Arrhythmias and Rhythm Management
- Cardiac Arrhythmias
- Catheter ablation therapy
- Atrial flutter
- Supraventicular tachycardias
- Atrial fibrillation
- Unusual cardiac arrhythmias
- Heart failure
- Cardiac Resynchronisation Therapy (CRT) pacemakers
- Implantable defibrillators (ICD)
- Useful links
Cardiac arrhythmias are abnormal heart rhythms that can be develop throughout life. Rhythm disturbances can occur from childhood to old age causing a range of symptoms that include palpitation (an awareness of abnormal or irregular heartbeats), breathlessness, lethargy, dizziness and blackouts, or feelings of chest discomfort and anxiety. The heart rhythm can be abnormal either because it may be beating too slowly, too rapidly or becomes irregular.
Arrhythmias are in the top 10 causes for hospital attendances. There are 700,000 people in the UK that suffer from these symptoms. Some arrhythmias such as ectopic beats are benign but others such as ventricular arrhythmias arising from the lower ventricular pumping chamber can be life threatening.
Intensive research over the last 2 decades has significantly improved our knowledge and understanding of the basic mechanisms of how arrhythmias occur and new treatments developed to cure these conditions.
The UK government has recently published guidelines for the treatment of cardiac arrhythmias in chapter 8 of the National Service Framework, a document setting out best practise and minimum standards in the treatment of arrhythmias in the UK. In this official document it is advised that patients with arrhythmias should be referred to a cardiac rhythm specialist to receive the most appropriate advice and treatment.
The basic function of the heart is to pump blood around the body for all the essential of the vital organs to keep us alive. In fact, we can only survive for a few minutes if the heart stopped pumping before irreversible damage and subsequent death would occur. The heart consists basically of 4 chambers, 2 upper atrial collection chambers which collects blood coming back to the heart, each is connected to a lower “high pressure” pumping chamber that are able to generate the forward driving pressure to pump blood around the body. The entire mechanical pump is driven by an electrical system. The sinus node is the area of the heart that initiates electrical signals (pacemaker) to start a heartbeat. Activation results in contraction of the upper atrial chamber passing this onto the lower ventricular pumps. The pacemaker signals then continues onto a relay station (AV node), which is connected to the lower pump by specialised bundles of electrical wiring (His Purkinje system).
There are a total of 4 one way valves in the heart that open and close in sequence during periods of filling and active pumping that keep blood flowing in one direction (Figure 1). Normally the His Bundle leading from the AV node, is the only connection between the top atrial chamber and the lower ventricle. Normally the whole process repeats itself always starting from the pacemaker area progressing from a top to bottom direction (Figure 2). Abnormities occur when the normal sequence is disrupted leading to cardiac arrhythmias.
Catheter ablation therapy
Focal areas of abnormal electrical activity or strands of abnormal wiring within the heart, key in causing or maintaining rapid arrhythmias can be eradicated or “ablated” by a percutaneous keyhole procedure. Catheter based ablation therapy can now be offered to permanently cure these arrhythmias. Long flexible wires or “catheters” can be introduced from a peripheral blood vessel into the heart and navigated to critical areas responsible for causing cardiac rhythm disorders. Delivery of a focal energy source from the tip of the catheter, either high frequency radiowaves causing heating of tissue or freezing cryo ablation can be delivered at the tip of these catheters (Figure 3), causing small discrete (4-5mm) irreversible areas of tissue destruction to render these abnormal areas of electrical activity non functional. The rest of the heart function is unaffected and the lesions created are usually permanent. A curative cathter ablation approach is preferred by many patients who have recurrent symptoms not controlled by drugs or who do not wish to take drugs long term which may have side effects (Figure 4).
This is the infamous arrhythmia that affected the Prime Minister Tony Blair. It is a very common cardiac rhythm disorder affecting an estimated 900 individuals per million of the population. Atrial flutter is 3 times more common in patients with structural heart disease (enlarged/impaired cardiac function, leaky valves, heart muscle disorders and chronic lung disease). It is associated with a very rapid but regular revolving electrical circuit (300 cycles per minute!) predominantly located in the right atrial chamber of the heart. Atrial flutter results in rapid heart rates, breathlessness, reduced exercise capacity and this condition has a small stroke risk.
