Heart Murmur


A murmur is a sound which can be heard through a stethoscope while a physician listens over the heart.

Also Known As: Heart Murmur

Basic Facts

  • A murmur is a sound which can be heard through a stethoscope while a physician listens over the heart.
  • The sound is usually created by blood moving through heart valves.
  • Most murmurs do not indicate a serious problem.  In some cases, significant heart valve abnormalities or congenital heart defects may first be detected because of a heart murmur.

A More Detailed Explanation

When fluid is forced out of a container through a small opening, turbulence is created and the fluid sprays out.  This spray can even create a sound, especially if the opening is very small or irregular and the force is large.  With every heart beat, our hearts move blood from containers (upper and lower chambers of the heart) through small openings (the heart valves).  So some turbulence of blood within our hearts is normal, and may even create a sound (murmur) which can be heard with a stethoscope.

Murmurs reflecting normal heart function can be heard in young people (because their hearts pump more vigorously in general), in thin individuals (because the stethoscope is physically closer to the heart), and in pregnant women (because of the more dynamic circulation required to supply blood to both the mother and fetus).  Since valve openings are actually pretty generous, the murmurs associated with normal heart function are usually quite soft.

In most normal individuals, valves “leak” a little when they are in the closed position.  In fact, echocardiograms (ultrasound evaluations of the heart) display a tiny leak in one or more heart valves in well over 80% of normal patients.  Because the “opening” in a closed leaky heart valve is usually very small, the murmur created can be fairly loud.  In fact, severe leaks (due to large openings) may produce very soft murmurs or no murmurs at all.

When valves are structurally abnormal (due to a congenital heart abnormality; due to prior damage from rheumatic fever; due to simple wear and tear over the years; etc.) the valve opening can be irregular or reduced in size, creating more turbulence of flow.  This can create a heart murmur.  The smaller, the more irregular the opening, the louder and higher pitched the murmur will be.  Most structural valve abnormalities worsen very gradually over time.  Physicians can use the changing sound characteristics of a heart murmur to detect progression of an underlying valve problem.

Some people are born with “holes” in their hearts – communications between the ventricles (pumping chambers) or atria (the upper chambers).  Usually the communication between ventricles (ventricular septal defect, VSD) is quite small, and can be associated with a very loud murmur and even a “thrill” (a vibration which can be felt by placing one’s hand on the patient’s chest).  Because the atria are low pressure chambers, communications between them (atrial septal defect, ASD) don’t usually produce a very loud murmur.

Sometimes, a heart murmur is present not because of a structural issue in the heart, but because the circulation of blood through the heart is exceptionally dynamic.  We have already mentioned young individuals and pregnant women.  Patients with anemia or an overactive thyroid may have a murmur due to the dynamic circulation caused by these conditions.

What to Expect

If your doctor has detected a murmur while listening over your heart with a stethoscope, he or she may order an echocardiogram  to determine the cause.  In most cases, the heart murmur will not be representative of a major health problem.  Sometimes, the murmur will point to an underlying structural heart abnormality, which will require follow-up and specific management.


**Source: Cardiosource- American College of Cardiology.



Cardiomyopathy refers to diseases of the heart muscle. These diseases have a variety of causes, symptoms, and treatments. In cardiomyopathy, the heart muscle becomes enlarged or abnormally thick or rigid. In rare cases, the muscle tissue in the heart is replaced with scar tissue.

Also Known As: Dilated Cardiomyopathy, Hypotrophic Cardiomyopathy, Restrictive Cardiomyopathy

Basic Facts

  • Cardiomyopathy refers to diseases of the heart muscle. It has a variety of causes, symptoms, and treatments.
  • In cardiomyopathy, the heart muscle becomes enlarged or abnormally thick or rigid. In rare cases, the muscle tissue in the heart is replaced with scar tissue.
  • The four major types of cardiomyopathy are dilated, hypertrophic, and restrictive cardiomyopathy and arrhythmogenic right ventricular dysplasia.
  • Some types of cardiomyopathy are caused by a gene mutation and run in families. Other types are a result of another disease or condition, such as damage to the heart from a heart attack, high blood pressure, or a viral infection. In many cases, the cause is unknown.
  • Cardiomyopathy can affect people of all ages, from babies to older adults. However, certain age groups are more likely to have certain types of cardiomyopathy.
  • Signs and symptoms of cardiomyopathy can include:
  • Tiredness
  • Weakness
  • Shortness of breath after exercise or even at rest
  • Swelling of the abdomen, legs, ankles, and feet
  • Dizziness, lightheadedness, or fainting during exercise
  • Abnormal heart rhythms (arrhythmias) or an extra or unusual sound heard during the heartbeat (heart murmur)
  • Cardiomyopathy is diagnosed using a medical history, physical exam, and tests such as chest x ray, electrocardiogram, echocardiogram, stress test, and blood tests.
  • Because cardiomyopathy often runs in families, doctors may recommend that the parents, brothers and sisters, and children of people with cardiomyopathy be tested for the disease.
  • Treatments depend on the type of cardiomyopathy, how severe the symptoms and complications are, and the age and overall health of the person.
  • The main goals of treatment are to manage any conditions that cause or contribute to the cardiomyopathy, control symptoms, stop the disease from getting worse, and reduce complications and the chance of sudden cardiac death.
  • Treatment may involve medicines, surgery, nonsurgical procedures, or lifestyle changes.
  • Cardiomyopathy can sometimes be prevented by managing or preventing the underlying condition that causes the disease. Cardiomyopathy that runs in families cannot be prevented.
  • Some people live long, healthy lives despite having cardiomyopathy. Some people don’t even realize that they have the disease because they have no symptoms. In other people, the disease develops rapidly, symptoms are severe, and serious complications develop. Current treatments can do much to reduce symptoms and help people live healthy lives.

Types of Cardiomyopathy

Dilated Cardiomyopathy

Dilated cardiomyopathy is the most common form of cardiomyopathy. It generally occurs in adults aged 20 to 60 years. Men are more likely than women to develop dilated cardiomyopathy.

Dilated cardiomyopathy affects the heart’s ventricles (VEN-trih-kuls) and atria. The ventricles are the two lower chambers of the heart, and the atria are the two upper chambers. Dilated cardiomyopathy usually starts in the left ventricle, where the heart muscle begins to dilate or stretch and become thinner. This leads to enlargement of the inside of the ventricle. The problem often spreads to the right ventricle and then to the atria as the disease gets worse.

When the chambers dilate, the heart can’t pump blood very well. The heart tries to cope by dilating the chambers even more. Over time, the heart becomes weaker and heart failure can occur. Symptoms of heart failure include feeling tired, swelling of the legs and feet, and shortness of breath. Dilated cardiomyopathy also can lead to heart valve problems, arrhythmias, and blood clots in the heart. Having advanced dilated cardiomyopathy is a common reason for needing a heart transplant.

Up to one-half of all cases of dilated cardiomyopathy may be hereditary (passed down in the genes from parent to child). These cases are called familial dilated cardiomyopathy. Dilated cardiomyopathy also can be a complication of many conditions, including coronary artery disease and high blood pressure. It also can be caused by viral infections, excessive use of alcohol, and exposure to certain drugs (including cocaine, amphetamines, and some drugs used in cancer treatments). In some cases, no cause can be found.

Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathy occurs when the heart muscle thickens abnormally. The thickening generally happens in the left ventricle, the heart’s main pumping chamber. This type of cardiomyopathy can affect people of any age.

Hypertrophic cardiomyopathy can be obstructive or nonobstructive. In the obstructive type, the septum (the wall that divides the left and right sides of the heart) thickens and bulges into the left ventricle. This bulge blocks the flow of blood out of the ventricle. The ventricle must work much harder to pump blood past the blockage and out to the body. Symptoms can include chest pain, dizziness, shortness of breath, or fainting.

