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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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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.

CLICK & SEE.…..>….(1.)..…………

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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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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Atrial Fibrillation

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Definition:
Atrial fibrillation (AF or A-fib) is the most common cardiac arrhythmia (abnormal heart rhythm) and involves the two upper chambers (atria) of the heart. Its name comes from the fibrillating (i.e. quivering) of the heart muscles of the atria, instead of a coordinated contraction. It can often be identified by taking a pulse and observing that the heartbeats don’t occur at regular intervals. However, a stronger indicator of AF is the absence of P waves on an electrocardiogram (ECG or EKG), which are normally present when there is a coordinated atrial contraction at the beginning of each heart beat. Risk increases with age, with 8% of people over 80 having AF.

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In AF, the normal electrical impulses that are generated by the sinoatrial node are overwhelmed by disorganized electrical impulses that originate in the atria and pulmonary veins, leading to conduction of irregular impulses to the ventricles that generate the heartbeat. The result is an irregular heartbeat which may occur in episodes lasting from minutes to weeks, or it could occur all the time for years. The natural tendency of AF is to become a chronic condition. Chronic AF leads to a small increase in the risk of death.

Atrial fibrillation is often asymptomatic, and is not in itself generally life-threatening, but may result in palpitations, fainting, chest pain, or congestive heart failure. People with AF usually have a significantly increased risk of stroke (up to 7 times that of the general population). Stroke risk increases during AF because blood may pool and form clots in the poorly contracting atria and especially in the left atrial appendage (LAA).[4] The level of increased risk of stroke depends on the number of additional risk factors. If a person with AF has none, the risk of stroke is similar to that of the general population. However, many people with AF do have additional risk factors and AF is a leading cause of stroke.

Atrial fibrillation may be treated with medications which either slow the heart rate or revert the heart rhythm back to normal. Synchronized electrical cardioversion may also be used to convert AF to a normal heart rhythm. Surgical and catheter-based therapies may also be used to prevent recurrence of AF in certain individuals. People with AF are often given anticoagulants such as warfarin to protect them from stroke.

Classification: The American College of Cardiology (ACC), American Heart Association (AHA), and the European Society of Cardiology (ESC) recommend in their guidelines the following classification system based on simplicity and clinical relevance.

AF Category…………… Defining Characteristics
First detected ……………….  only one diagnosed episode
Paroxysmal…………………..recurrent episodes that self-terminate in less than 7 days
Persistent……………………….recurrent episodes that last more than 7 days
Permanent……………………..an ongoing long-term episode

All atrial fibrillation patients are initially in the category called first detected AF. These patients may or may not have had previous undetected episodes. If a first detected episode self-terminates in less than 7 days and then another episode begins later on, the case has moved into the category of paroxysmal AF. Although patients in this category have episodes lasting up to 7 days, in most cases of paroxysmal AF the episodes will self-terminate in less than 24 hours. If instead the episode lasts for more than 7 days, it is unlikely to self-terminate and it is called persistent AF. In this case, the episode may be terminated by cardioversion. If cardioversion is unsuccessful or it is not attempted, and the episode is ongoing for a long time (e.g. a year or more), the patient’s AF is called permanent.

Episodes that last less than 30 seconds are not considered in this classification system. Also, this system does not apply to cases where the AF is a secondary condition that occurs in the setting of a primary condition that may be the cause of the AF.

Using this classification system, it’s not always clear what an AF case should be called. For example, a case may fit into the paroxysmal AF category some of the time, while other times it may have the characteristics of persistent AF. One may be able to decide which category is more appropriate by determining which one occurs most often in the case under consideration.

In addition to the above four AF categories, which are mainly defined by episode timing and termination, the ACC/AHA/ESC guidelines describe additional AF categories in terms of other characteristics of the patient.

