SADS - Maz died suddenly on the eve of his wedding

Sudden Arrhythmic Death Syndrome: a stealthy killer

Suzanne Lowry's son, Max, died suddenly on the eve of his wedding. A year on, his mother shares her sense of loss – and her hope that others may be spared the same fate.

• Suzanne Lowry
• theguardian.com, Tuesday 6 September 2011 08.00 BST

Max Lowry ... 'He was the cement in all our lives'

By eight o'clock on the evening before the wedding, the last jostlings in the table plan had ended and the numbers joining to dance after dinner had somehow been held to the level permitted.

I had seen the dress, hanging in its exquisite folds like a beautiful ghost, safely arrived from designer Georgina Chapman in New York (an old friend and schoolmate of the couple). Guests had gathered from far and near.

The bride, Jane, staying with her parents until the ceremony, made a goodnight call to her future husband (and my son), Max. He had just got back to their flat after a hard day's work at his studio, when he picked up the phone. They chatted briefly. "I love you," he said. And then, nothing, apart from a faint choking sound.

Across town, I was in my room, sending a few emails and looking forward to the next day. As the mother of the bridegroom, I reckoned, my role would be mainly to enjoy myself. That illusion faded when my hostess, Polly, burst in and thrust a phone into my hands. "It's Jane," she said. "Max is in an ambulance ..." I grabbed the phone and heard Jane say that he was on his way to Hammersmith Hospital and could I get there?

I don't remember leaving the house, only somehow being in a taxi. It dawned that I had no cash on me so we stopped at an ATM. As I waited for the notes to clunk out of the machine, I was thinking that perhaps we would have to postpone the wedding. A flickering hope.

At A&E I was shown to a room where I expected to see Max lying on a bed, but found only an anguished Jane holding her father's hand, tears streaming down her face. No one spoke. "Where is he?", I asked in panic. "Is he alive?" I spun around to find a doctor standing quietly by the door. "His heart stopped beating," he said gently. "We could not revive him."

Later during that long night Jane and I sat up with Polly, talking and weeping by turns, groping for comprehension. At dawn I went to bed, but my eyes seemed to be jammed open, "on stalks", like a cartoon character.

"You couldn't write this," Jane said. And after almost a year, this the first time I have tried. The aftermath of Max's death was so confused, and the fact of it so incredible, that even when - on what should have been his wedding day - I stood in the bleak little viewing room at the mortuary looking at him stretched out with something that looked like Grandma's velvet curtains draped over him, I could not believe it.

On the edge of his generous hand lying outside the cover I noticed a streak of green paint: a last reminder that Max was an artist. It was him and not him; here he was and yet here he was utterly absent. His hair was thrown back from his face; a small plastic tube was clenched in his mouth. I did not stay long, but left Jane talking and talking to him in a loving stream of consciousness, that she would never forget him, that he had shown her how to live.

That afternoon, most of the wedding guests, summoned by email and texts, walked en masse up Primrose Hill. At the top, Sam, the best man, addressed us and I began to understand just how much Max had meant to his legion of friends. "He was the cement in all our lives," Sam said, and at the end of his oration we all shouted "Max!" at the sky.

That was the first time that I felt suffused by a strange backwash of warmth, seeing off - briefly - the chill that was settling in me. The rush came again at the funeral, when even more - hundreds more - of his friends came to say goodbye. I have felt it many times since: early in the morning in my garden, or when I am with friends he loved, and sometimes when I am feeling low. Max specialised in the bear-hug, and I guess this is the best he can do from Over There.

So much has been written about death that I hesitate to add my spoonful of experience. It is a leveller, a common denominator, we are automatically signed up for it at birth. And yet its capacity to shock, and hurt, and bereave never diminishes - especially when, according to our hubristic programme, it comes too soon. As deaths go, Max had a good one: he had not suffered, he wasn't tortured or murdered, not wiped out in an accident, nor by a roadside bomb. He was at the peak of happiness and hitting his stride as an artist.

