Categories
Ailmemts & Remedies

Romano-Ward Syndrome.

Definition:
Romano-Ward syndrome is a condition that causes a disruption of the heart’s normal rhythm (arrhythmia). This disorder is a form of long QT syndrome, which is a heart condition that causes the heart (cardiac) muscle to take longer than usual to recharge between beats. The irregular heartbeats can lead to fainting (syncope) or cardiac arrest and sudden death.
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Romano-Ward syndrome is inherited in an autosomal dominant pattern. It is the most common form of inherited long QT syndrome, affecting an estimated 1 in 5,000 people worldwide, although more people may be affected but never experience any signs or symptoms of the condition.

Symptoms:
The list of signs and symptoms mentioned in various sources for Romano-Ward syndrome includes the 9 symptoms listed below:

•Partial loss of consciousness
•Total loss of consciousness
•Arrhythmias
•Long Q-T intervals
•Angina
•Grand mal seizures
•Lowered blood potassium level
•Fainting
•Heart attack

Causes:
Mutations in the ANK2, KCNE1, KCNE2, KCNH2, KCNQ1, and SCN5A genes cause Romano-Ward syndrome. The proteins made by most of these genes form channels that transport positively-charged ions, such as potassium and sodium, in and out of cells. In cardiac muscle, these ion channels play critical roles in maintaining the heart’s normal rhythm. Mutations in any of these genes alter the structure or function of channels, which changes the flow of ions between cells. A disruption in ion transport alters the way the heart beats, leading to the abnormal heart rhythm characteristic of Romano-Ward syndrome.

Unlike most genes related to Romano-Ward syndrome, the ANK2 gene does not produce an ion channel. The protein made by the ANK2 gene ensures that other proteins, particularly ion channels, are inserted into the cell membrane appropriately. A mutation in the ANK2 gene likely alters the flow of ions between cells in the heart, which disrupts the heart’s normal rhythm and results in the features of Romano-Ward syndrome.

This article incorporates public domain text from The U.S. National Library of Medicine

How do people inherit Romano-Ward syndrome?


This condition is typically inherited in an autosomal dominant pattern, which means one copy of the altered gene in each cell is sufficient to cause the disorder. In most cases, an affected person inherits the mutation from one affected parent. A small percentage of cases result from new mutations in one of the genes described above. These cases occur in people with no history of Romano-Ward syndrome in their family.

Diagnosis:
•High Blood Pressure: Home Testing
#Home Blood Pressure Hypertension Tests
#Home Blood Pressure Monitors
#Home Heart Tests

•Heart Health: Home Testing:
#Heart Rate Monitors
#Irregular Heartbeat Detection
#Heart Electrocardiogram (ECG)
#Home Blood Pressure Testing
#Home Cholesterol Testing

Treatment:
An imbalance between the right and left sides of the sympathetic nervous system may play a role in the etiology of this syndrome. The imbalance can be temporarily abolished with a left stellate ganglion block, which shorten the QT interval. If this is successful, surgical ganglionectomy can be performed as a permanent treatment

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose

Resources:
http://en.wikipedia.org/wiki/Romano-Ward_syndrome#Inheritance
http://ghr.nlm.nih.gov/condition/romano-ward-syndrome
http://www.wrongdiagnosis.com/r/romano_ward_syndrome/home-testing.htm

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Ailmemts & Remedies

Long QT Syndrome

Definition:
The long QT syndrome (LQTS) is a rare inborn heart condition in which delayed repolarization of the heart following a heartbeat increases the risk of episodes of torsade de pointes (TDP, a form of irregular heartbeat that originates from the ventricles). These episodes may lead to palpitations, fainting and sudden death due to ventricular fibrillation. Episodes may be provoked by various stimuli, depending on the subtype of the condition.
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You can be born with a genetic mutation that puts you at risk of long QT syndrome. In addition, certain medications and medical conditions may cause long QT syndrome.

The condition is so named because of the appearances of the electrocardiogram (ECG/EKG), on which there is prolongation of the QT interval.

Long QT syndrome is treatable. You may need to limit your physical activity, avoid medications known to cause prolonged Q-T intervals or take medications to prevent a chaotic heart rhythm. Some people with long QT syndrome need surgery or an implantable device.