#Lone atrial fibrillation (LAF) – absence of clinical or echocardiographic findings of other cardiovascular disease (including hypertension), related pulmonary disease, or cardiac abnormalities such as enlargement of the left atrium, and age under 60 years

#Nonvalvular AF – absence of rheumatic mitral valve disease, a prosthetic heart valve, or mitral valve repair

#Secondary AF – occurs in the setting of a primary condition which may be the cause of the AF, such as acute myocardial infarction, cardiac surgery, pericarditis, myocarditis, hyperthyroidism, pulmonary embolism, pneumonia, or other acute pulmonary disease

Although atrial fibrillation itself usually isn’t life-threatening, it is a medical emergency. It can lead to complications. Treatments for atrial fibrillation may include medications and other interventions to try to alter the heart’s electrical system.

Symptoms:
A heart in atrial fibrillation doesn’t beat efficiently. It may not be able to pump enough blood out to your body with each heartbeat.

Some people with atrial fibrillation have no symptoms and are unaware of their condition until it’s discovered during a physical examination. Those who do have atrial fibrillation symptoms may experience:

#Palpitations, which are sensations of a racing, uncomfortable, irregular heartbeat or a flopping in your chest
#Decreased blood pressure
#Weakness
#Lightheadedness
#Confusion
#Shortness of breath
#Chest pain

Atrial fibrillation may be:

#Occasional. In this case it’s called paroxysmal (par-ok-SIZ-mul) atrial fibrillation. You may have symptoms that come and go, lasting for a few minutes to hours and then stopping on their own.
#Chronic. With chronic atrial fibrillation, symptoms may last until they’re treated.

Time to see a doctor:-
If you have any symptoms of atrial fibrillation, make an appointment with your doctor. Your doctor should be able to tell you if your symptoms are caused by atrial fibrillation or another heart arrhythmia.

If you have chest pain, seek emergency medical assistance immediately. Chest pain could signal that you’re having a heart attack.

Causes:
To pump blood, your heart muscles must contract and relax in a coordinated rhythm. Contraction and relaxation are controlled by electrical signals that travel through your heart muscle.

Your heart consists of four chambers — two upper chambers (atria) and two lower chambers (ventricles). Within the upper right chamber of your heart (right atrium) is a group of cells called the sinus node. This is your heart’s natural pacemaker. The sinus node produces the impulse that starts each heartbeat.

Normally, the impulse travels first through the atria and then through a connecting pathway between the upper and lower chambers of your heart called the atrioventricular (AV) node. As the signal passes through the atria, they contract, pumping blood from your atria into the ventricles below. As the signal passes through the AV node to the ventricles, the ventricles contract, pumping blood out to your body.

.Sinus rhythm.

..Atrial fibrillation

In atrial fibrillation, the upper chambers of your heart (atria) experience chaotic electrical signals. As a result, they quiver. The AV node — the electrical connection between the atria and the ventricles — is overloaded with impulses trying to get through to the ventricles. The ventricles also beat rapidly, but not as rapidly as the atria. The reason is that the AV node is like a highway on-ramp — only so many cars can get on at one time.

The result is a fast and irregular heart rhythm. The heart rate in atrial fibrillation may range from 100 to 175 beats a minute. The normal range for a heart rate is 60 to 100 beats a minute.

Possible causes of atrial fibrillation :-

Abnormalities or damages to the heart’s structure are the most common cause of atrial fibrillation. Possible causes of atrial fibrillation include:

#High blood pressure
#Heart attacks
#Abnormal heart valves
#Congenital heart defects
#An overactive thyroid or other metabolic imbalance
#Exposure to stimulants such as medications, caffeine or tobacco, or to alcohol
#Sick sinus syndrome — improper functioning of the heart’s natural pacemaker
#Emphysema or other lung diseases
#Previous heart surgery
#Viral infections
#Stress due to pneumonia, surgery or other illnesses
#Sleep apnea
However, some people who have atrial fibrillation don’t have any heart defects or damage, a condition called lone atrial fibrillation. In lone atrial fibrillation, the cause is often unclear, and serious complications are rare.

