Tag Archives: American College of Cardiology

Easy Breathing

Breathing is an involuntary action, coordinated by respiratory centres deep in the brain. It is not really possible to die by voluntarily holding one’s breath, as without practice and training, apnoea (not breathing) cannot be sustained for more than 1-2 minutes. This is because “breath holding” results in accumulation of carbon dioxide in the blood and a drop in the blood pH. The respiratory centre in the brain is automatically stimulated. Breathing sets in.

Sleep apnoea (cessation of breathing during sleep) can occur in adults, usually middle-aged overweight males with a thick neck. It can occur in all ages and both sexes, especially if the tonsils or adenoids are enlarged, there is a deviated nasal septum or GERD (gastro esophageal reflux disease). Sleep apnoea can cause high blood pressure, stroke, heart disease, and daytime drowsiness. Academic performance and decision making at work can suffer. There may be daytime lapses in concentration, which can cause accidents.


Mild cases of sleep apnoea respond to weight loss and exercise. Severe cases may require CPAP (Continuous Positive Airways Pressure), or surgery.

Reactive Airways Disease or name bronchial asthma is a condition where the smaller airways in the lungs constrict when exposed to many triggers. These may be a viral or bacterial infection, pollen, food, or odours in the air. As the breathing pipes become smaller, the outflow of air is obstructed and there is whistling sound with each breath. The person may start coughing vigorously or panic as they feel the air supply is being cut off.

This can be tackled with nebulisers, inhalers and rotahalers. These devices deliver dilating medication directly to the breathing pipes. The effect is almost instantaneous and there are practically no side effects.

Our airways are designed to filter out dust and other harmful particles. Unfortunately our inbuilt air purification system can only filter out particles of 2·5 µm (PM2 ) in diameter. The smaller – found around us both indoors and out – can enter the lungs. Indoor pollution comes from the use of solid fuels, such as coal, wood, or charcoal (even when it is only used to heat water), burning rubbish and waste, particularly plastic. Cigarette smoke harms the smoker and the polluting particles secondarily affect others in the environment. Agarbattis release many polluting chemicals as do mosquito repelling coils, mats and liquids.

Industrialisation and urbanisation have? resulted in fossil fuels being used in factories and for transport. Smoke from factories is sent high into the sky through industrial chimneys, but that just means that the particles spread over a wider area. The petrol and diesel vehicles on the road also emit particulate material and harmful gases. Seven million deaths occur annually because of air pollution alone. Pregnant women and children are particularly vulnerable. Constant exposure to a polluted environment affects long-term growth and cognitive ability in children. If we keep polluting the environment like this, our IQ levels will be affected.
Eventually, constant exposure to pollutants over many years can also result in COPD (chronic obstructive pulmonary disease) with breathlessness with the slightest activity. This too is treated with nebulisers and inhalers.

• We all breathe but this does not mean we breathe correctly. Lungs need regular breathing exercises and correction of faulty breathing techniques. Yoga corrects the technique.

• Exercise early in morning when pollution is less or indoors in a gym.

• Keep indoor plants in your home. They reduce particulate matter and pollutants.

Source: The Telegraph (India, Kolkata)


Long QT Syndrome

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.
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.

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.

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.
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


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Atrial Fibrillation

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.



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.

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
#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.

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.


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)
#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.

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 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

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.

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.

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:

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.

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.


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Steps on Enlarged Heart ‘Uncovered’

Researchers in the US claim to have got new insight into the mechanisms that underlie an enlarged heart — a finding that could lead to development of new treatment for managing this common cardiac ailment.

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An enlarged heart can lead to heart failure (Image: CNRI, Science Photo Library)

According to them, high blood pressure, heart valve disease and heart attacks can lead to a abnormal thickening of the heart muscle, called myocardial hypertrophy, which plays a role in the pathological increase in the heart size.

At the molecular level, signals driving myocardial hypertrophy, like elevated levels of catecholamine hormones, activate the Myocyte Enhancer Factor (MEF) proteins. This alters gene expression in heart muscle cells and induces an adverse developmental paradigm known as “fetal gene response”.

“Previous research has shown that the signalling pathways leading to MEF2 are altered during pathological cardiac hypertrophy. Although we know that enzymes called histone deacetylases (HDACs) control MEF2 activity, it was not clear that HDACs and MEF2 were integrated into a larger signalling unit,” lead author John D Scott said.

To further identify the molecular mechanisms associated with cardiac hypertrophy, Scott and colleagues at the University of Washington studied cardiac A-Kinase Anchoring Proteins (AKAPs), which are known to play a critical role in organising signalling complexes in response to catecholamine hormones and transmitted signals within cells.

The researchers found that AKAP-Lbc functions as a scaffolding protein that selectively directs catecholamine signals to the transcriptional machinery to potentiate the hypertrophic response, the ‘Cell Press‘ journal reported.

“Our study supports a model where AKAP-Lbc facilitates activation of protein kinase D, which in turn phosphorylates the histone deacetylase HDAC5 to promote its export from the nucleus. The reduction in nuclear HDAC5 favoured MEF2 transcription and onset of cardiac hypertrophy,” Scott said.

Sources: The Times Of India

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Omega-3’s Protect Against Clogged Arteries

A diet rich in omega-3 fats may explain why middle-aged men in Japan have fewer problems with clogged arteries than similar men in theUnited States.s.

The research found that Japanese men living in Japan had twice the blood levels of omega-3 fats, and also lower levels of atherosclerosis, compared to middle-aged white men or Japanese-American men living in the United States.

Atherosclerosis is the buildup of plaque inside your arteries. Over time, they can lead to serious problems like heart attacks and stroke.

Nutritional studies show that intake of omega-3 fats averages 1.3 grams per day in Japan, compared to 0.2 grams per day in the United States.

Reuters July 28, 2008
Journal of the American College of Cardiology August 2008; 52:417-424

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