Is bringing a patient’s heart back to normal rhythm a treatment priority?

A patient’s symptoms and that patient’s risk of a stroke must be remembered when considering an attempt to keep the patient’s heart in normal rhythm. To date, the vast majority of the research done into returning people to normal rhythm does not demonstrate an outcome benefit. It demonstrates a symptomatic benefit, in that people feel better within themselves in normal rhythm; yet, returning people to normal rhythm surprisingly does not reduce risk of an adverse event in the long-term.

That means that these people are still having strokes. Even if a person has been returned to normal rhythm, there is a very good chance that the person will continue to flip in and out of atrial fibrillation and so still be at risk of a clot forming in the left atrial appendage and therefore still be at risk of stroke. Controlling the rhythm alone is not enough, as it is just not 100 percent effective.

In many situations, even if there appears to be good rhythm control, it might be necessary to look at rhythm control in combination with anticoagulation so that the patient’s symptoms and risk of stroke are covered together. Driven by the symptoms they are experiencing, many patients are quite attached to the idea of getting out of atrial fibrillation, sometimes by a feeling that ‘it’s just not right’ or they simply want it ‘fixed’.

My experience is that in a large number of patients for whom returning the heart to normal rhythm proves a difficulty, over time (probably six to 12 months) they gradually develop a tolerance to the presence of atrial fibrillation within their body. If we have controlled the rate so that the heart doesn’t race too much, the patient eventually becomes used to the heart functioning in that altered way. The symptomatic control, which was quite a major consideration early in the management, becomes less significant over time. It is also important to remember that medications used to maintain sinus rhythm potentially also have side-effects. We don’t want to push those too hard because the side-effects may become more trouble than the condition. As always, it comes down to an assessment of the pros and cons of any therapeutic strategy in relation to the individual patient.

timing

When looking to return a person to normal rhythm, importantly we try to ascertain when the person went into atrial fibrillation.

If a person presents within 48 hours of the onset of atrial fibrillation, the person can be returned to normal rhythm quickly, as long as there is no structural abnormality of the heart or any other coexisting conditions that could lead to any uncertainty around the safety of so doing. If we see a person within 48 hours, we will put that person on some anticoagulant to reduce the risk of the formation of a clot in the heart.

If the patient is seen beyond 48 hours, that person would be put on anticoagulation treatment for three to four weeks before making any attempt to restore normal rhythm. This is to ensure we minimise the risk of a clot being in the heart. The theory says that if we use anticoagulation, the fibrinolytic system (the clot break-down system) has a chance to clear that clot from the system. Remember, if we return normal contraction to the atria and there is a clot in the left atrial appendage, then the contraction may actually dislodge the clot.

Should it be decided to attempt to return a patient to sinus rhythm, there are two methods: pharmacological, using medications, and electrical, using electricity to restart the heart. Both can be used in the acute setting.

within 48 hours, pharmacological

Commonly, people present to accident and emergency for assessment with their first episode of atrial fibrillation. For the patient, there is quite a deal of apprehension associated with it. Medications used in this setting can be given either by mouth or through the vein. The most common agents used are beta-blockers, including metoprolol. Many cardiologists use flecainide, orally or through the vein, when patients have low blood pressure and it is unclear if they would tolerate beta blockade, they may be given amiodarone.

For patients who have previously been assessed and have structurally normal hearts, are not complicated medically and are symptomatic of their AF, then a ‘pill in the pocket’ regime can be employed, especially if they are having very infrequent episodes of atrial fibrillation. They implement the regime as soon as they are aware of the onset of atrial fibrillation.