Atrial flutter :
Atrial flutter is similar to atrial fibrillation, but slower. If you have atrial flutter, the abnormal heart rhythm in your atria is more organized and less chaotic than the abnormal patterns common with atrial fibrillation. Sometimes you may have atrial flutter that develops into atrial fibrillation and vice versa. The symptoms, causes and risk factors of atrial flutter are similar to those of atrial fibrillation. For example, strokes are a common concern in someone with atrial flutter. As with atrial fibrillation, atrial flutter is usually not life-threatening when it’s properly treated.

Risk Factors:-

Risk factors for atrial fibrillation include:

#Age. The older you are, the greater your risk of developing atrial fibrillation.
#Heart disease. Anyone with heart disease, including valve problems, history of heart attack and heart surgery, has an increased risk of atrial fibrillation.
#High blood pressure. Having high blood pressure, especially if it’s not well controlled with lifestyle changes or medications, can increase your risk of atrial fibrillation.
#Other chronic conditions. People with thyroid problems, sleep apnea and other medical problems have an increased risk of atrial fibrillation.
#Drinking alcohol. For some people, drinking alcohol can trigger an episode of atrial fibrillation. Binge drinking — having five drinks in two hours for men, or four drinks for women — may put you at higher risk.
#Family history. An increased risk of atrial fibrillation runs in some families.

Complications:-

Clots and stroke :
One of the most common complications with atrial fibrillation is the formation of blood clots in the heart. As the blood in the upper chambers of the heart (atria) of a patient with atrial fibrillation does not flow out in a normal manner and is very turbulent, there is a greater likelihood of blood clots forming. The clots may then find their way into the lower chambers of the heart (ventricles) and eventually end up in the lungs or in the general circulation. Clots in the general circulation may eventually block arteries in the brain, causing a stroke.

A patient with atrial fibrillation is twice as likely to develop a stroke compared to other people. 5% of patients with atrial fibrillation get a stroke each year. The risk is even greater the older the patient is. The following factors raise the risk of stroke even more for patients with atrial fibrillation:

#Hypertension (high blood pressure)
#Diabetes
#Heart failure
#A history of blood clots (embolism)

Strokes may be severe and can cause paralysis of part of the body, speech problems, and even death.

Heart failure:
If the atrial fibrillation is not controlled the heart is likely to get weaker. This may lead to heart failure. Heart failure is when the heart does not pump blood around the body efficiently or properly. The patient’s left side, right side, or even both sides of the body can be affected.

Alzheimer’s disease:
There is a strong relationship between atrial fibrillation and the development of Alzheimer’s disease, according to researchers at Researchers at Intermountain Medical Center in Salt Lake City.

Diagnosis:-
The evaluation of atrial fibrillation involves diagnosis, determination of the etiology of the arrhythmia, and classification of the arrhythmia. A minimal evaluation should be performed in all individuals with AF. This includes a history and physical examination, ECG, transthoracic echocardiogram, and routine bloodwork. Certain individuals may benefit from an extended evaluation which may include an evaluation of the heart rate response to exercise, exercise stress testing, a chest x-ray, trans-esophageal echocardiography, and other studies.

Screening
Screening for atrial fibrillation is not generally performed, although a study of routine pulse checks or ECGs during routine office visits found that the annual rate of detection of AF in elderly patients improved from 1.04% to 1.63%; selection of patients for prophylactic anticoagulation would improve stroke risk in that age category.[9]

Routine primary care visit
This estimated sensitivity of the routine primary care visit is 64%. This low result probably reflects the pulse not being checked routinely or carefully.

Minimal evaluation
The minimal evaluation of atrial fibrillation should generally be performed in all individuals with AF. The goal of this evaluation is to determine the general treatment regimen for the individual. If results of the general evaluation warrant it, further studies may be then performed.

History and physical examination
The history of the individual’s atrial fibrillation episodes is probably the most important part of the evaluation. Distinctions should be made between those who are entirely asymptomatic when they are in AF (in which case the AF is found as an incidental finding on an ECG or physical examination) and those who have gross and obvious symptoms due to AF and can pinpoint whenever they go into AF or revert to sinus rhythm.