Obstructive hypertrophic cardiomyopathy also can affect the heart’s mitral (MI-trul) valve, causing blood to leak backward through the valve.

In nonobstructive hypertrophic cardiomyopathy, the thickened heart muscle does not block the flow of blood out of the ventricle. The entire ventricle may become thicker (symmetric ventricular hypotrophy) or it may happen only at the bottom of the heart (apical hypertrophy). The right ventricle also may be affected.

In both kinds of hypertrophic cardiomyopathy, the thickened muscle makes the inside of the left ventricle smaller so that it holds less blood. The walls of the ventricles also may become stiff. As a result, they are less able to relax and fill with blood. This causes increased pressure in the ventricles and the blood vessels of the lungs. Changes also occur to the cells in the damaged heart muscle. This may interfere with the heart’s electrical signals, leading to arrhythmias.

Some people with hypertrophic cardiomyopathy have no symptoms, and the condition does not affect their lives. Others have severe symptoms or develop complications such as serious arrhythmias. A few people with the condition have sudden cardiac arrest because of dangerous arrhythmias.

Hypertrophic cardiomyopathy can be inherited because of a gene mutation or develop over time because of high blood pressure or aging. Often, the cause is unknown.

Restrictive Cardiomyopathy

Restrictive cardiomyopathy tends to mostly affect older adults. In this cardiomyopathy, the ventricles become stiff and rigid due to replacement of the normal heart muscle with abnormal tissue, such as scar tissue. As a result, the ventricles cannot relax normally and expand to fill with blood, which causes the atria to become enlarged. Eventually, blood flow in the heart is reduced, and complications such as heart failure or arrhythmias occur.

Restrictive cardiomyopathy can occur for no known reason, or it can develop because the person has another disease. Some of the diseases that can cause restrictive cardiomyopathy include hemochromatosis, sarcoidosis, amyloidosis, and connective tissue disorders. Restrictive cardiomyopathy also can occur as a result of radiation treatments, infections, or scarring after surgery.

Arrhythmogenic Right Ventricular Dysplasia

Arrhythmogenic right ventricular dysplasia (ARVD) is a rare type of cardiomyopathy. ARVD develops when the muscle tissue in the right ventricle dies and is replaced with scar tissue. This process causes problems in the heart’s electrical signaling, resulting in arrhythmias. Symptoms include a feeling of strong or irregular heartbeats (palpitations) and fainting after exercise.

ARVD usually develops in teens or young adults and is often the cause of sudden cardiac death in young athletes. ARVD is thought to be an inherited disease.

What Causes Cardiomyopathy?

Many times, the cause of cardiomyopathy is unknown. When this happens, the disease is called idiopathic (or primary) cardiomyopathy. The majority of cardiomyopathies in children are idiopathic.

Sometimes, cardiomyopathy is inherited (passed down in the genes from parent to child) or caused by another disease or condition.

Dilated Cardiomyopathy

Dilated cardiomyopathy can be inherited. It also can be caused by certain diseases, conditions, and substances, including:

  • Coronary artery disease and heart attacks (ischemic cardiomyopathy)
  • Infections, especially viral infections that cause the heart muscle to become inflamed (myocarditis)
  • Alcohol, especially when a person has a poor diet (alcoholic cardiomyopathy)
  • Complications during the last month of pregnancy or within 5 months of birth (peripartum cardiomyopathy)
  • Certain toxins, such as cobalt
  • Certain drugs, such as cocaine, amphetamines, and two medicines used to treat cancer (doxorubicin and daunorubicin)
  • Diseases such as diabetes and thyroid disease

Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathy can be inherited. It also can develop over time because of high blood pressure or aging. Often, the cause of hypertrophic cardiomyopathy is unknown.

Restrictive Cardiomyopathy

Certain diseases and conditions can cause restrictive cardiomyopathy, including:

  • Hemochromatosis, a condition in which too much iron is deposited into tissues, including heart tissue
  • Amyloidosis, a disease in which abnormal proteins are deposited into heart tissue
  • Sarcoidosis, a disease in which inflammation produces tiny lumps of cells in various organs in the body, including the heart
  • Connective tissue disorders

Arrhythmogenic Right Ventricular Dysplasia

Arrythmogenic right ventricular dysplasia is thought to be an inherited disease.

Who Is At Risk for Cardiomyopathy?

People of all ages can develop cardiomyopathy, but certain cardiomyopathies are more common in certain groups:

  • African Americans are more likely to have dilated cardiomyopathy compared to Caucasians.
  • Men are more likely to have dilated cardiomyopathy compared to women.
  • Teens and young adults are more likely to have arrhythmogenic right ventricular dysplasia compared to older people.

Major Risk Factors

Major risk factors for developing cardiomyopathy include:

  • Having a family history of cardiomyopathy, heart failure, or sudden cardiac death
  • Having a disease or condition that can lead to cardiomyopathy, such as:
  • Coronary artery disease
  • A previous heart attack
  • Myocarditis
  • Diseases that can damage the heart (for example, hemochromatosis, sarcoidosis, or amyloidosis)
  • Long-term alcoholism
  • Long-term high blood pressure
  • Diabetes and other metabolic diseases

Some people with cardiomyopathy never have symptoms. That is why it’s important to identify people who may be at high risk for this disease so that potential problems (such as serious arrhythmias or sudden cardiac death) can be prevented.

What Are the Signs and Symptoms of Cardiomyopathy?

Some people with cardiomyopathy never have symptoms, and others have no symptoms in the early stages of the disease. As cardiomyopathy progresses and the heart weakens, signs and symptoms of heart failure usually appear. These signs and symptoms include:

  • Tiredness
  • Weakness
  • Shortness of breath after exercise or even at rest
  • Swelling of the abdomen, legs, ankles, and feet

Other signs and symptoms can include dizziness, lightheadedness, fainting during exercise, abnormal heart rhythms (arrhythmias), and an extra or unusual sound heard during the heartbeat (heart murmur).

How Is Cardiomyopathy Diagnosed?

If cardiomyopathy is suspected, the diagnosis is based on a person’s:

  • Symptoms and medical history
  • Family history of cardiomyopathy, heart failure, or sudden cardiac arrest
  • Physical exam
  • Results on diagnostic tests and procedures

The physical exam will identify a number of findings in patients with cardiomyopathy. The doctor will use a stethoscope to listen to the person’s heart and lungs for sounds that may suggest the presence of cardiomyopathy. These sounds may even indicate a certain type of cardiomyopathy. For example, the loudness, timing, and location of a heart murmur may suggest that a person has hypertrophic obstructive cardiomyopathy. A “crackling” sound in the lungs may be a sign of heart failure, which often develops in the later stages of cardiomyopathy.

Physical signs also help the doctor diagnose cardiomyopathy. Swelling of the abdomen, legs, or feet may indicate excess fluid, which is a sign of heart failure.

Sometimes, doctors discover cardiomyopathy during a routine exam if they hear a heart murmur or if the patient has an abnormal electrocardiogram.