That regime may include some beta-blockers, heart rate regulators or specific antiarrhythmics. Those patients may also have an anticoagulant tablet to take immediately, to ensure that the blood is thin should the ‘pill in the pocket’ not work. They know that should the rhythm not settle down quickly, they need to present to hospital for review.

within 48 hours, electrical

The other option, when a person presents to an accident and emergency department, is the use of electrical current over the heart to restart the heart or shock it back into normal rhythm. This is Direct Current cardioReversion, DCR. It uses ‘paddles’ and requires a light general anaesthetic. It is very quick and generally very effective.

within 48 hours, my practice

In general terms, if a relatively well patient without structural heart disease or a history of heart problems presents with a new onset of atrial fibrillation, my normal practice is to put that person on anticoagulation immediately, often using one of the new novel oral anticoagulants as they are extremely effective.

I then ensure the patient has some heart rate control to improve the symptoms. I tend to use a reasonable dose of digoxin given intravenously in an attempt to achieve heart rate control as soon as possible.

I also give the patient some beta blockade as, very often, this may help return the patient to normal rhythm. With all that adrenaline pulsing through the patient because of the fear associated with the episode, it will dampen down some of the sympathetic drive.
Lastly, I sometimes use flecainide through the vein as an infusion over 30 minutes so that, if the heart returns to normal rhythm during the infusion, I have the opportunity to turn off the medication.

beyond 48 hours

If the patient has been in atrial fibrillation longer than 24-48 hours, we have crossed a threshold. The chance of a clot, or thrombus, forming in the left atrial appendage is too high to proceed directly to electrical or pharmacological cardioreversion, even with subsequent anticoagulant cover. In this situation we delay restoration of sinus rhythm until after three-to-four weeks of full anticoagulation.

beyond 48 hours, my practice

My preference is to wait a minimum of four weeks to give the body the best chance to clear, or break down, any possible clot that may be lurking in the left atrial appendage. I bring the patient back for review and check the ECG to assess rhythm. Sometimes the patient has reverted on the medications used to control rate. If that has happened, great, although the patient runs the unavoidable situation of the heart returning to normal rhythm while there is possibly a clot in the left atrium.

Should the patient still be in atrial fibrillation at four weeks, if the heart has a relatively normal structure and the patient is still troubled symptomatically, I will generally consider electrical cardioreversion as a planned procedure. This is a common procedure and relatively safe.

Before cardioreversion we look into the left atrial appendage to check there is no visible clot. This is done using a special ultrasound probe that goes down the patient’s gullet so that we can look from very close range, as the oesophagus rests adjacent to the left atrium at the level of the diaphragm. This gives us the chance to actually see into the left atrial appendage which is not possible using a standard echocardiogram which is done through the chest wall.

We call this special ultrasound a Trans (through) Oesophageal (gullet tube) Echocardiogram or TOE15. So, if the person is still in atrial fibrillation after four weeks and restoration of normal rhythm is indicated, we will proceed to a TOE DCR.

Often when I tell patients the next step is to slide a tube down their throat, have a close look at the heart, then, if all is OK, pull the tube out and give them a whack with electricity, they seem concerned. It sounds worse than it really is, although it is not without risk.

I explain they will have a light general anaesthetic for the entire procedure, so there will be no awareness of the TOE probe or the ‘whack’ of the DCR. I also make it really clear that we are doing the procedure because, based on the heart structure, there is a reasonable chance of success. I underline that we are undertaking this procedure to return them to normal rhythm, to make them feel better as the atrial fibrillation is causing unacceptable symptoms.

In explaining the risks involved, I try to ensure that patients understand that the risk of the procedure is outweighed by the benefit. I quote a complication rate of approximately 1-in-5000 of major complication with the TOE, a complication rate of approximately 1-in-10,000 for the DCR and a rate of 1-in-10-to-15,000 for the general anaesthetic. Although these risks are small, they are real. And it is not an exercise to be undertaken repeatedly without significant consideration of the pros and cons.

The need for repeated TOE DCR may be the start of the conversation about progressing to an electrophysiological ablation of the atrial fibrillation, or perhaps accepting permanent atrial fibrillation.