Routine bloodwork
While many cases of AF have no definite cause, it may be the result of various other problems (see below). Hence, renal function and electrolytes are routinely determined, as well as thyroid-stimulating hormone (commonly suppressed in hyperthyroidism and of relevance if amiodarone is administered for treatment) and a blood count.

In acute-onset AF associated with chest pain, cardiac troponins or other markers of damage to the heart muscle may be ordered. Coagulation studies (INR/aPTT) are usually performed, as anticoagulant medication may be commenced

Electrocardiogram
Atrial fibrillation is diagnosed on an electrocardiogram (ECG), an investigation performed routinely whenever an irregular heart beat is suspected. Characteristic findings are the absence of P waves, with unorganized electrical activity in their place, and irregular R-R intervals due to irregular conduction of impulses to the ventricles.

When ECGs are used for screening, the SAFE trial found that electronic software, primary care physicians and the combination of the two had the following sensitivities and specificities:

#Interpreted by software: sensitivity = 83%, specificity = 99%
#Interpreted by a primary care physician: sensitivity = 80%, specificity = 92%
#Interpreted by a primary care physician with software: sensitivity = 92%, specificity = 91%

If paroxysmal AF is suspected but an ECG during an office visit only shows a regular rhythm, AF episodes may be detected and documented with the use of ambulatory Holter monitoring (e.g. for a day). If the episodes are too infrequent to be detected by Holter monitoring with reasonable probability, then the patient can be monitored for longer periods (e.g. a month) with an ambulatory event monitor.

Echocardiography.
A non-invasive transthoracic echocardiogram (TTE) is generally performed in newly diagnosed AF, as well as if there is a major change in the patient’s clinical state. This ultrasound-based scan of the heart may help identify valvular heart disease (which may greatly increase the risk of stroke), left and right atrial size (which indicates likelihood that AF may become permanent), left ventricular size and function, peak right ventricular pressure (pulmonary hypertension), presence of left ventricular hypertrophy and pericardial disease.

Significant enlargement of both the left and right atria is associated with long-standing atrial fibrillation and, if noted at the initial presentation of atrial fibrillation, suggests that the atrial fibrillation is likely to be of a longer duration than the individual’s symptoms.

Extended evaluation
An extended evaluation is generally not necessary in most individuals with atrial fibrillation, and is only performed if abnormalities are noted in the limited evaluation, if a reversible cause of the atrial fibrillation is suggested, or if further evaluation may change the treatment course.

Chest X-ray
A chest X-ray is generally only performed if a pulmonary cause of atrial fibrillation is suggested, or if other cardiac conditions are suspected (particularly congestive heart failure.) This may reveal an underlying problem in the lungs or the blood vessels in the chest.  In particular, if an underlying pneumonia is suggested, then treatment of the pneumonia may cause the atrial fibrillation to terminate on its own.

Transesophageal echocardiogram
A normal echocardiography (transthoracic or TTE) has a low sensitivity for identifying thrombi (blood clots) in the heart. If this is suspected – e.g. when planning urgent electrical cardioversion – a transesophageal echocardiogram (TEE) is preferred.

The TEE has much better visualization of the left atrial appendage than transthoracic echocardiography. This structure, located in the left atrium, is the place where thrombus is formed in more than 90% of cases in non-valvular (or non-rheumatic) atrial fibrillation or flutter. TEE has a high sensitivity for locating thrombus in this area   and can also detect sluggish bloodflow in this area that is suggestive of thrombus formation.

If no thrombus is seen on TEE, the incidence of stroke, (immediately after cardioversion is performed), is very low.

Ambulatory holter monitoring
A Holter monitor is a wearable ambulatory heart monitor that continuously monitors the heart rate and heart rhythm for a short duration, typically 24 hours. In individuals with symptoms of significant shortness of breath with exertion or palpitations on a regular basis, a holter monitor may be of benefit to determine if rapid heart rates (or unusually slow heart rates) during atrial fibrillation are the cause of the symptoms.

