what is atrial fibrillation?

Atrial fibrillation is a disturbance within the electrical system of the heart which gives rise to a heart rhythm disorder or arrhythmia. This means that the person has an irregular, or abnormal, heartbeat. The term we use to describe it is ‘irregularly irregular’. Sudden, rapid, irregular and chaotic heartbeats may be a sign of this common heart rhythm problem. The impact of the condition on the patient ranges from inconvenience to black out, to chest pain and heart failure, with stroke another potential, devastating complication. While atrial fibrillation can be managed, at this time1 there is no cure.

the heart

The heart is the large muscle that pumps blood through our bodies. The blood supplies nutrients and oxygen, and also removes waste such as carbon dioxide. The heart can be likened to a car engine with compression chambers and valves, an electrical system and a set of fuel lines. It is the electrical system which will concern us primarily in the following pages.

As a car engine has an electrical system for timing, so does the heart. The electrical system in the heart ensures synchronicity and coordinated contraction throughout the heart. It also allows a mechanism for acceleration and deceleration.

The car has pistons and valves as part of its power-generating engine block while the heart has as its pistons the compression chambers, the main one being the ventricle, and valves which stop the blood flowing back from where it came.

To complete our analogy, the car engine also requires a fuel line to supply the engine block. In the human heart, the fuel lines are the coronary arteries that literally provide the life-blood to the engine block, the muscle of the heart.

This muscle, called the myocardium (myo, muscle; cardium, being of the heart), is a four-chambered structure. There are two chambers on the right- hand side and two chambers on the left-hand side. This means you have two pumps, one that accepts the blood back from the body and then pumps it to the lungs, and then a second pump that receives the blood from the lungs and then drives it around the body, the ‘right heart’ and the ‘left heart’, respectively. On each side of the heart there is a pre-pumping chamber, the atrium, and a main pumping chamber, the ventricle.

pistons and valves

Blood drains from the body through the veins, collecting into two major veins called the superior vena cava (SVC) and the inferior vena cava (IVC) which drain into the right side of the heart. This oxygen-poor, dark purple, carbon dioxide-rich blood arrives in the right atrium and is given a gentle pump through a one-way valve, the tricuspid valve, into the ventricle which then pumps the blood through another one-way valve, the pulmonary valve, into the pulmonary circulation which takes the blood to the lungs. There, by simple diffusion2, it is purified and oxygenated; carbon dioxide is released and leaves the body through the breath we exhale, while oxygen, from the air we breathe in, is absorbed.

Bright red, oxygen-rich arterial blood then flows through the four pulmonary veins to the left atrium. The left atrium gives a gentle pump and the blood passes through the mitral valve, another one-way valve, into the left ventricle which then contracts, squeezing blood through the aortic valve into the main artery of the body, the aorta, to begin its journey around the body. The contraction of the left ventricle makes the blood flow through the arteries and we feel this as our pulse.

fuel lines

The coronary arteries arise from the aorta as it comes from the left ventricle. They are the first branches in the circulation system. These are the fuel lines of the heart engine.

Cardiovascular disease involves heart and blood vessel diseases, and includes stroke. In a population of 25 million people, it affects one in six, or 3.7 million people, and kills one person every 12 minutes. Cardiovascular disease is often the main cause of hospitalisations in Western countries, in a given year. Although this book is about the electrical system, it is not uncommon for the fuel system and the electrical system to show features of wear and tear simultaneously.

A CLOSER LOOK
ARTERIES

It is useful to think of the arteries as the fuel lines supplying the cylinders of the car, transporting blood to different territories (pistons) of the heart muscle. This system consists of the right coronary artery and the left main coronary artery. Within one centimetre, the left coronary artery divides into two main arteries: the left anterior descending artery which provides blood to the anterior surface of the heart, that is the surface nearest the chest wall, and the circumflex artery which supplies blood to the back of the heart or the surface of the heart nearest the spine. The right coronary artery supplies the inferior surface of the heart or the surface that is nearest the diaphragm.
 