Symptoms :
Many people with long QT syndrome don’t have any signs or symptoms. They may be aware of their condition only from results of an electrocardiogram (ECG) performed for an unrelated reason, because they have a family history of long QT syndrome or because of genetic testing results.

For people who do experience signs and symptoms of long QT syndrome, the most common symptoms include:

*Fainting. This is the most common sign of long QT syndrome. In people with long QT syndrome, fainting spells (syncope) are caused by the heart temporarily beating in an erratic way. These fainting spells may happen when you’re excited, angry or scared, or during exercise. Fainting in people with long QT syndrome can occur without warning, such as losing consciousness after being startled by a ringing telephone.

Signs and symptoms that you’re about to faint include lightheadedness, heart palpitations or irregular heartbeat, weakness and blurred vision. However, in long QT syndrome, such warning signs before fainting are unusual.

*Seizures. If the heart continues to beat erratically, the brain becomes increasingly deprived of oxygen. This can then cause generalized seizures.

*Sudden death. Normally, the heart returns to its normal rhythm. If this doesn’t happen spontaneously and paramedics don’t arrive in time to convert the rhythm back to normal with an external defibrillator, sudden death will occur.Signs and symptoms of inherited long QT syndrome may start during the first months of life, or as late as middle age. Most people who experience signs or symptoms from long QT syndrome have their first episode by the time they reach age 40.

Rarely, signs and symptoms of long QT syndrome may occur during sleep or arousal from sleep.

Causes:
Your heart beats about 100,000 times a day to circulate blood throughout your body. To pump blood, your heart’s chambers contract and relax. These actions are controlled by electrical impulses created in the sinus node, a group of cells in the upper right chamber of your heart. These impulses travel through your heart and cause it to beat.

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After each heartbeat, your heart’s electrical system recharges itself in preparation for the next heartbeat. This process is known as repolarization. In long QT syndrome, your heart muscle takes longer than normal to recharge between beats. This electrical disturbance, which often can be seen on an electrocardiogram (ECG), is called a prolonged Q-T interval.

Prolonged Q-T interval
An electrocardiogram (ECG, also called an EKG) measures electrical impulses as they travel through your heart. Patches with wires attached to your skin measure these impulses, which are displayed on a monitor or printed on paper as waves of electrical activity.

An ECG measures electrical impulses as five distinct waves. Doctors label these five waves using the letters P, Q, R, S and T. The waves labeled Q through T show electrical activity in your heart’s lower chambers.

The space between the start of the Q wave and the end of the T wave (Q-T interval) corresponds to the time it takes for your heart to contract and then refill with blood before beginning the next contraction.

By measuring the Q-T interval, doctors can tell whether it occurs in a normal amount of time. If it takes longer than normal, it’s called a prolonged Q-T interval. The upper limit of a normal Q-T interval takes into account age, sex, and regularity and speed of the heart rate.

Long QT syndrome results from abnormalities in the heart’s electrical recharging system. However, the heart’s structure is normal. Abnormalities in your heart’s electrical system may be inherited or acquired due to an underlying medical condition or a medication.

Inherited long QT syndrome
At least 12 genes associated with long QT syndrome have been discovered so far, and hundreds of mutations within these genes have been identified. Mutations in three of these genes account for about 70 to 75 percent of long QT syndrome, and cause the forms referred to as LQT1, LQT2 and LQT3.

Doctors have described two forms of inherited long QT syndrome:

*Romano-Ward syndrome. This more common form occurs in people who inherit only a single genetic variant from one of their parents.

*Jervell and Lange-Nielsen syndrome. Signs and symptoms of this rare form usually occur earlier and are more severe than in Romano-Ward syndrome. It’s seen in children who are born deaf and have long QT syndrome because they inherited genetic variants from each parent.

Additionally, scientists have been investigating a possible link between SIDS and long QT syndrome and have discovered that about 10 percent of babies with SIDS had a genetic defect or mutation for long QT syndrome.

Acquired long QT syndrome
More than 50 medications, many of them common, can lengthen the Q-T interval in otherwise healthy people and cause a form of acquired long QT syndrome known as drug-induced long QT syndrome.

Medications that can lengthen the Q-T interval and upset heart rhythm include certain antibiotics, antidepressants, antihistamines, diuretics, heart medications, cholesterol-lowering drugs, diabetes medications, as well as some antifungal and antipsychotic drugs.