Exercise stress testing
Some individuals with atrial fibrillation do well with normal activity but develop shortness of breath with exertion. It may be unclear if the shortness of breath is due to a blunted heart rate response to exertion due to excessive AV node blocking agents, a very rapid heart rate during exertion, or due to other underlying conditions such as chronic lung disease or coronary ischemia. An exercise stress test will evaluate the individual’s heart rate response to exertion and determine if the AV node blocking agents are contributing to the symptoms.

Treatments:-
In some people, a specific event or an underlying condition, such as a thyroid disorder, may trigger atrial fibrillation. If the condition that triggered your atrial fibrillation can be treated, you might not have any more heart rhythm problems — or at least not for quite some time. If your symptoms are bothersome or if this is your first episode of atrial fibrillation, your doctor may attempt to reset the rhythm

The treatment option best for you will depend on how long you’ve had atrial fibrillation, how bothersome your symptoms are and the underlying cause of your atrial fibrillation. Generally, the goals of treating atrial fibrillation are to:

#Reset the rhythm or control the rate
#Prevent blood clots
The strategy you and your doctor choose depends on many factors, including whether you have other problems with your heart and if you’re able to take medications that can control your heart rhythm. In some cases, you may need a more invasive treatment, such as surgery or medical procedures using catheters.

Resetting your heart’s rhythm
Ideally, to treat atrial fibrillation, the heart rate and rhythm are reset to normal. To correct your condition, doctors may be able to reset your heart to its regular rhythm (sinus rhythm) using a procedure called cardioversion, depending on the underlying cause of atrial fibrillation and how long you’ve had it.

Cardioversion can be done in two ways:

#Cardioversion with drugs. This form of cardioversion uses medications called anti-arrhythmics to help restore normal sinus rhythm. Depending on your heart condition, your doctor may recommend trying intravenous or oral medications to return your heart to normal rhythm. This is often done in the hospital with continuous monitoring of your heart rate. If your heart rhythm returns to normal, your doctor often will prescribe the same anti-arrhythmic or a similar one to try to prevent more spells of atrial fibrillation.
#Electrical cardioversion. In this brief procedure, an electrical shock is delivered to your heart through paddles or patches placed on your chest. The shock stops your heart’s electrical activity momentarily. When your heart begins again, the hope is that it resumes its normal rhythm. The procedure is performed during anesthesia.
Before cardioversion, you may be given a blood-thinning medication, such as warfarin (Coumadin), for several weeks to reduce the risk of blood clots and stroke. Unless the episode of atrial fibrillation lasted less than 24 hours, you’ll need to take warfarin for at least four to six weeks after cardioversion to prevent a blood clot from forming even after your heart is back in normal rhythm. Warfarin is a powerful medication that can have dangerous side effects if not taken exactly as directed by your doctor. If you have any concerns about taking warfarin, talk to your doctor.

Or, instead of taking warfarin, you may have a test called transesophageal echocardiography — which can tell your doctor if you have any heart blood clots — just before cardioversion. In transesophageal echocardiography, a tube is passed down your esophagus and detailed ultrasound images are made of your heart. You’ll be sedated during the test.

Maintaining a normal heart rhythm
After electrical cardioversion, anti-arrhythmic medications often are prescribed to help prevent future episodes of atrial fibrillation. Commonly used medications include:

#Amiodarone (Cordarone, Pacerone)
#Propafenone (Rythmol)
#Sotalol (Betapace)
#Dofetilide (Tikosyn)
Although these drugs can help maintain a normal heart rhythm in many people, they can cause side effects, including:

#Nausea
#Dizziness
#Fatigue
Rarely, they may cause ventricular arrhythmias — life-threatening rhythm disturbances originating in the heart’s lower chambers. These medications may be needed indefinitely. Even with medications, the chance of another episode of atrial fibrillation is high.

