.
If a patient bleeds on warfarin, we also give them plasma to thicken their blood, but we can administer Vitamin K to fully reverse the blood thinning process.
This can take a day or two.
With the direct thrombin inhibitors, we wait the 12-24 hours for the drug to work its way through the system.
It is now more than three years later and the face of anticoagulation in atrial fibrillation is changing.
I would argue that because these drugs are easier to use, more patients who should be on blood thinners for atrial fibrillation are indeed on them.
Controversy still exists about the use of anticoagulants in emergency settings and what to do if a patient indeed has a bleed on these agents.
In general, blood thinners make many people — patients and physicians — uncomfortable.
And they should: There’s a risk involved in being on a blood thinner.
But as with everything, that risk should be weighed against the benefit of treatment.
Like any good physician, I sat with Marjorie and explained all of this to her.
We weighed the risks and the benefits and I gave her some information to take home and to read.
She thanked me for picking up the diagnosis and for explaining everything to her
And, she went on a “new” blood thinner.
For more information on atrial fibrillation: http://www.stopafib.org
Dr. Ali Zentner is the medical consultant for Global National’s “Health Matters” segment.
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