People who develop drug-induced long QT syndrome may also have some subtle genetic defects in their hearts, making them more susceptible to disruptions in heart rhythm from taking drugs that can cause prolonged Q-T intervals.

Risk Factors:
People at risk of long QT syndrome include:

*Children, teenagers and young adults with unexplained fainting, unexplained near drownings or other accidents, unexplained seizures, or a history of cardiac arrest

*Family members of children, teenagers and young adults with unexplained fainting, unexplained near drownings or other accidents, unexplained seizures, or a history of cardiac arrest

*Blood relatives of people with known long QT syndrome

*People taking medications known to cause prolonged Q-T intervals

Long QT syndrome often goes undiagnosed or is misdiagnosed as a seizure disorder, such as epilepsy. However, researchers believe that long QT syndrome may be responsible for some otherwise unexplained deaths in children and young adults. For example, an unexplained drowning of a young person may be the first clue to inherited long QT syndrome in a family.

People with low potassium, magnesium or calcium blood levels — such as those with the eating disorder anorexia nervosa — may be susceptible to prolonged Q-T intervals. Potassium, magnesium and calcium are all important minerals for the health of your heart’s electrical system.

Diagnosis:
The diagnosis of LQTS is not easy since 2.5% of the healthy population have prolonged QT interval, and 10–15% of LQTS patients have a normal QT interval. A commonly used criterion to diagnose LQTS is the LQTS “diagnostic score”. The score is calculated by assigning different points to various criteria (listed below). With four or more points, the probability is high for LQTS; with one point or less, the probability is low. A score of two or three points indicates intermediate probability.

*QTc (Defined as QT interval / square root of RR interval)
#>= 480 msec – 3 points
#460-470 msec – 2 points
#450 msec and male gender – 1 point

*Torsades de pointes ventricular tachycardia – 2 points

*T wave alternans – 1 point

*Notched T wave in at least 3 leads – 1 point

*Low heart rate for age (children) – 0.5 points

*Syncope (one cannot receive points both for syncope and torsades de pointes)
#With stress – 2 points
#Without stress – 1 point

*Congenital deafness – 0.5 points

*Family history (the same family member cannot be counted for LQTS and sudden death)
#Other family members with definite LQTS – 1 point
#Sudden death in immediate family (members before the age 30) – 0.5 points
Treatment options:
Those diagnosed with long QT syndrome are usually advised to avoid drugs that would prolong the QT interval further or lower the threshold for TDP.  In addition to this, there are two intervention options for individuals with LQTS: arrhythmia prevention and arrhythmia termination.

Arrhythmia prevention:
Arrhythmia suppression involves the use of medications or surgical procedures that attack the underlying cause of the arrhythmias associated with LQTS. Since the cause of arrhythmias in LQTS is after depolarizations, and these after depolarizations are increased in states of adrenergic stimulation, steps can be taken to blunt adrenergic stimulation in these individuals. These include:

*Administration of beta receptor blocking agents which decreases the risk of stress induced arrhythmias. Beta blockers are the first choice in treating Long QT syndrome.
In 2004 it has been shown that genotype and QT interval duration are independent predictors of recurrence of life-threatening events during beta-blockers therapy. Specifically the presence of QTc >500ms and LQT2 and LQT3 genotype are associated with the highest incidence of recurrence. In these patients primary prevention with ICD (Implantable cardioverter-defibrillator) implantation can be considered.

*Potassium supplementation. If the potassium content in the blood rises, the action potential shortens and due to this reason it is believed that increasing potassium concentration could minimize the occurrence of arrhythmias. It should work best in LQT2 since the HERG channel is especially sensitive to potassium concentration, but the use is experimental and not evidence based.

*Mexiletine. A sodium channel blocker. In LQT3 the problem is that the sodium channel does not close properly. Mexiletine closes these channels and is believed to be usable when other therapies fail. It should be especially effective in LQT3 but there is no evidence based documentation.

*Amputation of the cervical sympathetic chain (left stellectomy). This may be used as an add-on therapy to beta blockers but modern therapy mostly favors ICD implantation if beta blocker therapy fails.