Heart rate control
Sometimes atrial fibrillation can’t be converted to a normal heart rhythm. Then the goal is to slow the heart rate to between 60 and 100 beats a minute (rate control). Heart rate control can be achieved two ways:

#Medications. Traditionally, doctors have prescribed the medication digoxin (Lanoxin). It can control heart rate at rest, but not as well during activity. Most people require additional or alternative medications, such as calcium channel blockers or beta blockers.
#Atrioventricular (AV) node ablation. If medications don’t work, or you have side effects, AV node ablation may be another option. The procedure involves applying radio frequency energy to the pathway connecting the upper and lower chambers of your heart (AV node) through a long, thin tube (catheter) to destroy this small area of tissue.

The procedure prevents the atria from sending electrical impulses to the ventricles. The atria continue to fibrillate, though, and anticoagulant medication is still required. A pacemaker is then implanted to establish a normal rhythm. After AV node ablation, you’ll need to continue to take blood-thinning medications to reduce the risk of stroke, because your heart rhythm is still atrial fibrillation.

Other surgical and catheter procedures
Sometimes medications or cardioversion to control atrial fibrillation doesn’t work. In those cases, your doctor may recommend a procedure to destroy the area of heart tissue that’s causing the erratic electrical signals and restore your heart to a normal rhythm. These options can include:

#Radiofrequency catheter ablation. In many people who have atrial fibrillation and an otherwise normal heart, atrial fibrillation is caused by rapidly discharging triggers, or “hot spots.” These hot spots are like abnormal pacemaker cells that fire so rapidly that the upper chambers of your heart quiver instead of beating efficiently.

Radiofrequency energy directed to these hot spots through a catheter inserted in an artery near your collarbone or leg may be used to destroy these hot spots, scarring the tissue so the erratic electrical signals are normalized. This corrects the arrhythmia without the need for medications or implantable devices. In some cases, other types of catheters that can freeze the heart tissue (cryotherapy) are used.

#Surgical maze procedure. The maze procedure is often done during an open-heart surgery. Using a scalpel, doctors create several precise incisions in the upper chambers of your heart to create a pattern of scar tissue. Because scar tissue doesn’t carry electricity, it interferes with stray electrical impulses that cause atrial fibrillation. Radiofrequency or cryotherapy can also be used to create the scars, and there are several variations of the surgical maze technique. The procedure has a high success rate, but because it usually requires open-heart surgery, it’s generally reserved for people who don’t respond to other treatments or when it can be done during other necessary heart surgery, such as coronary artery bypass surgery or heart valve repair. Some people need a pacemaker implanted after the procedure.

Preventing blood clots
Most people who have atrial fibrillation or who are undergoing certain treatments for atrial fibrillation are at especially high risk of blood clots that can lead to stroke. The risk is even higher if other heart disease is present along with atrial fibrillation. Your doctor may prescribe blood-thinning medications (anticoagulants) such as warfarin (Coumadin) in addition to medications designed to treat your irregular heartbeat. Many people have spells of atrial fibrillation and don’t even know it — so you may need lifelong anticoagulants even after your rhythm has been restored to normal. If you’re prescribed warfarin, carefully follow your doctor’s instructions on taking it. Warfarin is a powerful medication that can have dangerous side effects.

Change of Lifestyle :

You may need to make lifestyle changes that improve the overall health of your heart, especially to prevent or treat conditions such as high blood pressure. Your doctor may suggest that you:

#Eat heart-healthy foods and avoid Junk or Fast food
#Reduce your salt intake, which can help lower blood pressure
#Increase your physical activity
#Quit smoking
#Pratice regular Exercise Or walk for about 45 minutes daily

Avoid drinking more than one drink of alcohol for women or more than two drinks for men a day.

Prevention:-
There are some things you can do to try to prevent recurrent spells of atrial fibrillation. You may need to reduce or eliminate caffeinated and alcoholic beverages from your diet, because they can sometimes trigger an episode of atrial fibrillation. It’s also important to be careful when taking over-the-counter (OTC) medications. Some, such as cold medicines containing pseudoephedrine, contain stimulants that can trigger atrial fibrillation. Also, some OTC medications can have dangerous interactions with anti-arrhythmic medications.