CASE STUDY – JEFF
dilated right atrium

When I met him, Jeff was 46 years old. He had just completed a 1/2 marathon, a 1/2 marathon running uphill and in good time! After the event he developed atrial fibrillation and ended up in the accident and emergency department with an irregular pulse.

When I saw him in A&E, the ECG was normal. We anticoagulated him, slowing his heart down with digoxin, immediately. Because his heart was structurally sound, based on his exercise capacity, I also gave him flecainide to try to revert the heart:
150 mg intravenously, as an infusion over 30 minutes. That didn’t revert him. Twelve hours later, I repeated the flecainide but this time gave
him only 100 mg. This worked. He returned to sinus rhythm and he felt considerably better. We sent him home soon afterwards. He had anticoagulant tapering for the next couple of days and we followed him up in clinic.

The follow-up was interesting because when we looked at his Holter monitor he was getting extra beats from the top of his heart. We call these atrial extras (extras, extra beats) or supraventricular (supra, above; ventricular, main pumping chamber) atrial ectopic beats or atrial ectopics (ectopic, out of place). We also did an ultrasound of his heart to look at its structure and function. Interestingly, the right atrium appeared to be dilated; the left appeared normal. I had been expecting to see a normal-looking heart and I wasn’t really sure what to make of this subtle and unexpected finding.

Jeff was in and out of hospital several times during the next year or so, with episodes of atrial fibrillation that were months apart and which responded reasonably well to therapy in the accident and emergency department.

Initially, we tried him on beta-blocker. He didn’t tolerate that particularly well and I was comfortable switching him over to calcium channel blocker which can sometimes be slightly more effective in the setting of atrial ectopic beats.

I was, however, intrigued by the increase in the size of the right atrium. This was unusual and I wondered if it could be contributing to his low atrial fibrillation threshold. I ordered imaging of the connections of his heart, using cardiac CT imaging, so we could see how the great vessels interrelated with each other. As suspected, this showed an abnormality. It showed that two of the right upper lobe pulmonary veins drained directly into the right atrium. This meant that blood which should have been draining into the left atrium, then ventricle and then around the body, was draining instead into the wrong side of the heart, so that the right atrium was receiving blood, not only from the body but also from the lungs. This increase in blood flow caused an increase in volume and that increase in volume had stretched the right atrium. This was the cause of the anatomical observation of his right atrium being dilated. I believe this was a contributory factor in his development of atrial fibrillation in an otherwise structurally normal heart, in an otherwise well patient, without any other clear-cut risks.

Currently, Jeff is on a good dose of the calcium channel blocker, verapamil. I also have him on a blood pressure-lowering agent, the angiotensin- converting-enzyme (ACE) inhibitor, perindopril, as this may help with the remodelling of the chambers of the heart.

I am pleased to say that Jeff is well and stable. He carries with him a ‘pill in the pocket’ regime so that if he does develop atrial fibrillation, he is able to take extra verapamil and can start an anticoagulant to immediately reduce the risk of stroke. Of course, he is instructed to present as soon as possible after an event so that it might be dealt with appropriately.

He is having perhaps one, maybe two, episodes of atrial fibrillation a year. Although we have spoken about the possibility of using electrophysiological ablation to try to reduce the risk of recurrence, the frequency is not sufficient to justify that procedure at this stage.
Jeff is going well. I think he has an interesting, likely contributing factor in his development of atrial fibrillation. We catch up on a regular basis for on-going re-evaluation of the management plan that is now in place.

IMPORTANT POINTS    
SINUS RHYTHM

•    Returning a patient to sinus rhythm has symptomatic benefits; surprisingly it does not reduce the risk of an adverse event in the long term.
•    Sinus rhythm is restored by drugs or electrcity.
•    Treatment needs to look at rhythm control as well as anticoagulation and is dependent on
-    the timing of presentation in relation to the episode
-    the structure of the patient’s heart
-    the general medical condition of the patient.
•    Over time, patients become used to living with AF.