Arrhythmia termination:
Arrhythmia termination involves stopping a life-threatening arrhythmia once it has already occurred. One effective form of arrhythmia termination in individuals with LQTS is placement of an implantable cardioverter-defibrillator (ICD). Alternatively, external defibrillation can be used to restore sinus rhythm. ICDs are commonly used in patients with syncopes despite beta blocker therapy, and in patients who have experienced a cardiac arrest.

It is hoped that with better knowledge of the genetics underlying the long QT syndrome, more precise treatments will become available.
Prognosis:
The risk for untreated LQTS patients having events (syncopes or cardiac arrest) can be predicted from their genotype (LQT1-8), gender and corrected QT interval.

*High risk (>50%)
QTc>500 msec LQT1 & LQT2 & LQT3 (males)

*Intermediate risk (30-50%)
QTc>500 msec LQT3 (females)

QTc<500 msec LQT2 (females) & LQT3

*Low risk (<30%)
QTc<500 msec LQT1 & LQT2 (males)

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose

Resources:
http://www.bbc.co.uk/health/physical_health/conditions/longqt1.shtml
http://www.mayoclinic.com/health/long-qt-syndrome/DS00434
http://en.wikipedia.org/wiki/Long_QT_syndrome
http://paramedicine101.blogspot.com/2009/09/long-qt-syndrome-part-iii.html
http://www.itriagehealth.com/disease/long-qt-syndrome-(qt-prolongation)

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Categories
Ailmemts & Remedies

Arrhythmia

Definition:
The heart is a pump that functions by pushing the blood through its four chambers. The blood is “pushed” through in a controlled sequence of muscular contractions. The sequence is controlled by bundles of cells which control the electrical activity of the heart. When the sequence is disturbed, heart arrhythmias occur.

Arrhythmias are abnormal rhythms of the heart.  Arrhythmias cause the heart to pump blood less effectively.  Most cardiac arrhythmias are temporary and benign.  Most temporary and benign arrhythmias are those where your heart skips a beat or has an extra beat. The occasional skip or extra beat is often caused by strong emotions or exercise. Nonetheless, some arrhythmias may be life-threatening and require treatment.

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Types of Arrhythmias:
Arrhythmias can be divided into two main categories ventricular and supraventricular.  Supraventricular arrhythmias occur in the heart’s two upper chambers called the atrium.  Ventricular arrhythmias occur in the heart’s two lower chambers called the ventricles.


Electrical conduction in the heart originates in the SA node and travels through the AV node to the ventricles, resulting in a heart beat.
Supraventricular and Ventricular arrhythmias are further defined by the speed of the heartbeats: very slow, very fast and fast uncoordinated.  A very slow heart rate is called bradycardia.  In bradycardia, the heart rate is less than 60 beats per minute. A very fast heart rate is called Tachycardia meaning the heart beats faster than 100 beats per minute. A fast uncoordinated heart rate is called Fibrillation.  Fibrillation is the most serious form of arrhythmia are contractions of individual heart muscle fibers.  Arrhythmias cause nearly 250,000 deaths each year.

Supraventricular Arrhythmia

A very common long term arrhythmia is atrial fibrillation. Atrial fibrillation is very abnormal.  A normal heart beats between 60 and 100 times a minute. However, in atrial fibrillation, the atria (upper lobes of the heart) beat 400 to 600 times per minute. In response to this, the ventricles usually beat irregularly at a rate of 170 to 200 times per minute. So in Atrial Fibrillation, the upper part of the heart may beat up to 8 times as much as a normal heart.  Unfortunately, atrial fibrillation is seen in many types of heart disease; once established, it usually lasts a lifetime.

Ventricular Arrhythmia
One of the most serious arrhythmias is sustained ventricular tachycardia. In sustained ventricular tachycardia, there are consecutive impulses that arise from the ventricles at a heart rate of 100 beats or more per minute until stopped by drug treatment or electrical conversion. This condition is very dangerous.  It is dangerous because it may degenerate further into a totally disorganized electrical activity known as ventricular fibrillation. In ventricular fibrillation, heart’s action is so disorganized that it quivers and does not contract, thus failing to pump blood.

SADS:
SADS, or sudden arrhythmic death syndrome, is a term 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.[citation needed] Approximately 300,000 people die suddenly of this cause every year in the US.[citation needed] 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.

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

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 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.