In the last decade we have developed a full understanding of this arrhythmia, and now we can offer patients catheter ablation treatment as a definitive cure for this arrhythmia. Atrial flutter is a loop like circuit revolving around the right atrium (Figure 5), spreading out and passing through a narrow channel called the isthmus (Figure 6). By passing a catheter from a vein in the groin under local anaesthesia, this circuit can be successfully cut internally by a moving catheter and rendered these circuits non-functional, providing a “cure” in 95% of cases, with minimal of risk (<1% risk). In fact these cases usually take under an hour to perform and can be done as day cases without the need for an overnight stay. If patients only only have flutter, all cardiac rhythm drugs including blood thinners (Warfarin) can be stopped soon after the procedure.
Drugs are generally not very effective when used to terminate or prevent flutter. Although an electrical current can be used to jolt the heart back to normal (DC cardioversion), there is over 50% chance within 2 year of a recurrence of this condition. The Prime Minister also had a cardioversion but developed the same problem within a few months.
Supraventricular tachycardias (SVT) are rapid arrhythmias that originate from above the ventricles. Although this including atrial flutter and fibrillation, the term is generally used to describe arrhythmias caused by an abnormal piece of wiring within the heart or accessory pathway. The presence of a second, abnormal connection, from the atrium to ventricle, forms the requirement for loop like "reentry" circuits, allowing signals to go down one connection, revolve around the chamber then up the other connection to the second chamber in a self perpetuating loop like process (Figure 7).
Wolff Parkinson White Syndrome cannot only cause symptoms, but is a type of accessory pathway that can cause life threatening arrhythmias. It is reported that there is a 0.2% annual risk of sudden cardiac death but recent reports suggest this can be as high as 1-2% even in patients with no symptoms.
These arrhythmias occur in 1% of the population and often beginnings early in life. SVTs are not life threatening except for a condition called Wolff Parkinson White Syndrome. The difficulty of SVTs is the unpredictable nature of how they behave, when they occur, how long an attack may persist and when it would end. Drugs are often effective in complete control of the arrhythmia in half of all cases and the drugs are effective only for the duration that they are taken. This means that young patients may face the prospect of several decades of take drugs therapy with potential long-term side effects from medication.
Because these arrhythmias arise from abnormal focal strands of wiring and their behaviour has been well categorised and understood, catheter ablation techniques can now locate these abnormal strands of muscle acting as bridging pieces of electrical wiring and focal delivery of high frequency radiowaves (Figure 8) can completely cure these arrhythmias (Figure 9). Even left sided pathways can be easily treated with procedural risk of up to 1%.
Atrial fibrillation (AF) is the commonest arrhythmia in man, with an estimated prevalence of 1% under 60 years and increases rapidly with age to more than 10% in those over 80 years (Figure 10). AF is the commonest arrhythmic cause for hospitalisations, and is associated with increased morbidity (adverse events) and mortality (risk of death). Two decades ago the only treatment options for AF were largely limited to achieving heart rate control. However, extensive research in recent years has provided greater understanding of the pathophysiology and mechanisms that lead to AF. A number of recent clinical trials have provided evidence of improved outcomes using these newer therapeutic strategies for AF management. Patients should now be given the option of these new treatments in a balanced and rational approach to risks and benefits.
Patients with AF typically present with symptoms, which include palpitations, chest pain and breathlessness, that compromise their quality of life and functional capacity. However, some patients may have asymptomatic AF discovered as an incidental finding. In highly symptomatic individuals, conventional rate control strategies may be an unacceptable option, particularly in young patients facing the prospect of several decades of AF combined with the potential side effects of long-term drug therapy. Therefore, for many patients the more attractive alternative is to try to restore and maintain normal cardiac (sinus) rhythm.
Restoration of sinus rhythm from AF can be achieved by electrically jolting the heart back to normal rhythm (DC cardioversion) or by rhythm controlling (anti-arrhythmic) drugs. Despite an acute success rate of over 80% for electrical DC cardioversion, there is a high relapse rate back to AF of more than 70% within 1 year, which may be reduced to 50% by serially trying different antiarrhythmic drugs (Figure 11).