Diagnostic Tests and Procedures

Doctors may order one or more tests to diagnose cardiomyopathy, including:

  • EKG (electrocardiogram). This test measures the rate and regularity of the heartbeat and can detect arrhythmias.
  • Holter monitor (ambulatory EKG/ECG). This test records the EKG readings for a continuous 24-hour period. It can detect arrhythmias that occur only rarely throughout the day. A small monitoring device is attached to patches (electrodes) that are placed on the patient’s chest. The device is carried in a pouch around the neck or attached to a belt.
  • Echocardiogram. This test uses sound waves to create a moving picture of your heart. Echocardiogram provides information about the size and shape of your heart and how well your heart chambers and valves are functioning. The test also can identify areas of poor blood flow to the heart, areas of heart muscle that are not contracting normally, and previous injury to the heart muscle caused by poor blood flow.
  • There are several different types of echocardiograms, including a stress echocardiogram. During this test, an echocardiogram is done both before and after your heart is stressed either by having you exercise or by injecting a medicine into your bloodstream that makes your heart beat faster and work harder. A stress echocardiogram is usually done to find out if you have decreased blood flow to your heart (coronary artery disease). Echocardiogram is a good way to diagnose hypertrophic cardiomyopathy because it shows the thickened walls of the heart.
  • Transesophageal (tranz-ih-sof-uh-JEE-ul) echocardiography (TEE). In this test, the doctor inserts an ultrasound probe into the throat after the patient is sedated. TEE provides a view of the back of the heart.
  • Stress Test. Some heart problems are easier to diagnose when your heart is working harder and beating faster than when it’s at rest. During stress testing, you exercise (or are given medicine if you are unable to exercise) to make your heart work harder and beat faster while heart tests are performed.
  • During exercise stress testing, your blood pressure and EKG readings are monitored while you walk or run on a treadmill or pedal a bicycle. Other heart tests, such as nuclear heart scanning or echocardiography, also can be done at the same time. These would be ordered if your doctor needs more information than the exercise stress test can provide about how well your heart is working.
  • If you are unable to exercise, a medicine can be injected through an intravenous line (IV) into your bloodstream to make your heart work harder and beat faster, as if you are exercising on a treadmill or bicycle. Nuclear heart scanning or echocardiography is then usually done.
  • During nuclear heart scanning, radioactive tracer is injected into your bloodstream, and a special camera shows the flow of blood through your heart and arteries. Echocardiography uses sound waves to show blood flow through the chambers and valves of your heart and to show the strength of your heart muscle.
  • Your doctor also may order two newer tests along with stress testing if more information is needed about how well your heart works. These new tests are magnetic resonance imaging (MRI) and positron emission tomography (PET) scanning of the heart. MRI shows detailed images of the structures and beating of your heart, which may help your doctor better assess if parts of your heart are weak or damaged. PET scanning shows the level of chemical activity in different areas of your heart. This can help your doctor determine if enough blood is flowing to the areas of your heart. A PET scan can show decreased blood flow caused by disease or damaged muscles that may not be detected by other scanning methods.
  • Chest x ray. A chest x ray takes a picture of the organs and structures inside the chest, including the heart, lungs, and blood vessels. This test can show whether the heart is enlarged or whether fluid is building up in the lungs.
  • Blood tests, such as complete blood count, blood chemistries, and cardiac enzymes. These tests are done to provide information on the condition of the heart and to rule out other conditions.

The doctor may order additional tests to confirm the diagnosis or if surgery is planned. These tests may include:

  • Cardiac catheterization. With this test doctors can check the pressure and blood flow in the heart’s chambers, collect blood samples from the heart, and examine the arteries of the heart using x ray. A thin, flexible tube (catheter) is passed through an artery in the upper thigh (groin) or in the arm to reach the coronary arteries. This allows the doctor to study the inside of the arteries to look for blockages.
  • Coronary angiography. This test is usually performed along with cardiac catheterization. Angiography enables the doctor to see the flow of blood to the heart muscle. A dye that can be seen on an x ray image is injected into the coronary arteries. Dye also can be injected into the chambers to evaluate the pumping function of the heart.
  • Myocardial biopsy. In this test, the doctor removes a piece of heart muscle to look at under a microscope. The biopsy can be done during a cardiac catheterization and is useful in diagnosing some types of cardiomyopathy.

Because some types of cardiomyopathy run in families, the doctor may recommend looking for the disease in the parents, brothers and sisters, and children of people with cardiomyopathy.

Genetic counseling may be recommended. Genetic counseling is useful to help define and explain how the disease runs in families and to determine the chances of parents passing it on to their children.

How Is Cardiomyopathy Treated?

Not everyone with cardiomyopathy needs treatment. People who have no symptoms may not need treatment. In some cases, dilated cardiomyopathy that comes on suddenly may even go away on its own. For other people with cardiomyopathy, treatment is necessary.

Specific treatments depend on the type of cardiomyopathy, how severe the symptoms and complications are, and the age and overall health of the person.

Goals of Treatment

The main goals of treating cardiomyopathy are to:

  • Manage any conditions that cause or contribute to the cardiomyopathy
  • Control symptoms so that the person can live as normally as possible
  • Stop the disease from getting worse
  • Reduce complications and the chance of sudden cardiac death

Specific Types of Treatment

Treatments for cardiomyopathy may include medicines, surgery, nonsurgical procedures, and lifestyle changes.


A number of medicines may be used to treat cardiomyopathy, including:

  • Diuretics, which remove excess fluid and sodium from the body.
  • Angiotensin-converting enzyme (ACE) inhibitors, which lower blood pressure and reduce stress on the heart.
  • Beta-blockers, which slow the heart rate by reducing the speed of the heart’s contractions. These medicines also lower blood pressure.
  • Calcium channel blockers, which slow a rapid heartbeat by reducing the force and rate of heart contractions. These medicines also lower blood pressure.
  • Digoxin, which increases the force of heart contractions and slows the heartbeat.
  • Anticoagulants, which prevent blood clots from forming. Anticoagulants are often used in the treatment of dilated cardiomyopathy.
  • Antiarrhythmia medicines, which keep the heart beating in a normal rhythm.
  • Antibiotics, which are used before dental or surgical procedures. Antibiotics help to prevent endocarditis, an infection of the heart walls, valves, and vessels.
  • Corticosteroids, which reduce inflammation.


Doctors can use several different types of surgery to treat cardiomyopathy, including removing part of the enlarged heart muscle (septal myectomy) and implanting devices that help the heart beat more effectively. Heart transplant is sometimes used in cases of severe heart failure.

Septal myectomy. Septal myectomy (also called septal myomectomy) is open-heart surgery for people with hypertrophic obstructive cardiomyopathy and severe symptoms. It is generally used in younger patients and when medicines aren’t working well.

In septal myectomy, a surgeon removes part of the thickened septum that is bulging into the left ventricle. This widens the pathway in the ventricle that leads to the aortic valve and improves blood flow through the heart and out to the body. The tissue that is removed does not grow back. If necessary, the mitral valve can be repaired or replaced at the same time. This surgery is often successful, and the person can return to a normal life with no symptoms.

Surgically implanted devices. Surgeons can place several different types of devices in the heart to help it beat more effectively. One device is a pacemaker, which electronically helps maintain normal heart rhythm. Sometimes, doctors choose to use a biventricular pacemaker, which coordinates contractions between the heart’s left and right ventricles.

A left ventricular assist device (LVAD) helps the heart pump blood to the body. LVAD can be used as a long-term therapy or as a short-term treatment for people who are waiting for a heart transplant.

An implantable cardioverter defibrillator (ICD) is used in people who are at risk of life-threatening arrhythmia or sudden cardiac death. This small device is implanted in the chest and connected to the heart with wires. If the ICD senses a dangerous change in heart rhythm, it will send an electric shock to the heart to restore a normal heartbeat.

Heart transplant. In this surgery, a doctor replaces a person’s diseased heart with a healthy heart from a person who has recently died. It is a last resort for people with heart failure when all other treatments have failed.

Nonsurgical Procedure

Alcohol septal ablation. In this procedure, a doctor injects ethanol (a type of alcohol) through a catheter into the small artery that supplies blood to the thickened area of heart muscle. The alcohol kills the cells and the thickened tissue shrinks to a more normal size. Blood can flow freely through the pathway in the ventricle that leads to the aortic valve, and symptoms improve.