The terms ‘right dominant’ or ‘left dominant’ can be used in reference to the origin of the artery that supplies blood to the bulk of the inferior surface of the heart. This is generally from the right coronary artery but sometimes the right coronary artery is smaller, and the circumflex is ‘dominant’, or bigger, supplying the majority of the inferior surface of the heart. This is called ‘left dominant’. This becomes important in terms of the amount of the heart that may be affected by a blockage of the artery, the dominant artery providing blood to a larger territory.

The left anterior descending artery supplies blood to the anterior wall of the heart (nearest the chest wall). Most often, the left anterior descending artery is the largest and most important of the three main coronary arteries. It can be 12 to 14 cm long, while only two to five millimetres in diameter. This is little thicker than a pen refill, yet its blockage can be disastrous. A dominant right coronary artery can be approximately the same size and a non-dominant circumflex can be six to eight centimetres long and 1.5 to three millimetres in diameter.

The major arteries are comprised of fewer than 35 cm in total length and fewer than five millimetres in diameter at their largest.

This is a very vulnerable system.

electrical system coordinates powerful pump

A healthy heart is a highly efficient pump coordinated by its electrical system. The atria and ventricles work together, alternately contracting and relaxing, to pump blood through the heart and into the body. The heartbeat is triggered by electrical impulses. The heart pumps three to four litres of blood every minute, with the healthy heart rate between 50 and 100 beats per minute.

Normally, the contractions of the atria are set off by the heart’s natural pacemaker, a small area of the heart called the sinoatrial (SA) node, located in the top of the right atrium. This is where the electrical activity ‘beats the drum’ to which the rest of the heart ‘marches’.

Electrical impulses travel rapidly throughout the atria, a bit like a Mexican wave, causing the muscle fibres to contract, squeezing blood into the ventricles. To get to the ventricles, these electrical impulses pass through the atrioventricular (AV) node, a cluster of cells in the centre of the heart, between the atria and the ventricles. This node acts as a gatekeeper. Passing through this node slows the electrical impulses before they enter the ventricles, thus giving the atria time to contract before the ventricles then contract. Once in the ventricles, the electrical impulse is carried via special cells, Purkinje fibres, that act like wires delivering the signal to the apex of the heart, ensuring that blood is expelled from the furthest point first.

This normal heart rhythm is known as sinus rhythm because it is controlled by the sinoatrial, or sinus, node. In a healthy heart, this beating occurs in a synchronistic and smooth manner. Visualise, if you can, a squid moving through the water. Synchronous. Coordinated. Smooth.

break-down

When this synchronicity breaks down, arrhythmia occurs.

One of the most common forms of heart arrhythmia is atrial fibrillation4 which, according to the European Society of Cardiology (ESC), is one of the major causes of stroke, heart failure, sudden death and cardiovascular disease in the world. The ESC also predicts that its prevalence will rise steeply in coming years.

Atrial fibrillation results in chaotic, or irregular, electrical activity leading to the atria not contracting properly. Instead they shake, vibrate, tremor; they fibrillate. Between 20 and 30 percent of all strokes are due to atrial fibrillation6. Long-term atrial fibrillation can damage the structure of the heart and sometimes existing heart problems can trigger atrial fibrillation; hence the association with cardiac morbidity and mortality.

classifications

There are two types of atrial fibrillation: the type that the patient feels, called overt or symptomatic atrial fibrillation, and the type of which the patient is not aware, called silent or asymptomatic atrial fibrillation.

Atrial fibrillation classification is also referred to in terms of the time the patient is in the abnormal rhythm: paroxysmal, persistent or permanent atrial fibrillation.

symptoms

In overt, or symptomatic, atrial fibrillation, the person is aware when the condition occurs and/or is present. Sufferers will feel palpitations in the chest, an irregularity, a fluttering which they can describe quite clearly. Some will have shortness of breath on exertion, for example while climbing the stairs or carrying the groceries. Others will notice a decrease in their exercise capacity. Because atrial fibrillation can occur very suddenly, and because the heart is not pumping normally, it can also be associated with low blood pressure and patients may present with a collapse.