But the "good" aspects made his loss harder to take for those left behind, simply because he was young and seemed so fit and well. We were repeatedly told - by the coroner, the heart specialist's autopsy - that there had been nothing wrong with him. His heart was healthy, nothing toxic in his system, he was in good shape. At the inquest, the verdict recorded was simply "natural causes."

But there was a specific cause, and a stealthy one. He died of Sads - Sudden Arrhythmic Death Syndrome (sometimes called Sudden Adult Death Syndrome), an umbrella term for around a dozen conditions that kill at least 600 people under 35 a year in the UK. These deaths, linked to anomalies in electrical workings of the heart, have been compared to cot deaths in infancy. They have a special poignancy because there are few prior symptoms and the victims appear, like Max, to be in prime health.

Athletes on the sports field, a young girl thrilled by her first kiss, a teenager collapsing on to his birthday cake, a girl on her morning jog, somebody's son at the wheel, waiting for the lights to change - these are among the long roll of stories in the archives of Cry (Cardiac Risk in the Young). This charity works to raise awareness of Sads and helps to fund important research and a screening programme for under-35s.

Max's family and friends miss his presence every day - his smile, his warmth and humour. However, as an artist, he left his work behind. Next week, just ahead of the first anniversary of his death, some of his pictures and prints will be exhibited in London. It will be a celebration of his life and work, but also, it is hoped, will raise money for Cry, and their campaign to save others from his fate.

• Max Lowry 1976-2010: A Retrospective. Mall Galleries, The Mall (near Admiralty Arch), London SW1, 12-18 September.

SADS - Many young people dies of SADS

Reducing unexpected deaths

Every week three young people die unexpectedly from rare heart conditions they didn’t know they had. This is called Sudden Arrhythmic Death Syndrome (SADS).

The rhythm of the heart beat is controlled by natural electrical currents in our heart cells. Disruption of this electrical current can cause a disturbance to the heart beat that can lead to SADS.

Sudden arrhythmic death syndrome booklet An inherited heart condition can affect one or several members of the same family. Sadly,some inherited cardiac conditions are often not diagnosed until one person dies suddenly and unexpectedly. Download or order our Sudden Arrhythmic Death Syndrome booklet.

Our ground-breaking research into SADS

Our scientists have been investigating the electrical and structural problems that lead to SADS, so that we can get better at identifying people at risk and provide treatments to prevent these tragic deaths.

Genetic clues

Professor Bill McKenna and his team were supported by your donations to identify genetic clues that might explain how this condition occurs.

A state of the art Magnetic Resonance Imaging (MRI) machine we provided helped the team learn more about how these genes might work to control heart function. 

Predicting SADS risk

With help from our research funding, researchers at Papworth Hospital have developed a way to predict SADS risk by measuring electrical ‘disorganisation’ in the heart.

By identifying this type of electrical disturbance, the researchers hope to prevent SADS in people suffering from a range of different heart diseases. 

Saving lives

In the 1990s research by BHF Professor John Camm demonstrated the benefits of a device called an internal cardioverter defibrillator (ICD) for patients at high risk of ventricular fibrillation.

He pioneered the use of these devices for people at risk of SADS. Patients at high risk can be fitted with an internal cardioverter defibrillator, which helps prevent SADS by giving the heart a kick-start when its rhythm is disrupted.

The future for SADS research

We fund a great many research projects looking at the genes and proteins that control the spread of electrical currents across the heart muscle.

It is thought that disruptions in this control might hold the key to understanding heart rhythm disturbances that cause SADS.

_________________________________________________________________________________

Every 16.8hrs an Australian child dies of SADS

This website is in memory of those who have passed as a result of SADS or Sudden Arrhythmic Death Syndrome.

It has also been created to increase awareness of Sudden Arrhythmic Death Syndrome and to provide helpful and supportive online community where family members can reach out to others.