Lifestyle Changes

The doctor may recommend lifestyle changes to manage a condition that is causing the cardiomyopathy. These changes may help reduce symptoms. Lifestyle changes may include:

  • Quitting smoking
  • Losing excess weight
  • Eating a low-salt diet
  • Getting moderate exercise, such as walking, and avoiding strenuous exercise
  • Avoiding the use of alcohol and illegal drugs
  • Getting enough sleep and rest
  • Reducing stress
  • Treating underlying conditions, such as diabetes and high blood pressure

How Can Cardiomyopathy Be Prevented?

People can make lifestyle choices to reduce the risk of conditions that may lead to cardiomyopathy, such as coronary artery disease, high blood pressure, and heart attack. Examples of lifestyle choices include:

  • Quitting smoking
  • Eating a healthy diet and maintaining a healthy weight
  • Getting regular physical exercise
  • Avoiding the use of alcohol and illegal drugs

People also can control high blood pressure, high blood cholesterol, and diabetes by:

  • Getting regular checkups with their doctors
  • Following their doctors’ advice about lifestyle changes
  • Taking medicines as directed

Some types of cardiomyopathy, such as inherited forms, can’t be prevented. Restrictive cardiomyopathy can’t always be prevented because it occurs as the result of another disease. Sometimes, underlying diseases can be prevented or treated early enough to stop restrictive cardiomyopathy from developing.

It may be possible to prevent sudden cardiac death if doctors can identify a person at high risk of this event and treat him or her with an implantable cardioverter defibrillator.

Living With Cardiomyopathy

Some people—especially those with hypertrophic cardiomyopathy—may live a healthy life with few problems or symptoms. Others may have serious symptoms and complications. Very rarely, cardiomyopathy can cause sudden death in young people.

Here are some things you can do if you have cardiomyopathy:

  • Take all of your medicines as your doctor prescribes.
  • Make all of the lifestyle changes recommended by your doctor.
  • Go to all of your medical appointments.

You may need to take antibiotics before seeing the dentist or having certain medical procedures. This is important because it can prevent an infection in your heart (endocarditis).

Ongoing Health Care Needs

You should talk to your doctor if you notice new or worse symptoms, such as swelling in your legs or feet. These could be a sign that your condition is getting worse.

You also should talk with your doctor to find out how much exercise is right for you. People with hypertrophic cardiomyopathy should not exercise vigorously, but moderate exercise, such as walking, is often a good idea.

Your doctor can help you decide what kind of diet is right for you. Doctors will often recommend that people with hypertrophic cardiomyopathy drink lots of water and other fluids. Your doctor also may suggest a diet low in salt and fat.

Cardiomyopathy often runs in families. Your doctor may suggest that your parents, brothers and sisters, and children get checked every once in a while to see whether they have cardiomyopathy.


If you are diagnosed with cardiomyopathy, you should ask your doctor about any research studies available that you may be eligible to enroll in. Research studies often provide focused attention on questions about diagnosis and treatment. The researchers conducting studies are generally experts in the field, and they may assist you and your doctor, while also gaining information that could be helpful to other patients with cardiomyopathy.


**Source: Cardiosource- American College of Cardiology.

Acute Pericarditis


Pericarditis (PER-i-kar-DI-tis) is a condition in which the membrane, or sac, around your heart is inflamed. This sac is called the pericardium (per-i-KAR-de-um). The pericardium holds the heart in place and helps it work properly. The sac is made of two thin layers of tissue that enclose your heart. Between the two layers is a small amount of fluid. This fluid keeps the layers from rubbing against each other and causing friction. In pericarditis, the layers of tissue become inflamed and can rub against the heart. This causes chest pain—a common symptom of pericarditis.

Also Known As: Pericarditis

Basic Facts

  • Pericarditis is a condition in which the membrane, or sac, around your heart is inflamed. This sac is called the pericardium.
  • The pericardium holds the heart in place and helps it work properly. The sac is made of two thin layers of tissue that enclose your heart.
  • In pericarditis, the layers of tissue become inflamed and can rub against the heart, causing chest pain. The chest pain may feel like pain from a heart attack. If you have chest pain, you should call 9–1–1 right away, as you may be having a heart attack.
  • Many factors can cause pericarditis. Viruses and infections are common causes. Less often, pericarditis occurs after a heart attack or heart surgery.  Lupus, scleroderma, rheumatoid arthritis, or other autoimmune disorders also can cause the condition. In about half of all cases, the cause is unknown.
  • Pericarditis can be acute or chronic. “Acute” means that it occurs suddenly and usually doesn’t last long. “Chronic” means that it develops over time and may take longer to treat.
  • Both acute and chronic pericarditis can disrupt your heart’s normal function and possibly (although rarely) lead to death.
  • Pericarditis occurs in people of all ages. However, men between the ages of 20 and 50 are more likely to get it.
  • Sharp, stabbing chest pain and fever are common symptoms of acute pericarditis. Other symptoms are weakness, trouble breathing, and coughing. Chronic pericarditis often causes tiredness, coughing, and shortness of breath. In severe cases, it can lead to swelling in the stomach and legs and low blood pressure.
  • Two serious complications of pericarditis are cardiac tamponade and chronic constrictive pericarditis. These conditions can disrupt your heart’s normal function. If left untreated, they may lead to death.
  • Your doctor will diagnose pericarditis based on your medical history and the results from a physical exam and tests.
  • Most cases of pericarditis are mild and clear up on their own or with rest and simple treatment. Other times, more intense treatment is needed to prevent complications. Treatment may include medicines and, less often, procedures and/or surgery.
  • You usually can’t prevent acute pericarditis. But, you can take steps to reduce your chances of having another acute episode, having complications, or getting chronic pericarditis. Get prompt treatment, follow your treatment plan, and get ongoing medical care (as your doctor advises).
  • In some cases, it may take weeks or months to recover from pericarditis. Full recovery is likely with rest and ongoing care. These measures also can help reduce the chances of having the condition again.

Causes and Risk Factors

The cause of about half of all pericarditis cases (both acute and chronic) is unknown.

Viral infections are likely the most common cause of acute pericarditis, but the virus may never be found. Pericarditis often occurs after a respiratory infection. Bacterial, fungal, and other infections also can cause pericarditis.

Less often, pericarditis is caused by:

  • Autoimmune disorders, such as lupus, scleroderma, and rheumatoid arthritis
  • Heart attack and heart surgery
  • Kidney failure, HIV/AIDS, cancer, tuberculosis, and other health problems
  • Injury from accidents or radiation therapy
  • Certain medicines, like phenytoin (an antiseizure medicine), warfarin and heparin (blood-thinning medicines), and procainamide (a medicine to treat abnormal heartbeats)

The causes of acute and chronic pericarditis are the same.

Risk Factors

Pericarditis occurs in people of all ages. However, men between the ages of 20 and 50 are more likely to get it.

People who are treated for acute pericarditis may get it again. This may happen in 15 to 30 percent of people who have the condition. A small number of these people go on to develop chronic pericarditis.

Signs and Symptoms

Sharp, stabbing chest pain is a common symptom of acute pericarditis. The pain usually comes on quickly. It often is felt in the middle or the left side of the chest.

[box]Figure A shows the pericardium—the sac surrounding the heart. Figure B is an enlarged cross-section of the pericardium that shows its two layers of tissue and the fluid between the layers.[/box]

The pain tends to ease when you sit up and lean forward. Lying down and deep breathing worsens it. For some people, the pain feels like a dull ache or pressure in their chests.

The chest pain may feel like pain from a heart attack. If you have chest pain, you should call 9–1–1 right away, as you may be having a heart attack.

Fever is another common symptom of acute pericarditis. Other symptoms are weakness, trouble breathing, and coughing.