Atrio-ventricular node ablation with pacemaker implantation
Patient symptoms are often related to a rapid irregular ventricular rate. One treatment option involves destroying the normal atrioventicular (AV) nodal connection using thermal heat delivered through a small catheter tip (radiofrequency ablation), which has to be combined with implantation of a ventricular pacemaker. This “ablate and pace” strategy is an effective treatment particularly in older more frail patients, but the process of AV disconnection is irreversible, and commits patients to lifelong dependence on pacing. In particular it should be avoided in young patients who will require multiple revisions of their pacing system during their lifetime. Perhaps what is more disappointing with this approach is that AF continues, thromboembolic stroke risks remain unaltered, and the need for long-term anticoagulation persists. In addition, the incidence of heart failure and mortality in patients with structural heart disease treated with AV node ablation and pacemaker implantation has been shown to be as high as 40%, probably because right ventricular pacing induces inco-ordination (dyssynchrony), shown to adversely affect cardiac performance.
Despite the prevalence of this condition, it was not until 1998 that the primary cause of AF, due to paroxysmal (intermittent) rapid firing focal triggers located in the left atrium was discovered. These areas usually located around the pulmonary veins that deliver oxygen rich blood back to the heart from the lungs, for some reason has retained autonomous and inappropriate rapid firing electrical activity, capable of sending the whole chamber into complete chaos, resulting in clinical symptoms. Clinical trials of ablation treatment techniques began soon after this discovery. These techniques aim to either eliminate rapid AF triggers or to electrically isolate them to disconnect them from the atrium (Figure 12). Although a number of small trials have shown the efficacy of this approach, it was only recently that large scale studies have directly comparing pulmonary vein isolation against rate control was published. In one non randomised Italian study, almost 1200 patients were enrolled over a 3-year follow-up period. For the first time this preliminary study has shown highly significant acute and medium term improvements (>50% risk reduction) in both cardiovascular and total mortality, and morbidity from heart failure and strokes in the ablation compared with rate control groups. Patient quality of life and functional capacity were also found to be significantly better in the ablation group. A higher success rate of AF prevention was achieved in patients with paroxysmal (85%) compared to persistent (62%) AF ablation. These results are in line with a number of other studies with similar reported success rates of preventing AF recurrence.
Despite the promising results from this study, there are small but significant risks associated with AF ablation. These include the risk from transeptal puncture and anticoagulation (blood thinners required during the procedure), procedure related stroke, pericardial effusion (seepage of blood into the sack that surround the heart that may lead to cardiac compression and compromise) and pulmonary vein stenosis (narrowing of the veins draining from the lungs <2%), culminating in an average overall risk of approximately 5% of which up to 1% may be serious. Clearly, this aggressive strategy is not suitable for all patients, but should be considered in highly symptomatic individuals intolerant or refractory to antiarrhythmic drugs.
In the short space of 8 years, from identifying the triggers of AF, therapeutic strategies to potentially cure this arrhythmia have been developed. It is anticipated that as our understanding of the pathophysiology evolves, techniques and results will also continue to improve. It therefore appears that far from being simplified, the management of AF is likely to become more complex, as evidence from large clinical trials continue to suggests better long term outcome from more aggressive therapeutic strategies.
It is clear that warfarin is far superior compared to aspirin for thromboembolic risk reduction. Therefore, as a minimum, we should be advising formal anticoagulation for patients at thromboembolic risk from AF, unless there are clear contraindications. Those below the age of 60-65 years with structurally normal heart can be treated with aspirin alone.
It is inappropriate to treat all patients using a single approach, and treatment plans should be tailored for each patient according to suitability and careful risk-benefit assessment, aimed at reducing long-term morbidity and mortality, with acceptable clinical risks in mind. It is strongly advised that symptomatic patients, particularly those unresponsive to or have side effects from drugs should be referred to a Cardiac Rhythm Specialist for assessment. Expansion of interventional AF treatment, accumulating as the volume of evidence of long term outcome with time, improving results and lower complication rates is likely to increase the numbers of patients treated by these techniques. Clinicians should be aware of the range of treatment options available, to offer patients the highest quality of care.