Sudden Arrhythmic Death Syndrome is common in people aged 5 - 35 it is an inherited disease which creates an abnormality in the heart, causing it to speed up/slow down to the point where it can no longer pump blood, in some cases, however, the heart will stop completely.

A heart condition such as this is hard to detect as there are very few, sometimes no prior symptoms ; most GP's and health professionals remain unaware of this 'SILENT KILLER'.

SADS - Cardiac dysrhythmia

Cardiac dysrhythmia

From Wikipedia, the free encyclopedia

Cardiac dysrhythmia (also known as arrhythmia or irregular heartbeat) is any of a large and heterogeneous group of conditions in which there is abnormal electrical activity in the heart. The heartbeat may be too fast or too slow, and may be regular or irregular. A heart beat that is too fast is called tachycardia and a heart beat that is too slow is called bradycardia. Although many arrhythmias are not life-threatening, some can cause cardiac arrest.

Arrhythmias can occur in the upper chambers of the heart, (atria), or in the lower chambers of the heart, (ventricles). Arrhythmias may occur at any age. Some are barely perceptible, whereas others can be more dramatic and can even lead to sudden cardiac death.

Some arrhythmias are life-threatening medical emergencies and can result in cardiac arrest. Cardiac arrythmias are one of the most common causes of death when travelling to a hospital. Others cause symptoms such as an abnormal awareness of heart beat (palpitations) and may be merely uncomfortable. These palpitations have also been known to be caused by atrial/ventricular fibrillation, wire faults, and other technical or mechanical issues in cardiac pacemakers/defibrillators. Still others may not be associated with any symptoms at all, but may predispose the patient to potentially life threatening stroke orembolism.

The term sinus arrhythmia refers to a normal phenomenon of mild acceleration and slowing of the heart rate that occurs with breathing in and out. It is usually quite pronounced in children and steadily decreases with age. This can also be present during meditation breathing exercises that involve deep inhaling and breath holding patterns. Proarrhythmia is a new or more frequent occurrence of pre-existing arrhythmias, paradoxically precipitated by antiarrhythmic therapy, which means it is a side effect associated with the administration of some existing antiarrhythmic drugs, as well as drugs for other indications. In other words, it is a tendency of antiarrhythmic drugs to facilitate emergence of new arrhythmias. Some arrhythmias are minor and can be regarded as normal variants. In fact, most people will on occasion feel their heart skip a beat or give an occasional extra strong beat; neither of these is usually a cause for alarm.

Classification

Arrhythmia may be classified by rate (normal sinus rhythm, tachycardia, bradycardia) or mechanism (automaticity, reentry, junctional, fibrillation).

It is also appropriate to classify by site of origin:

Atrial

• Premature Atrial Contractions (PACs)
• Wandering Atrial Pacemaker
• Multifocal atrial tachycardia
• Atrial flutter
• Atrial fibrillation (Afib)

Junctional arrhythmias

• Supraventricular tachycardia (SVT)
• AV nodal reentrant tachycardia is the most common cause of Paroxysmal Supra-ventricular Tachycardia (PSVT)
• Junctional rhythm
• Junctional tachycardia
• Premature junctional contraction

Ventricular

• Premature Ventricular Contractions (PVC) sometimes called Ventricular Extra Beats (VEBs)
  • Premature Ventricular beats occurring after every normal beat are termed "ventricular bigeminy"
  • PVCs that occur at intervals of 2 normal beats to 1 PVC are termed "PVCs in trigeminy"
  • Three premature ventricular grouped together is termed a "run of PVCs"; runs lasting longer than three beats are generally referred to as ventricular tachycardia
• Accelerated idioventricular rhythm
• Monomorphic Ventricular tachycardia
• Polymorphic ventricular tachycardia
• Ventricular fibrillation

Heart blocks

These are also known as AV blocks, because the vast majority of them arise from pathology at the atrioventricular node. They are the most common causes of bradycardia:

• First degree heart block, which manifests as PR prolongation
• Second degree heart block
  • Type 1 Second degree heart block, also known as Mobitz I or Wenckebach
  • Type 2 Second degree heart block, also known as Mobitz II
• Third degree heart block, also known as complete heart block.