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/Atrial_fibrillation
http://www.mayoclinic.com/health/atrial-fibrillation/DS00291
http://www.medicalnewstoday.com/info/atrial-fibrillation/

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Categories
Health Quaries

Some Health Quaries & Answers

Towering disturbance:-…....CLICK & SEE

Q: I own a flat on the third (top) floor of a building. The residents’ association has leased out the terrace to a cell phone company which has erected a tower there. I have a pacemaker and am worried about the impact of the signals from the tower on my heart. What should I do?

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A: Signals from microwaves and cell phones do affect pacemakers. Irregularities in the heart rate have been noticed when a phone is held even 15cm away from the pacemaker. When you are living just under a phone tower, the signal is likely to be strong and powerful. The first symptoms of the pacemaker being affected are a feeling of faintness and irregularity in your pulse rate. You can be fitted with a 24-hour monitoring device by your cardiologist. This will document any irregularity, so you know it is real and not psychological.

If there are any changes, it may make sense to move. Your building association is unlikely to cancel a financially lucrative enterprise and get the tower relocated.

Circumcise to protect:-

Q: I read that circumcision offers protection against AIDS. I wonder if I should get my one-year-old son circumcised.

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A: Circumcision is a surgical procedure that involves removal of the skin and mucosal tissue that covers the glans, the tip of the penis. Circumcision is unconditionally practised by Jews and Muslims. It is a part of their religious culture. In others it is usually performed if the foreskin gets stuck (phimosis) or infected. It does help in the prevention of AIDS and other sexually transmitted diseases. But it does not give 100 per cent protection.

All operations can have complications. Problems like infection or bleeding, though rare, can arise after the surgery. Unless your son’s paediatrician has advised circumcision for a particular reason, it does not make sense to put him through elective surgery. When he is older, teaching him about responsibility, sexual norms and safe sex may be a better option.

Yellow vs white:-

Q: There are natural and “artificial” eggs available in the market. The colour of the yolk in the two differs. Is there a difference in their nutritive values? Is eating eggs healthy?

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A: Eggs contain easily digestible proteins, fats, vitamins and antioxidants. They are a complete food in themselves. The recommended intake is one egg a day for those with a normal lipid profile (cholesterol and triglycerides). If the lipids are raised, cutting down on yolks to a maximum of two per week would be fine. Egg whites do not add to the cholesterol level, and you can eat as many of these as you like.

The colour of the yolk only depends on the type of feed the hen has received. It does not affect the egg’s nutritive value. By natural eggs, I think you mean those laid by hens that roam free, and by “artificial” the ones that are laid in hatcheries. Nutrition-wise, both are the same.

Music mania:-

Q: My daughter listens to music the whole day. I don’t like it, but do not want to put a stop to it unless it is harmful.

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A: If your daughter is listening to music instead of doing her homework or studying, perhaps you need to interfere. But do check her academic performance first. Listening to music does have many positive effects. It soothes, pacifies and relieves tension in children and in adults. Music during exercise provides a cognitive boost, in addition to the other benefits of regular activity. Loud music, on the other hand, can damage hearing, increase the heart rate and produce paradoxical excitement.

Unequal feet:

Q: My shoes never fit both the feet perfectly. One is always a little loose or tight.

A: A person’s feet may not be identical in shape and size. One is usually marginally larger than the other. If this difference is marked, footwear will never fit properly. It is better to buy a bigger size and wear two socks on the foot that is smaller. Otherwise, you have to buy two pairs of shoes.

Cauliflower ear:

Q: I pierced my ear in the upper part, in addition to the ear lobe. It has become red, swollen and painful. My ear now looks ugly and deformed. What should I do?

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A: The condition you are describing is called “cauliflower ear”. It occurs when a blood clot develops in the cartilage of the ear as a result of injury. The accumulated blood becomes infected and this destroys the cartilage, making it shrunken and shrivelled.

As soon as there is pain and swelling owing to an injury (even piercing), it should be treated with ice packs and antibiotics. Once it becomes misshapen, cosmetic reconstruction by a plastic surgeon is the only option.

Sources: The Telegraph (Kolkata, India)

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