Chronic pericarditis often causes tiredness, coughing, and shortness of breath. Chest pain is often absent in this type of pericarditis. Severe cases of chronic pericarditis can lead to swelling in the stomach and legs and low blood pressure (hypotension).


Two serious complications of pericarditis are cardiac tamponade (tam-po-NAD) and chronic constrictive pericarditis.

Cardiac tamponade occurs when too much fluid collects in the pericardium (the sac around the heart). The extra fluid puts pressure on the heart. This prevents the heart from properly filling with blood. As a result, less blood leaves the heart. This causes a sharp drop in blood pressure. If left untreated, cardiac tamponade can cause death.

Chronic constrictive pericarditis is a rare disease that develops over time. It leads to scar-like tissue throughout the pericardium. The sac becomes stiff and can’t move properly. In time, the scarred tissue compresses the heart and prevents it from working correctly.


Your doctor will diagnose pericarditis based on your medical history and the results from a physical exam and tests.

Medical History

To learn more about your medical history, your doctor may ask whether you:

  • Have had a recent respiratory infection or flu-like illness
  • Have had a recent heart attack or injury to your chest
  • Have any other medical conditions

Your doctor also may ask about your symptoms. If you have chest pain, he or she will ask you to describe how it feels, where it’s located, and whether it’s worse when you lie down, breathe, or cough.

Physical Exam

When the pericardium (the sac around your heart) is inflamed, the amount of fluid between its two layers of tissue increases. As part of the exam, your doctor will look for signs of excess fluid in your chest.

A common sign is the pericardial rub. This is the sound of the pericardium rubbing against the outer layer of your heart. Your doctor will place a stethoscope on your chest to listen for this sound.

Your doctor may hear other chest sounds that are signs of fluid in the pericardium (pericardial effusion) or the lungs (pleural effusion). These are more severe problems related to pericarditis.


Your doctor may order one or more tests to diagnose your condition and show how severe it is. The most common tests are:

  • EKG (electrocardiogram). This simple test detects and records the electrical activity of your heart. Certain EKG results suggest pericarditis.
  • Chest x ray.  A chest x ray takes pictures of your heart and lungs. The images can show whether you have an enlarged heart. This is a sign of excess fluid in your pericardium.
  • Echocardiography. This painless test uses sound waves to create pictures of your heart. The pictures show the size and shape of your heart and how well your heart is working. This test can show whether fluid has built up in the pericardium.
  • Cardiac CT (computed tomography). This is a type of x ray that takes a clear, detailed picture of your heart and pericardium. CT helps rule out other causes of chest pain.
  • Cardiac MRI (magnetic resonance imaging). This test uses powerful magnets and radio waves to create detailed pictures of your organs and tissues. MRI can show changes in the pericardium.

Your doctor also may order blood tests. These tests can help your doctor find out whether you’ve had a heart attack, the cause of the pericarditis, and how inflamed your pericardium is.


Most cases of pericarditis are mild and clear up on their own or with rest and simple treatment. Other times, more intense treatment is needed to prevent complications. Treatment may include medicines and, less often, procedures and/or surgery.

The goals of treatment are to:

  • Reduce pain and inflammation
  • Treat the underlying cause, if it’s known
  • Check for complications

Specific Types of Treatment

As a first step in your treatment, your doctor may advise you to rest until you feel better and have no fever.

He or she may tell you to take over-the-counter, anti-inflammatory medicines, such as aspirin or ibuprofen, to reduce pain and inflammation. You may need stronger medicine if your pain is severe.

If your pain continues to be severe, your doctor may prescribe a medicine called colchicine and, possibly, prednisone (a steroid medicine).

If an infection is causing your pericarditis, your doctor will prescribe an antibiotic or other appropriate medicine to treat the infection.

You may need to stay in the hospital during treatment so your doctor can check you for complications.

The symptoms of acute pericarditis can last from a few days to 3 weeks. Chronic cases may last several months.

Other Types of Treatment

If you have complications of pericarditis, you’ll need treatment for those problems. Two serious complications of pericarditis are cardiac tamponade and chronic constrictive pericarditis.

Cardiac tamponade is treated with a procedure called periocardiocentesis (PER-e-o-KAR-de-o-sen-TE-sis). A needle or tube (called a catheter) is inserted into the chest wall to remove excess fluid that has collected inside the pericardium. This relieves pressure on the heart.

If time allows, the fluid may be removed with a special catheter or tube put through a small cut in the chest.

The only cure for chronic constrictive pericarditis is surgery to remove the pericardium. This is known as a pericardiectomy (PER-i-kar-de-EK-to-me).

The treatments for these complications require hospital stays.


You usually can’t prevent acute pericarditis. But, you can take steps to reduce your chances of having another acute episode, having complications, or getting chronic pericarditis.

These steps include getting prompt treatment, following your treatment plan, and having ongoing medical care (as your doctor advises).


**Source: Cardiosource- American College of Cardiology.

Heart Failure


Heart failure does not mean that your heart has stopped working.  Heart failure refers to a large number of conditions which affect the structure or function of the heart, making it harder and harder for the heart to supply sufficient blood flow to meet the body’s needs. It occurs when one or more of the heart’s four chambers lose its ability to maintain proper blood flow.  This can happen because the heart can’t fill well enough with blood or because the heart can’t contract strongly enough to propel the blood with enough force to maintain proper circulation. In some people, both filling and contraction problems can occur.

Basic Facts (see below for more information)

  • In the United States, 5.7 million people have HF and it afflicts 10 in every 1,000 people over the age of 65.
  • The three major contributors to heart failure: coronary artery disease, hypertension, and dilated cardiomyopathy. HF can also result from heart defects, arrhythmias, unhealthy lifestyles, and more.
  • The most common signs of HF are shortness of breath, fatigue, and swelling in the feet, ankles, legs, and abdomen.
  • Medication can help stem progression of HF and most patients take a combination of a diuretic, ACE inhibitor, and beta-blocker. Lifestyle changes are critical to slowing heart failure.
  • Some patients may need cardiac resynchronization therapy, ICDs, pacemakers, or heart assist devices.
  • Patients with end-stage heart failure require heart transplantation to survive.


The problems associated with heart failure depend a lot on what part or parts of the heart are most affected. Because the left ventricle is responsible for pumping oxygen-rich blood throughout the body, it is, in many ways, the most important of the four heart chambers and critical for normal heart function. When the left ventricle cannot contract normally, as might occur after a heart attack,, not enough  oxygenated blood is propelled into the circulation. This can cause fatigue, shortness of breath, and a buildup of fluid in the lungs.  If the left ventricle stiffens and the chamber can’t relax normally, as might occur with longstanding poorly controlled hypertension, the heart cannot fill properly when resting between heart beats. This can cause fatigue, shortness of breath, and a buildup of fluid in the lungs.  Indeed, problems with either left ventricular muscle contraction or relaxation or both can result in the exact same clinical presentation.  Although failure of the right ventricle can occur on its own, the most common cause of right ventricular failure is failure of the left ventricle (as left ventricular failure causes increased fluid pressures in the lungs, which eventually begin to affect the right ventricle).

Changes to the heart’s structure and function may precede the development of symptoms by months or even years (as with chronic hypertension) or may lead to heart failure quickly (as after a large heart attack).

The illustration on the right summarizes the various symptoms people with heart failure may experience:

Blood and fluid can back up into the lungs because of failure of the left ventricle.  This is called pulmonary edema and may cause coughing, breathlessness with activities, and/or breathlessness when lying down.

Fluid can build up in the feet, ankles, legs and elsewhere (edema) as a result of higher pressures in the lungs, especially when the right ventricle is affected.

Most heart failure patients experience shortness of breath and fatigue.