SADS

SADS, or sudden arrhythmic death syndrome, is a term (as part of, Sudden unexpected death syndrome) used to describe sudden death due to cardiac arrest brought on by an arrhythmia in the absence of any structural heart disease on autopsy. The most common cause of sudden death in the US is coronary artery disease. Approximately 180,000 to 250,000 people die suddenly of this cause every year in the US. SADS occurs from other causes. There are many inherited conditions and heart diseases that can affect young people and subsequently cause sudden death. Many of these victims have no symptoms before dying suddenly.^{[citation needed]}

Causes of SADS in young people include viral myocarditis, long QT syndrome, Brugada syndrome, Catecholaminergic polymorphic ventricular tachycardia, hypertrophic cardiomyopathy and arrhythmogenic right ventricular dysplasia.^{[A: 1]}

Signs and symptoms

The term cardiac arrhythmia covers a very large number of very different conditions.

The most common symptom of arrhythmia is an abnormal awareness of heartbeat, called palpitations. These may be infrequent, frequent, or continuous. Some of these arrhythmias are harmless (though distracting for patients) but many of them predispose to adverse outcomes.

Some arrhythmias do not cause symptoms, and are not associated with increased mortality. However, some asymptomatic arrhythmias are associated with adverse events. Examples include a higher risk of blood clotting within the heart and a higher risk of insufficient blood being transported to the heart because of weak heartbeat. Other increased risks are of embolisation and stroke, heart failure and sudden cardiac death.

If an arrhythmia results in a heartbeat that is too fast, too slow or too weak to supply the body's needs, this manifests as a lower blood pressure and may cause lightheadedness or dizziness, or syncope (fainting).

Some types of arrhythmia result in cardiac arrest, or sudden death.

Medical assessment of the abnormality using an electrocardiogram is one way to diagnose and assess the risk of any given arrhythmia.

Differential diagnosis

Normal electrical activity

Main article: Electrical conduction system of the heart

Each heart beat originates as an electrical impulse from a small area of tissue in the right atrium of the heart called the sinus node or Sino-atrial node or SA node. The impulse initially causes both atria to contract, then activates the atrioventricular (or AV) node which is normally the only electrical connection between the atria and the ventricles (main pumping chambers). The impulse then spreads through both ventricles via the Bundle of His and the Purkinje fibres causing a synchronised contraction of the heart muscle and, thus, the pulse.

In adults the normal resting heart rate ranges from 60 to 80 beats per minute. The resting heart rate in children is much faster. In athletes though, the resting heart rate can be as slow as 40 beats per minute, and be considered as normal.

Bradycardias

Normal sinus rhythm, with solid black arrows pointing to normal P waves representative of normal sinus node function, followed by a pause in sinus node activity (resulting in a transient loss of heart beats). Note that the P wave that disrupts the pause (indicated by the dashed arrow) does not look like the previous (normal) P waves — this last P wave is arising from a different part of the atrium, representing an escape rhythm.

A slow rhythm (less than 60 beats/min), is labelled bradycardia. This may be caused by a slowed signal from the sinus node (sinus bradycardia), a pause in the normal activity of the sinus node (sinus arrest), or by blocking of the electrical impulse on its way from the atria to the ventricles (AV block or heart block). Heart block comes in varying degrees and severity. It may be caused by reversible poisoning of the AV node (with drugs that impair conduction) or by irreversible damage to the node. Bradycardias may also be present in the normally functioning heart of endurance athletes or other well-conditioned persons.

Tachycardias

In adults and children over 15, resting heart rate faster than 100 beats/minute is labelled tachycardia. Tachycardia may result in palpitation; however, tachycardia is not necessarily an arrhythmia. Increased heart rate is a normal response to physical exercise or emotional stress. This is mediated by the sympathetic nervous system on the sinus node and called sinus tachycardia. Other things that increase sympathetic nervous system activity in the heart include ingested or injected substances, such as caffeine or amphetamines, and an overactive thyroid gland (hyperthyroidism).