Unusual cardiac arrhythmias
There are also a number of more unusual cardiac arrhythmias which either occur from a rapidly discharging focal source, or form a loop like “re-entrant” circuit. These are complex and are frequently found in patients with structural heart abnormalities with areas of scar or development of abnormal “pacemaker” activity. The majority of these can now be successfully mapped and cured or at least ameliorated by ablation therapy using complex 3-dimensional global mapping systems. Rhythm specialists with adequate experience now successfully cure a large number of previously unmappable and untreatable arrhythmias using newer technology.
Heart failure is the syndrome of clinical manifestations and symptoms that patients experience when the function of the heart is inadequate to meet the body’s requirements. This usually arises from significant damage to large parts of the heart’s muscle as a result of blocked arteries from a heart attack, or from a disease process of the muscle itself, which can arise from viral infections, certain genetic disorders or rarely other causes. The end result is enlargement and weakening of the heart as a mechanical pump.
Patients develop breathlessness, lethargy, poor exercise tolerance and swollen lower limbs and stomach area due to fluid retention. Symptomatic patients have difficulty lying flat or sleeping, it may be difficult to wear normal footwear because of swelling in their feet, and poor appetite with nausea is often encountered due to backpressure on the gut from impaired cardiac function.
The incidence of heart failure increases with age and 1 in 10 patients over the age of 80 may develop this condition. Heart failure has a very bleak outlook. It is estimated even with the best heart failure drugs currently available, half of all symptomatic patients may not survive beyond 2-3 years.
It is estimated that as many as 20-30% of all heart failure patients have significant damage or malfunction of the normal electrical wiring within the heart resulting in areas of early and late pump activation. This defect would introduce marked incoordination into the pumping action of a already weakened heart and worsen heart failure.
Cardiac Resynchronisation Therapy (CRT) pacemakers
A new form of pacemaker to resynchronise this incoordination was developed to correct this defect. 2 wires place on either side of the lower left ventricular chamber responsible for pumping blood around the body (Figure 17) has now been shown to improve cardiac function, patient quality of life, improve exercise distance (Figure 18) and reduce heart failure events Figure 19. Dramatic 77% reduction in days spent in hospital for heart failure was achieved by patients who the CRT devices (Figure 20). Further recent trials have also shown that selected heart failure patients with dyssynchrony, deaths can be reduced by 36% in 2 and a half years follow-up (Figure 21 and 22). In selected patient, they not only feel better, but also live longer with CRT. Not all patients with heart failure are suitable for this treatment, but it is thought that up to 30% of this population may benefit from CRT.
Implantable defibrillators (ICD)
As we have seen above, a large number of patient with heart failure die suddenly. In fact, those with the poorest cardiac function tend to die of pump failure, but those with better heart function tend to die suddenly (Figure 23). These are the result of developing malignant arrhythmias that stop the heart from pumping (cardiac arrest). Those patients resuscitated from ventricular tachycardia or cardiac arrest, are at highest risk of developing further arrhythmic events.
A number of clinical trials have now shown that anti-arrhythmic drugs have little effect in reducing mortality in heart failure patients. The implantable defibrillator (Figure 24 and 25), a device like a pacemaker (but larger) that can be fully implanted within the body under local anaesthetic taking approximately an hour, can protect heart failure patients from risk of sudden death. They can terminate rapid heart rhythms by use of the pacemaker function of the device, which is painless and is successful in 80% of cases. But when the heart is so rapid or irregular that it has stopped pumping, the device will deliver a shock to reset and restore normal rhythm (Figure 26). A number of clinical trials have shown that the ICD is highly effective in reducing the risk of sudden death in patients who have had arrhythmias by 30-50% in 5 years (Figure 27).
More recently the indications for use of ICDs have also expanded to include certain patients with impaired heart function whom have never had an abnormal rhythm event but considered at significant risk (primary prevention). Trials of patients with a previous heart attack or cardiomyopathy (heart muscle disorder but normal coronary circulation) with severely impaired cardiac function have shown mortality reduction of over 20-31% (Figure 28 and 29). On the strength of these powerful studies, the National Institute of Clinical Excellence, European and American Cardiac Societies have now made clear guidelines for patient selection and device implantation to prevent sudden cardiac death. A cardiac rhythm specialist should be consulted to assess for suitability and benefit from these devices.
London Arrhythmia Network www.londonarrhythmianetwork.co.uk