Most conditions which cause heart failure affect both sides of the heart to some degree and most frequently include some impairment of left ventricular function. One measurement that helps determine whether the left ventricle is working well is called the ejection fraction. This calculates the percentage of blood being pumped out of the ventricle with each heartbeat. Because not all blood is ever squeezed out, a left ventricular ejection fraction (LVEF) of about 50% to 70% is considered normal. (Right ventricular ejection fractions will be lower.)  An LVEF between 35% and 40% indicates systolic heart failure; an LVEF below 35% increases the risk of deadly arrhythmias, making this degree of EF reduction especially worrisome.

Because heart failure worsens over time, it is considered a chronic condition and may be underway before there is any obvious indication that something is wrong. Initially, the heart tries to compensate for any loss of pumping action or capacity. It can do this in various ways: it enlarges, allowing it to stretch and contract more strongly to pump more blood; it develops more muscle mass to increase pumping strength; or it pumps faster to increase output.

Your body also attempts to aid the faltering heart in various ways. Blood vessels may narrow to increase blood pressure in an attempt to counteract the heart’s decreasing power. Or the body may redirect blood flow away from less important parts (top priority is always given to the heart and brain). Ultimately, however, these attempts to maintain normal function fail to compensate for the failing heart, leaving the individual chronically tired and perhaps experiencing breathing problems or other symptoms prompting medical evaluation.

Chronic stable heart failure can deteriorate due to any number of factors, such as an unrelated illness or heart attack. Known as acute decompensated heart failure (ADHF), it is the leading cause of hospitalization for patients over the age of 65 and is the most costly cardiovascular disease in Western countries.  This is because ADHF is associated with a greater risk of death and complications. Once it has occurred, the risk of subsequent ADHF is high: about 1 in 5 will be rehospitalized within 30 days and half will be readmitted within six months.

There are various treatments for heart failure, and treatments will be more or less effective depending on the history and cause of the disease. When heart failure worsens and does not respond to any therapies (called end-stage heart failure), a heart transplant may be the only option for survival.

By the Numbers

Heart failure (HF) is a major and growing public health problem in the U.S. It is the primary reason for 12 to 15 million office visits and 6.5 million hospital days each year. Fully 75% of patients have hypertension before they develop heart failure. At 40 years of age, the lifetime risk of developing heart failure for both men and women is 1 in 5. The number of people experiencing heart failure has increased steadily during the last 2 decades; thanks to better treatment and improved survival rates, although this improvement has been less evident among women and elderly persons.

Heart failure is the most common hospital discharge diagnosis among individuals served by Medicare and more Medicare dollars are spent for the diagnosis and treatment of heart failure than for any other diagnosis. The increasing incidence of diabetes is having a huge impact on heart failure. In just 20 years, four times as many people diagnosed with heart failure have diabetes and the combination of these two diseases greatly increases risk of death. Fully 1 of every 8 death certificates issued in the United States mentions heart failure as a cause of death.

The more risk factors you have for heart disease, the greater your risk of eventually developing heart failure. If a parent has proven heart failure, the risk among offspring is greater (1.7-fold elevated risk) than someone without a parent who had heart failure.

Causes and Risk Factors

After age 65, 10 of every 1,000 people have heart failure. Many factors can lead to heart failure. Hypertension (high blood pressure) is a major contributor to numerous heart problems and conditions including heart failure: the lifetime risk of heart failure doubles in people whose blood pressure is greater than160 mmHg systolic /90 mmHg diastolic versus those whose blood pressure is less than 140/90 mm Hg.

Many of the behaviors that can lead to heart disease and heart attacks — such as poor diet, lack of physical activity, and substance abuse — also can cause heart failure. These lifestyle choices are linked to heart failure via the diseases that most often cause heart failure in the Western world: coronary artery disease, hypertension, and dilated cardiomyopathy. The latter is a disease of the heart muscle; any damage to the heart muscle, whether from previous heart attack, other diseases, a viral infection, or substance abuse, increases the chance of developing heart failure.

Heart valve problems, whether caused by disease, infection, or a defect present at birth, also can produce heart failure, as can irregular heartbeats (arrhythmias). Indeed, up to 40% of patients with heart failure experience a specific type of arrhythmia called atrial fibrillation and individuals with this combination of heart problems are at high risk for cardiac death.

Diabetes, especially because it increases one’s risk of developing hypertension and coronary artery disease, is another major contributor to the development of heart failure. In this case, gender makes a big difference in risk. According to the current American College of Cardiology (ACC) guidelines, diabetes only modestly increases the risk of heart failure for men, but it increases the relative risk of heart failure more than 3-fold among women.

Sleep apnea, which affects one’s breathing and reduces the amount of oxygen to the heart, does not necessarily cause heart failure but it can make it worse by increasing the heart’s workload.

Other factors also can injure heart muscle and subsequently lead to heart failure.  These include treatments for cancer, such as radiation or chemotherapy; thyroid disorders; and HIV/AIDS. Good news: While heart failure may appear many years after cancer chemotherapy, it often improves greatly in response to appropriate therapy.

Beyond those contributing factors already mentioned, others that increase the risk for heart failure include:

  • Age — People 65 years and older are at risk because aging can weaken heart muscle. Also, older individuals may have developed heart disease years earlier that subsequently led to heart failure. In this age group, heart failure is the number one reason for hospital visits.
  • Ethnicity — African Americans are more likely than those of other races to have heart failure and they tend to suffer more severe forms, develop symptoms younger, get worse faster, go to the hospital more, and are more likely to die from heart disease than any other group.
  • Obesity — The more overweight a person is, the more strain is put on the heart. Obesity also contributes to many other problems, such as diabetes and hypertension, that can cause heart failure.
  • Gender — Men have heart failure at a higher rate than women, but more women end up with this condition because they tend to live to an older age when the disease is more common.

Signs and Symptoms

As mentioned above, the most common signs and symptoms of heart failure are

  • shortness of breath or trouble breathing
  • fatigue, tiredness
  • swelling in the ankles, feet, legs, and abdomen; occasionally in neck veins.

Breathing problems can manifest in several ways. If you are out of breath just from walking stairs or doing simple activities, you have what doctors call “dyspnea”. If you wake up at night and are breathless, you have “paroxysmal nocturnal dyspnea”. If breathlessness occurs when you’re lying flat, you may feel the need to sit up or be propped up with pillows. This inability to breathe easily unless sitting up straight or standing erect is called “orthopnea”.

It should be noted that some heart failure patients have exercise intolerance but little evidence of fluid retention, whereas others complain primarily of edema and report few symptoms of dyspnea or fatigue. When fluid build-up is present, there also may be weight gain, increased urination, and a cough that worsens at night and/or while lying down. Because not all patients have congestion in and around the lungs due to edema, the term “heart failure” is preferred today over the older term “congestive heart failure.”

Testing and Diagnosis

Heart failure is a complex clinical problem and no one test can confirm the diagnosis. First, a doctor or nurse will likely obtain a thorough patient history, including past and current use of alcohol, illicit drugs, standard or “alternative” drug therapies, and any history of radiation or chemotherapy. During a complete physical examination, your doctor will listen to your heart for telltale signs that suggest heart function problems and will listen to your lungs looking for any abnormal sounds. The exam goes beyond the heart and lungs to look for signs of heart failure, such as swelling in your ankles, and there will be an assessment of your ability to perform everyday tasks.