Tachycardia that is not sinus tachycardia usually results from the addition of abnormal impulses to the normal cardiac cycle. Abnormal impulses can begin by one of three mechanisms: automaticity, reentry or triggered activity. A specialised form of re-entry problem is termed fibrillation.

Although the term "tachycardia" is known over one hundred year, basis for the classification of arrhythmias are still being discussed.

Heart defects causing tachycardia

Congenital heart defects are structural or electrical pathway problems in the heart that are present at birth. Anyone can be affected with this because overall health does not play a role in the problem. Problems with the electrical pathway of the heart can cause very fast or even deadly arrhythmias. Wolf-Parkinson-White syndrome is due to an extra pathway in the heart that is made up of electrical muscle tissue. This tissue allows the electrical impulse, which stimulates the heartbeat, to happen very rapidly. Right Ventricular Outflow Tract Tachycardia is the most common type of ventricular tachycardia in otherwise healthy individuals. This defect is due to an electrical node in the right ventricle just before the pulmonary artery. When the node is stimulated, the patient will go into ventricular tachycardia, which does not allow the heart to fill with blood before beating again. Long QT Syndrome is another complex problem in the heart and has been labeled as an independent factor in mortality. There are multiple methods of treatment for these including cardiac ablations, medication treatment, or altering your lifestyle to have less stress and exercise. It is possible to live a full and happy life with these conditions.

Automaticity

Automaticity refers to a cardiac muscle cell firing off an impulse on its own. All of the cells in the heart have the ability to initiate an action potential; however, only some of these cells are designed to routinely trigger heart beats. These cells are found in the conduction system of the heart and include the SA node, AV node, Bundle of His and Purkinje fibers. The sinoatrial node is a single specialized location in the atrium which has a higher automaticity (a faster pacemaker) than the rest of the heart and, therefore, is usually responsible for setting the heart rate and initiating each heart beat.

Any part of the heart that initiates an impulse without waiting for the sinoatrial node is called an ectopic focus and is, by definition, a pathological phenomenon. This may cause a single premature beat now and then, or, if the ectopic focus fires more often than the sinoatrial node, it can produce a sustained abnormal rhythm. Rhythms produced by an ectopic focus in the atria, or by the atrioventricular node, are the least dangerous dysrhythmias; but they can still produce a decrease in the heart's pumping efficiency, because the signal reaches the various parts of the heart muscle with different timing than usual and can be responsible for poorly coordinated contraction.

Conditions that increase automaticity include sympathetic nervous system stimulation and hypoxia. The resulting heart rhythm depends on where the first signal begins: If it is the sinoatrial node, the rhythm remains normal but rapid; if it is an ectopic focus, many types of dysrhythmia may ensue.

Re-entry

Re-entrant arrhythmias occur when an electrical impulse recurrently travels in a tight circle within the heart, rather than moving from one end of the heart to the other and then stopping.

Every cardiac cell is able to transmit impulses of excitation in every direction but will only do so once within a short time. Normally, the action potential impulse will spread through the heart quickly enough that each cell will only respond once. However, if there is some essential heterogeneity of refractory period or if conduction is abnormally slow in some areas (for example in heart damage) so the myocardial cells are unable to activate the fast sodium channel, part of the impulse will arrive late and potentially be treated as a new impulse. Depending on the timing, this can produce a sustained abnormal circuit rhythm.

As a sort of re-entry, the vortices of excitation in the myocardium (autowave vortices) is considered to be the main mechanism of life-threatening cardiac arrhythmias. In particular, the autowave reverberator is a typical in thin walls of the atria, with the atrial flutter producing. Re-entry are also responsible for most paroxysmal supraventricular tachycardia, and dangerous ventricular tachycardia. These types of re-entry circuits are different from WPW syndromes in which the real pathways existed.