In silent, or asymptomatic, atrial fibrillation, the person does not feel it at all. It is discovered as an incidental finding. This can occur when the person goes to the general practitioner for a check, say, a blood pressure check, and the doctor notices that the person’s pulse is irregular, instead of being strong and regular as a normal sinus rhythm beat should be. The irregularity in the pulse could be atrial fibrillation. Three percent of the population over 75 years of age will have AF and not be aware of having the condition.
 
Occasionally, the possibility of atrial fibrillation being present is indicated by something else.

An unfortunate and common modern situation is in the setting of a stroke. This is when a blood clot has gone from the heart to the brain. This neurological problem can result in localised weakness, difficulty with speech, difficulty with vision and even lead to death. A stroke that lasts momentarily is called a Transient (doesn’t last very long) Ischaemic (lack of blood flow) Attack or TIA. A stroke and TIAs are triggers in which to look for AF as a potential cause.

Large numbers of people today have heart-related devices implanted, pacemakers, in particular. The interrogation of these devices can be as often as every six months or as long as every 12 months. Either way, when these devices are checked, the heart rhythm can be evaluated. So, it is possible to find that people being seen for pacemaker issues may have atrial fibrillation detected incidentally during a check to ensure the device is working properly.

Important to know!

The incidental finding of atrial fibrillation can occur when an ECG (electrocardiogram) is taken.

An example in the hospital where my consulting rooms are located is the pre-operative ECG which is very commonly undertaken for patients over a certain age undergoing procedures with a certain complexity.

It is a really good way to pick up asymptomatic AF, a valuable opportunity to make the diagnosis and initiate appropriate therapy.

A CLOSER LOOK
STROKE

We know stroke is a devastating occurrence. In the simplest terms, stroke is an interruption of the blood flow to the brain, an organ which needs a good supply of blood at all times. If there is any change in that flow, the tissue of the brain can be damaged. Damage to the tissue of the brain from a change in, or interruption to, the blood flow is a stroke.

There are two main ways a stroke can occur, resulting in an haemorrhagic stroke or an ischaemic stroke.

If a blood vessel supplying an area, or territory, in the brain bursts or ruptures, it bleeds into that territory causing damage. This is an haemorrhagic stroke in which too much blood goes into that area of the brain because the artery has been damaged.

It can be associated with abnormalities of the blood vessels in which there is a thinning and a rupture at that location. It can be related to points of strain within the arteries of the brain when high blood pressure over time causes weakness within the arteries and that can also, with age, lead to situations when blood may rupture from the blood vessel into the tissue of the brain.

Haemorrhagic strokes account for about 15 percent of strokes.

An ischaemic stroke occurs when a clot, also called a thrombus, blocks the artery, leading to a lack of blood flow.

An ischaemic stroke arises when a clot dislodges from a location within the body and travels to the brain, lodging itself in an artery and thus blocking the artery.

Ischaemic strokes account for the other 85 percent of strokes.

In relation to an ischaemic stroke, there are two main locations where the clot may form. The most common location is within the large blood vessels in the neck, the carotid arteries. A build-up of plaque in these arteries can lead to rupture of that plaque. A clot forms, breaks off, moves to the brain, lodges in one of the blood vessels and stops the blood supply, causing a stroke. Strokes originating in the carotid arteries account for about 50 to 55 percent of ischaemic strokes.

The other major clot source is the heart as a consequence of atrial fibrillation.

When the left atrium is not contracting properly, blood  can  pool  within a recess in the left atrium, the left atrial appendage. If blood pools in the appendage, a clot can form and subsequently dislodge.

Such a clot will float into the left atrium, sweep through the mitral valve into the left ventricle. The ventricle will expel blood, including the clot, into the aorta. It will then come to the arch of the aorta where there is an opportunity for that clot to travel to the brain via either of the carotid arteries, and subsequently become lodged in a blood vessel within the brain, leading to an ischaemic stroke.

If the clot passes the brain arteries, it will continue to travel with the blood flow until it finds a place to rest which could be any organ or tissue beyond the brain: the gut, kidneys, liver, spleen or even a toe.