Causes:
Many types of heart disease cause arrhythmia.  Coronary disease is often a trigger.  It triggers arrhythmia because coronary heart disease produces scar tissue in the heart.  This scar tissue disrupts the transmission of signals which control the heart rhythm.  Some people are born with arrhythmias, meaning the condition is congenital. Atherosclerosis is also a factor in causing arrhythmia. Other medical conditions such as diabetes and high blood pressure also are factors. Furthermore,  stress, caffeine, smoking, alcohol, and some over-the-counter cough and cold medicines can affect your heart’s natural beating pattern.

Diagnosis:
Many different techniques are used to diagnose arrhythmia.  The techniques include:

•A standard electrocardiogram (ECG or EKG).
An EKG is the best test for diagnosing arrhythmia. This test helps doctors analyze the electrical currents of your heart and determines the type of arrhythmia you have.

•Holter monitoring.
Holter monitoring gets a continuous reading of your heart rate and rhythm over a 24-hour period (or more). You wear a recording device (the Holter monitor), which is connected to small metal disks on your chest. With certain types of monitors, you can push a “record” button to capture a rhythm when you feel symptoms. Doctors can then look at a printout of the recording to find out what causes your arrhythmia.

•Trans telephonic monitoring. Transtelephonic monitoring documents problems that may not be detected within a 24-hour period. The devices used for this type of test are smaller than a Holter monitor. One of the devises is about the size of a beeper, the other device is worn like a wristwatch. Like with Holter monitoring, you wear the recording device. When you feel the symptoms of an arrhythmia, you can telephone a monitoring station, where a record can be made. If you cannot get to a telephone during your symptoms, you can turn on the device’s memory function. Later, you can send the recorded information to a monitoring station by using a telephone. These devices also work during episodes of fainting.

•Electrophysiology studies (EPS). Electrophysiology studies are usually performed in a cardiac catheterization laboratory. In this procedure, a long, thin tube (called a catheter) is inserted through an artery in your leg and guided to your heart. A map of electrical impulses from your heart is sent through the wire to find out what kind of arrhythmia you have and where it starts. During the study, doctors can give you controlled electrical impulses to show how your heart reacts. Medicines may also be tested at this time to see which medicines will stop the arrhythmia. Once the electrical pathways causing the arrhythmia are found, radio waves can be sent through the catheter to destroy them.

•A tilt-table exam. A tilt-table exam is a way to evaluate your heart’s rhythm in cases of fainting. The test is noninvasive, which means that doctors will not use needles or catheters. Your heart rate and blood pressure are monitored as you lie flat on a table. The table is then tilted to 65 degrees. The changing angle puts stress on the area of the nervous system that maintains your heart rate and blood pressure. Doctors can see how your heart responds under carefully supervised conditions of stress.

Treatment:

Treatment of arrhythmia depend on the type of arrhythmia, the patients age, physical condition and age.  Methods are available for prevention of arrhythmia.  These methods include relaxation techniques to reduce stress, limit intake of caffeine, nicotine, alcohol and stimulant drugs. Many arrhythmias require no treatment, they are naturally controlled by the body’s immune system. However if it is  necessary that arrhythmias must be controlled, they can be controlled by drugs, Cardioversion, Automatic implantable defibrillators or an Artificial pacemaker. Arrhythmias are very serious.

Arrhythmias that start in the lower chambers of the heart (the ventricles) are more serious than those that start in the upper chambers (the atria).

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 (you may click to see: supraventricular tachycardias). Parasympathetic nervous supply to the heart is via the vagus nerve, and these maneuvers are collectively known as vagal maneuvers.

Antiarrhy
thmic drugsMain 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.

Click  to learn more about  arrhythmia

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:
http://www.mamashealth.com/ardiag.asp
http://www.mamashealth.com/arrhythmia.asp
http://hrssc.com/hrssc-patient-resource-how-to-diagnose-arrhythmias.html
http://www.nsmc.partners.org/web/service/heart_arrhythmia
http://www1.ecardio.com/PS/Cardiac.aspx
http://www.medicompinc.com/holter_service.html

http://www.nhlbi.nih.gov/health/dci/Diseases/ekg/ekg_during.html

http://commons.wikimedia.org/wiki/File:Heart_conduct_atrialfib.gif

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