Although omega-3 fatty acids from fish oil can be protective against arrhythmias, in the case of re-entrant arrhythmias, fish oil can worsen the arrhythmia.

Fibrillation

When an entire chamber of the heart is involved in a multiple micro-reentry circuits and, therefore, quivering with chaotic electrical impulses, it is said to be in fibrillation.

Fibrillation can affect the atrium (atrial fibrillation) or the ventricle (ventricular fibrillation); ventricular fibrillation is imminently life-threatening.

• Atrial fibrillation affects the upper chambers of the heart, known as the atria. Atrial fibrillation may be due to serious underlying medical conditions and should be evaluated by aphysician. It is not typically a medical emergency.
• Ventricular fibrillation occurs in the ventricles (lower chambers) of the heart; it is always a medical emergency. If left untreated, ventricular fibrillation (VF, or V-fib) can lead to death within minutes. When a heart goes into V-fib, effective pumping of the blood stops. V-fib is considered a form of cardiac arrest. An individual suffering from it will not survive unless cardiopulmonary resuscitation (CPR) and defibrillation are provided immediately.

CPR can prolong the survival of the brain in the lack of a normal pulse, but defibrillation is the only intervention that can restore a healthy heart rhythm. Defibrillation is performed by applying an electric shock to the heart, which resets the cells, permitting a normal beat to re-establish itself.

Triggered beats

Triggered beats occur when problems at the level of the ion channels in individual heart cells result in abnormal propagation of electrical activity and can lead to sustained abnormal rhythm. They are relatively rare and can result from the action of anti-arrhythmic drugs. See early and delayed Afterdepolarizations.

Diagnostic approach

Cardiac dysrhythmias are often first detected by simple but nonspecific means: auscultation of the heartbeat with a stethoscope, or feeling for peripheral pulses. These cannot usually diagnose specific dysrhythmias, but can give a general indication of the heart rate and whether it is regular or irregular. Not all the electrical impulses of the heart produce audible or palpable beats; in many cardiac arrhythmias, the premature or abnormal beats do not produce an effective pumping action and are experienced as "skipped" beats.

The simplest specific diagnostic test for assessment of heart rhythm is the electrocardiogram (abbreviated ECG or EKG). A Holter monitor is an EKG recorded over a 24-hour period, to detect dysrhythmias that may happen briefly and unpredictably throughout the day.

A more advanced study of the heart's electrical activity can be performed to assess the source of the aberrant heart beats. This can be accomplished in an Electrophysiology study. A minimally invasive procedure that uses a catheter to "listen" to the electrical activity from within the heart, additionally if the source of the arrhythmias is found, often the abnormal cells can be ablated and the arrhythmia can be permanently corrected.

Management

The method of cardiac rhythm management depends firstly on whether or not the affected person is stable or unstable. Treatments may include physical maneuvers, medications, electricity conversion, or electro or cryo cautery.

Physical maneuvers

A number of physical acts can increase parasympathetic nervous supply to the heart, resulting in blocking of electrical conduction through the AV node. This can slow down or stop a number of arrhythmias that originate above or at the AV node (see main article: supraventricular tachycardias). Parasympathetic nervous supply to the heart is via the vagus nerve, and these maneuvers are collectively known as vagal maneuvers.

Antiarrhythmic drugs

Main article: Antiarrhythmic agents

There are many classes of antiarrhythmic medications, with different mechanisms of action and many different individual drugs within these classes. Although the goal of drug therapy is to prevent arrhythmia, nearly every antiarrhythmic drug has the potential to act as a pro-arrhythmic, and so must be carefully selected and used under medical supervision.

Other drugs

A number of other drugs can be useful in cardiac arrhythmias.

Several groups of drugs slow conduction through the heart, without actually preventing an arrhythmia. These drugs can be used to "rate control" a fast rhythm and make it physically tolerable for the patient.