IMPORTANT POINTS    
A STROKE

A stroke can be
•    haemorrhagic, bleeding into the brain tissue (about 15 percent)
•    ischaemic, from reduced blood flow (about 85 percent)
-    from problems within the carotid arteries (50-55 percent)
-    from the atrium (left atrial appendage) as a consequence of atrial fibrillation (about 30 percent)

CASE STUDY – PETER
an incidental finding

Peter was a 65-year-old man when his atrial fibrillation was found incidentally. A week or so before I met him, late in 2017 , Peter was undergoing a routine colonoscopy, a test to look in his lower bowel. The anaesthetist who was looking after him found his pulse to be ‘irregularly irregular’ with a controlled rate. An ECG and subsequent monitoring confirmed that Peter was in atrial fibrillation, although he had had no clue as to his situation as he had experienced no symptoms. This is not entirely uncommon. A number of people do walk around with silent or asymptomatic fibrillation.

When I spoke with Peter, it turned out that he had seen his GP about three months earlier. His blood pressure and pulse, which were checked at the time, were said to be okay. This suggests that he had gone into fibrillation in that intervening period. Peter’s general health also included some hypertension for which he was on therapy and central adiposity or weight around the belly. This can be a marker of prediabetes and is worth keeping in mind. He did not exercise much.

When we looked at Peter’s risk of a stroke on the CHA₂DS₂-VASc score (a clinical predictor for estimating the risk of stroke in patients with atrial fibrillation) he had a score of two: one for age and one for hypertension. I would have added an extra score for prediabetes. However, with a score of two, his risk of stroke was considered mild to moderate with the recommendation that he should be on full anticoagulation.

We also had other information available. A 24-hour heart rate monitor showed that in the asymptomatic state, on average, Peter’s heartbeat in atrial fibrillation was nearly 100 beats a minute, going as high as 180 beats a minute at times of exertion. For someone in his mid-60s, that’s a very fast heartbeat and I was quite surprised that he was asymptomatic.
 
An ultrasound of his heart showed that the structure and function of Peter’s heart were relatively normal, although his atria were mildly to moderately dilated.

As a result of the CHA₂DS₂-VASc score, I started Peter on full anticoagulation. I also included in the therapy a drug to try to slow the heartbeat down. A heart that’s revving so quickly simply does not fill properly and therefore doesn’t pump properly, and so patients almost invariably describe some shortness of breath. This should give him more puff as the heart pumps better.

Another consideration for Peter was whether or not we should attempt to restore sinus rhythm. On occasions, we can be caught between trying to restore normal rhythm and leaving people in atrial fibrillation. The lack of symptoms, as in the case of Peter, can suggest an approach that simply controls the heart rate.

However, in this particular situation, the patient is relatively young. My observation over the years, and there is some research coming through to support this, is that if we restore sinus rhythm we may have a positive effect on any morphological, or structural, change the heart could undergo. What I mean by that is, if we leave people in atrial fibrillation for many years, we see changes in the heart as a consequence of that atrial fibrillation. The most notable alteration is that the atria dilate or enlarge. Another observation, and I have a number of cases in which this has occurred, is the atrioventricular ring that connects the atrium to the ventricle also dilates as the atria dilate. If the AV ring dilates, then the fixtures for the valves that it holds, particularly for the tricuspid valve which is on the right side of the heart, can be stretched. As it stretches, the cusps of that tricuspid valve do not come together as well as they should. So, although I haven’t yet8 attempted to restore sinus rhythm in Peter, it’s a serious consideration so that the structure of his heart can be maintained in its best condition for as long as possible.

Regardless of whether I return him to sinus rhythm or not, Peter will be on anticoagulation for the remainder of his life. The CHA₂DS₂-VASc score is high enough, and with his being completely unaware of symptoms, I wouldn’t begin to rely on him to tell me when he’s in and out of the rhythm.

time in rhythm

If atrial fibrillation is experienced for a short time, between 24 and 48 hours but no longer than a week, it is called paroxysmal atrial fibrillation, meaning that it comes and goes. This classification is characterised by a short period when the patient has the abnormal rhythm and then the heart reverts back to sinus rhythm.

If the abnormal rhythm is present in the patient for longer than seven days, it is called persistent (staying there longer) AF.

Permanent (long-standing) atrial fibrillation means it has been present for longer than a year.

What if the patient is asymptomatic?