If heart failure is suspected, various blood tests will be ordered, which may help confirm the diagnosis and reveal the presence of disorders or conditions that can lead to or exacerbate heart failure. For example, thyroid-function tests can reveal overactivity (hyperthyroidism) and underactivity (hypothyroidism) of the thyroid gland, both of which can be a primary or contributory cause of heart failure. Another blood test will evaluate levels of a marker known as brain natriuretic peptide (BNP); increased levels of BNP have been associated with abnormal heart function, helping confirm the presence of heart failure in patients whose main complaint is breathlessness.  BNP is also elevated during a heart attack, and in other settings, so your doctor will need to weigh the BNP result relative to your overall health status.

A chest x-ray may be taken as well an electrocardiogram (ECG), which measures your heart’s electrical activity. An echocardiogram (commonly called an echo), may be performed to measure your heart’s structure and function. This ultrasound examination (performed much like a baby ultrasound in pregnant patients) provides exquisite detail of the heart and how well it is working. The speed and direction of blood flow can also be assessed, providing an evaluation of heart valve function. The echo is also helpful in diagnosing right-side heart failure and measuring pressures in the lungs. Your doctor also may order an exercise stress test to see how your heart responds to an increased workload.

Another type of test is called radionuclide ventriculography, can be performed to assess LVEF.  This test uses a small dose of an injected radioactive material to follow blood flow through the heart chambers.  Finally, if necessary, coronary  angiography may be performed. In this test, a small tube (catheter) is inserted into a blood vessel in your arm or groin area, threaded through the body’s vasculature to your heart where a dye is released. X-ray imaging helps reveal if any your heart arteries are blocked.  Coronary angiography would be considered in someone who has clear risk factors for coronary artery disease, especially if other tests are suggestive of a prior heart attack.

Once diagnosed, heart failure often is categorized using the New York Heart Association (NYHA) Functional Classification system, which is based on symptoms and limitations to physical activity. NYHA stage I refers to patients who have no symptoms; NYHA stage IV refers to patients who have symptoms at rest.  Stages II and III refer to situations where patients experience symptoms with progressively less exertion.

Guidelines issued by the ACC and American Heart Association (AHA) (presented in the summary slide) concentrate more on progressive stages of heart damage, beginning with a detectable insult or injury to the heart and key advances in staging based on structural changes and asymptomatic or symptomatic phases.

Important: Once heart failure has been diagnosed, at each visit your healthcare provider should measure your body weight as well as sitting and standing blood pressure. You’ll also be examined for fluid build up (in your arms and legs, for example). This is very important: you’re being assessed for what’s called “volume status” or level of fluid retention, which can influence drug therapy and suggest whether you are doing fine or perhaps getting slowly worse. With heart failure, it is critically important to detect sometimes subtle changes and intervene early (by altering medication, for example) rather than wait for the development of critical problems such as acute decompensated heart failure (ADHF). This emergency situation causes serious trouble breathing and can occur when fluid management and restriction does not work. ADHF requires emergency treatment including hospitalization, and puts additional strain on an already overworked heart.


Heart failure itself is not a reversible disease, but there are many treatments that can reverse underlying causes and improve symptoms. Many of the drugs target changes in the body’s hormone status.  Some hormones are naturally released by the body in response to heart failure but they can paradoxically  either directly or indirectly damage the heart itself. Treatment goals for all stages of heart failure are geared toward keeping the disease from worsening and increasing both the length and the quality of life.

Lifestyle Changes

One reason for a thorough history and physical examination is to identify behaviors that might cause heart failure or accelerate its progression. Therefore, first and foremost, an individual with heart failure should focus on lifestyle changes. Controlling high blood pressure and weight are critical to improving the disease; both require a heart-healthy diet and increased physical activity/exercise. Your diet should be low in sodium, which not only helps with blood pressure levels but can also help reduce swelling (edema) in your legs, feet, and abdomen.

Recommendations regarding increasing activity and exercise have changed dramatically over the years. A hallmark of heart failure is a reduced ability to perform aerobic exercise, such as walking, swimming, or riding a bicycle. For generations, the management of heart failure included sharp restrictions of physical activity and exercise. Then, during the 1990s, 15 controlled trials of exercise training in heart failure demonstrated significant improvements in the amount of exercise that could be performed. Another 10 trials, during roughly the same period, reported other important improvements when heart failure patients exercised, including quality-of-life measures. As for the risks of activity, studies consistently showed a very low rate of adverse events during either supervised or home-based exercise programs.

Subsequently, the ACC and AHA guidelines formally recognized exercise training for patients with current or prior symptoms of heart failure. The guidelines state that exercise training leads to improvements “comparable” to that achieved with drug therapy and is in addition to the benefits of drug therapy. There is even evidence today that patients with heart failure benefit from cardiac rehabilitation programs, which had previously been recommended primarily for patients who had experienced a heart attack or undergone heart surgery.

Is exercise worth the time and effort? A recent large-scale trial, called HF-ACTION, placed half of the trial patients, all of whom had mild to severe heart failure symptoms (NYHA class II to IV), into an aerobic exercise program versus the other half, who simply had usual care. Those that exercised improved the amount of activity they could perform — enhancing the ability to perform day-to-day activities — plus they reported an improved sense of well being. Importantly, exercise was deemed safe in this group of fairly sick patients. There was almost what could be called a “dose-response” effect, meaning that the more exercise a patient achieved the greater the benefits.

Your doctor can discuss types of activities you can undertake, ranging from walking to bicycling, swimming, or low-impact aerobics; all of which provide excellent benefits and can be accomplished without straining your budget.

If you smoke or use illicit drugs, you should stop, and you should moderate your alcohol consumption per your doctor’s recommendations. You will hear these recommendations almost universally if you have heart disease — appropriate lifestyle choices truly are the foundation of good overall health and they can be especially critical in terms of managing heart failure.


There are various treatments for heart failure, most of which are geared towards treating specific underlying conditions. However, you should always tell your doctor about any and all medications, vitamin supplements, or “alternative” therapies you may be taking, including over-the-counter drugs. Some drugs can exacerbate heart failure and there are many potentially dangerous drug-drug interactions. This includes medications you take temporarily; for example, some cough and cold treatments may increase blood pressure while some anti-inflammatory agents (such as ibuprofen) may cause sodium retention and negatively affect kidney function. Even some herbal products may have unintended consequences in patients with heart failure, so remember that something seemingly innocuous or helpful may really be quite harmful in someone with heart failure.

Guidelines written to guide medical therapy recommend different treatments for those who are at risk of developing heart failure versus those at different stages of the disease. Different agents — even those in the same class of drugs — can be more effective or less effective at different stages. In brief, specific drugs are used to target particular problems, which is why your doctor needs to determine to the fullest extent possible how your heart failure started (or could start) and what structures or conditions are actually involved.

Most of the drugs used to treat heart failure target the renin-angiotensin-aldosterone system (RAAS). This is a hormone system that regulates blood pressure and water (fluid) balance in the body. The drugs that target the RAAS are the principle means of controlling high blood pressure (hypertension), heart failure, kidney failure, and the harmful effects of diabetes.

Typical heart failure medications include

  • Diuretics — Also known as water pills, these drugs help reduce fluid build up in the body.  They lessen congestion in the lungs and help diminish swelling in the abdomen, legs, and feet.
  • ACE inhibitors — Known as angiotensin-converting enzyme inhibitors, these drugs target the RAAS by reducing the formation of angiotensin, a substance that causes blood vessels to constrict resulting in increased blood pressure. ACE inhibitors lower blood pressure and reduce strain on the heart.   Angiotensin receptor blockers (ARBs) — Working at a different place in the angiotensin pathway, these agents block the action of angiotensin so that it has no or limited deleterious effect on the blood vessels and thus the heart.
  • Beta-blockers — These drugs slow your heart rate and help lower blood pressure.  This helps counteract the heart’s tendency to compensate for heart muscle weakness by pumping faster.
  • Vasodilators — This class of drugs helps the blood vessel walls to widen or relax (called vasodilation), which helps normalize blood flow and reduce strain on the heart.
  • Aldosterone antagonists — Again, the target is the RAAS. By helping the body get rid of salt and fluid, these drugs reduce the actual volume of blood the heart must pump.
  • Digitalis — This specific drug helps the heart beat more strongly by increasing the force of the heart’s contractions.  It has a mild effect on stabilizing some heart rhythm abnormalities as well.