Some arrhythmias promote blood clotting within the heart, and increase risk of embolus and stroke. Anticoagulant medications such as warfarin and heparins, and anti-platelet drugs such as aspirin can reduce the risk of clotting.

Electricity

Dysrhythmias may also be treated electrically, by applying a shock across the heart — either externally to the chest wall, or internally to the heart via implanted electrodes.

Cardioversion is either achieved pharmacologically or via the application of a shock synchronised to the underlying heartbeat. It is used for treatment of supraventricular tachycardias. In elective cardioversion, the recipient is usually sedated or lightly anesthetized for the procedure.

Defibrillation differs in that the shock is not synchronised. It is needed for the chaotic rhythm of ventricular fibrillation and is also used for pulseless ventricular tachycardia. Often, more electricity is required for defibrillation than for cardioversion. In most defibrillation, the recipient has lost consciousness so there is no need for sedation.

Defibrillation or cardioversion may be accomplished by an implantable cardioverter-defibrillator (ICD).

Electrical treatment of dysrhythmia also includes cardiac pacing. Temporary pacing may be necessary for reversible causes of very slow heartbeats, or bradycardia, (for example, from drug overdose or myocardial infarction). A permanent pacemaker may be placed in situations where the bradycardia is not expected to recover.

Electrical cautery

Some cardiologists further sub-specialise into electrophysiology. In specialised catheter laboratories, they use fine probes inserted through the blood vessels to map electrical activity from within the heart. This allows abnormal areas of conduction to be located very accurately, and subsequently destroyed with heat, cold, electrical or laser probes.

This may be completely curative for some forms of arrhythmia, but for others, the success rate remains disappointing. AV nodal reentrant tachycardia is often curable. Atrial fibrillation can also be treated with this technique (e.g. pulmonary vein isolation), but the results are less reliable.

References

• Books

1. ^ Jump up to:^a b Mandel, William J., ed. (1995). Cardiac Arrhythmias: Their Mechanisms, Diagnosis, and Management (3 ed.). Lippincott Williams & Wilkins. ISBN 978-0-397-51185-3.
2. Jump up^ Moskalenko, A. (2012). "Tachycardia as “Shadow Play”". In Yamada, Takumi. Tachycardia. Croatia: InTech. pp. 97–122. ISBN 978-953-51-0413-1.

• Papers

1. Jump up^ Chugh, Sumeet S.; Reinier, Kyndaron; Teodorescu, Carmen; Evanado, Audrey; Kehr, Elizabeth; Al Samara, Mershed; Mariani, Ronald; Gunson, Karen et al. (2008). "Epidemiology of Sudden Cardiac Death: Clinical and Research Implications". Progress in Cardiovascular Diseases 51 (3): 213–28. doi:10.1016/j.pcad.2008.06.003. PMC 2621010.PMID 19026856. 
2. Jump up^ Wiener, Norbert; Rosenblueth, Arturo (1946). "The mathematical formulation of the problem of conduction of impulses in a network of connected excitable elements, specifically in cardiac muscle". Archivos del Instituto de Cardiología de México 16 (3): 205–65. PMID 20245817.
3. Jump up^ Allessie, M. A.; Bonke, F. I.; Schopman, F. J. (1976). "Circus movement in rabbit atrial muscle as a mechanism of tachycardia. II. The role of nonuniform recovery of excitability in the occurrence of unidirectional block, as studied with multiple microelectrodes". Circulation Research 39 (2): 168–77. doi:10.1161/01.RES.39.2.168. PMID 939001.
4. Jump up^ Denruijter, H; Berecki, G; Opthof, T; Verkerk, A; Zock, P; Coronel, R (2007). "Pro- and antiarrhythmic properties of a diet rich in fish oil". Cardiovascular Research 73 (2): 316–25.doi:10.1016/j.cardiores.2006.06.014. PMID 16859661.

• Web-sources

1. Jump up^ www.arrhythmiaaliiance.org.uk
2. Jump up^ familydoctor.org