Deciding whether the atrial fibrillation is paroxysmal, persistent or permanent is almost impossible to ascertain, if this is the case. How do you know when it started? Simply, you don’t!

Some clues can be found from other investigations. The simplest hint is the longer a person has been in atrial fibrillation, the greater the likelihood there will be changes in the atria of the heart. Dilation of the atria will be more pronounced the longer the heart has been out of rhythm.

While one of the management strategies is to attempt to return a patient to sinus rhythm, this is not the case for all sufferers of persistent or permanent atrial fibrillation. The clinician will need to decide if the patient’s condition is to be accepted long-term, based on factors relevant and specific to that patient. If the decision is to leave the person in atrial fibrillation, then controlling the rate of the heartbeat and management of the risk of clot formation within the heart become the foci.

effective management

Atrial fibrillation is associated with a poorer quality of life for sufferers as symptoms include lethargy, palpitations, breathlessness, chest tightness, sleeping difficulties and psychosocial distress.

AF cannot be cured.

In managing atrial fibrillation, medical carers look to the efficiency of the heart as a pump, its rate and its rhythm, and stroke mitigation as the significant concerns. The condition, regardless of its type and time in arrhythmia, can be managed with medication, lifestyle adjustments and, sometimes, through procedural interventions.

IMPORTANT POINTS    
AN OVERVIEW

Atrial fibrillation
•    is characterised by the loss of coordinated atrial activity so that the person’s heartbeat becomes ‘irregularly irregular’
•    leads to the decreased efficiency of the heart as a pump
•    is associated with a significant increased risk of stroke
•    can be either overt (with symptoms) or silent (no symptoms)
•    can be paradoxical (lasting hours), persistent (lasting days or longer) or permanent (ongoing)
•    currently has no cure, but it can be managed

ANSWERING AN IMPORTANT QUESTION
ARE ALL CLOTS THE SAME?

Clotting is a normal function that is required in the body for our existence. Otherwise, if we were to cut ourselves we would bleed to death. There are times, though, when clots can cause problems and threaten our existence.

A clot which forms in an artery of the heart, blocking the artery, can cause a heart attack. Bad.

If a clot forms in the left atrial appendage of the heart, it can break free and travel to the brain through the arteries which supply blood and oxygen. A block in an artery to the brain causes a stroke. Bad again.

If the clot forms in a carotid artery and moves to the brain, it can also cause a stroke. Still bad.

There are, however, other places in the body where clots can form. Most well-known are the legs. A Deep Vein Thrombosis (DVT) can form there due to immobility for a variety of reasons such as a long aeroplane flight or after surgery. If the clot breaks off, it travels back to the heart passing through the right heart and into the lungs causing a very serious medical problem, pulmonary (pertaining to the lungs) thromboembolism (blood clot that moves through the bloodstream). You guessed it. Very bad.

Problems from blood clotting are treated according to where the clot originated in the body. In particular, clots formed within the coronary arteries (heart attack) and the carotid arteries (ischaemic stroke) are treated with agents to reduce the stickiness of platelets in the blood. Aspirin and other antiplatelet agents are used. These agents seem to work best in the arterial circulation which is a high velocity and high- pressure setting.

Where blood pools in slow-flow areas, such as in the legs (during periods of immobility) and in the left atrial appendage (during periods of atrial fibrillation), the antiplatelet agents are far less effective and so anticoagulants are used for treatment. Heparin, low molecular weight heparin, warfarin and the Non-vitamin K Oral AntiCoagulants (NOACs, also an acronym for Novel Oral AntiCoagulant) reduce the risk of, or treat, clots that form in these slow-flow and low-pressure settings.

The 2017 COMPASS Study9 asked the question: Can we have an each-way bet, putting patients on some aspirin and some anticoagulant, in particular the NOAC rivaroxaban? In a group of high risk patients, the study demonstrated that having a bet each way was a successful approach, working particularly well within the group of people on which it was tested who had bad arteries in their legs.

IMPORTANT POINTS    
CLOTS

•    Clots are needed to stop us from bleeding. Good.
•    They can form when we don’t want them to do so. Bad.
•    They can develop in different locations in the body and are treated differently depending on where they form. Tricky.