Successful treatment of hypertension often requires at least two different types of drugs to control blood pressure. In the case of heart failure, blood pressure is only one of the targets of therapy. Consequently, heart failure patients will be routinely managed with a combination of a diuretic, an ACE inhibitor, and a beta-blocker. (Sometimes patients don’t tolerate ACE inhibitor therapy; these people often receive an ARB instead.) There is strong and compelling evidence that drugs are best used in combination for managing heart failure, so most patients with heart failure will end up taking at least 3 separate medications. Guidelines also recommend including digoxin, if necessary, as a fourth agent to help reduce symptoms, increase exercise tolerance, control heart rhythms, and help prevent hospitalization.

Heart Failure with Preserved Ejection Fraction

While low ejection fraction (EF) is typically used as a chief indicator of heart failure, approximately 15 to 20 million heart failure patients worldwide (one-third to one-half of heart failure patients) have relatively normal heart muscle contraction  or preserved EF (40% or higher.) This is the predominant form of heart failure in elderly patients, particularly elderly women, most of whom have hypertension, diabetes, or both.   Often these patients also have other heart issues including coronary artery disease or atrial fibrillation. Despite their preserved EF, they still have many of the typical symptoms and signs of heart failure, including shortness of breath, fluid buildup, and reduced quality of life. The main issue in many of these patients appears to be abnormal heart muscle relaxation.  Individuals with preserved EF do have a better life expectancy than those with a low EF, but they still are at significant risk for dying and for requiring hospitalization at some point during the course of their illness.

Clinical trials are currently assessing how heart failure therapy might be different for individuals with preserved LVEF. Right now, guidelines for doctors suggest basing therapy on the control of factors like blood pressure, heart rate, and on addressing any health issues which may contribute to this form of heart failure (such as coronary artery disease, severe heart valve abnormalities, sleep apnea, and heart rhythm disorders).    Many of the same medications which are used to treat patients with low EF are also used to treat heart failure patients whose EF is preserved.

Research eventually may suggest that individuals with preserved EF may do better on some drugs and not as well as others compared to heart failure with reduced LVEF. For example, a few recent studies have shown that ARB-type medications have not been very effective in improving survival or lowering hospitalization rates in patients with preserved EF-type heart failure.  So it is possible that this class of drugs may not be as helpful for heart failure patients with normal ejection fractions as it is for those with reduced EFs.  Much more research needs to be done in this area before firm conclusions can be made, however.

Two important points

First: Heart failure in elderly patients may be inadequately recognized and treated because both patients and physicians frequently attribute the symptoms of heart failure to aging. Furthermore, because the elderly are most likely to have heart failure with preserved EF, this condition may be missed with routine testing unless doctors are attuned to the possibility of this scenario. . If you have symptoms of heart failure (trouble breathing or inability to perform normal tasks of everyday living), and you are told that you don’t have heart failure,  you might want to ask your doctor if you could have heart failure with preserved EF.

Second: No matter the kind of heart failure, there are no hard and fast rules about how an individual is affected by the disease. Patients with a very low EF may have no symptoms or physical limitations, whereas patients with preserved LVEF may have severe disability. Likewise, it’s hard to predict how someone will respond to therapy. Although medications may produce rapid changes in important markers of heart failure, signs and symptoms of the disease may improve slowly over weeks or months or not at all. That’s why an all-encompassing approach is important and includes recommended drug therapy, good compliance with prescribed medications, lifestyle changes, and attention to details such as weight gain or peripheral edema that might indicate disease progression. Your doctor can help a lot by getting you on appropriate drug therapy but your contribution with all the other aspects of the disease is important, too.

Acute decompensated heart failure

Fluid retention is the primary cause of hospitalization among ADHF patients older than age 65, with more than 1 million hospitalizations reported each year. Current treatments for ADHF have significant safety concerns and often are inadequate in managing fluid retention, especially without affecting kidney function or mineral balance in the body.

One big problem with treating ADHF is a lack of clinical trial data on which to base treatment decisions. Available guidelines suggest that reducing congestion is the primary objective, usually through salt and water restriction and diuretic therapy.  However, there is not enough data to know whether this therapy, does much to change outcomes like rehospitalization and mortality. . A large registry of ADHF patients, called ADHERE, is collecting information about ADHF patients to help define successful treatment strategies for this critical disease.

Treating the whole patient

People with heart failure often have other health problems, too. Some drugs that might be quite effective as therapy for one condition might be problematic when given to individuals with another disease. Your particular treatment regimen may therefore vary from the regimens of other patients, depending upon your overall health situation.  Nevertheless, it’s always wise to periodically go over your prescriptions with your health care provider, to make sure you understand the rationale for each medication and to know that no potentially beneficial medications are missing from your regimen.

On the flip side, some drugs used to treat other disorders actually have some benefit in heart failure patients.  For example, metformin, which is the most widely prescribed drug in the U.S. for type II diabetes, has been shown to actually have specific beneficial effects on heart failure when given as diabetes therapy. Metformin was safe, even in patients with advanced heart failure, although the drug should be avoided in patients with severe kidney disease. Metformin should also not be used in patients without diabetes.

Surgery and Mechanical Assistance

To help deal with some of the underlying causes of heart failure, surgery may be one option to get the heart back into shape. For instance, if heart failure stems from a valve problem, valve repair or replacement surgery may be very beneficial. If coronary artery disease has blocked multiple arteries, coronary artery bypass graft (CABG) surgery may be necessary. If artery blockage can be handled via angioplasty or stent implantation, the result may include a lessening of heart failure symptoms.

Another therapy used for heart failure is enhanced external counterpulsation (EECP), which uses three sets of inflating pneumatic cuffs attached to the patient’s legs that rapidly inflate and deflate. (They look like over-sized blood pressure cuffs.) The cuffs are applied to the calves, lower thigh, and upper thigh; then, they are inflated and deflated sequentially and timed to your heartbeat. A typical EECP treatment regimen consists of 1-hour sessions for 35 days. EECP improves blood pressure and blood flow, and in trials with heart failure patients, it improves exercise capacity and duration, NYHA class, and quality of life.

Despite optimal medical therapy and lifestyle changes, there may come a time when these interventions no longer control heart failure symptoms. This often occurs to individuals in NYHA class III or IV heart failure. In these cases, doctors may rely on mechanical means to help keep the heart beating in as strong a rhythm as possible. Some options include:

  • Cardiac resynchronization therapy (CRT) — When the left and right sides of the heart no longer work together, the heart becomes less efficient in its ability to pump blood through the body.  CRT “resynchronizes” the two sides to work in sequence and improve  pumping function. CRT involves implanting a pacemaker-type device with electrical leads to specific areas of the heart, such as the left ventricle. The CRT device stimulates the left and right ventricles to help restore a coordinated, synchronous pattern to the heart’s pumping action. This is also referred to as bi-ventricular pacing.
  • Implantable cardioverter-defibrillator (ICD) — For heart failure patients with recurrent, rapid, irregular heart rhythms who are at risk of sudden cardiac arrest, ICDs can check the actual speed and rhythm of the heart and shock it appropriately to return it to normal rhythm. Some ICD devices have pacing capability, too. These combination devices can convert some sustained arrhythmias to normal rhythm without the need of an electrical shock to the heart.
  • Left ventricular assist device (LVAD) — This surgically implanted device helps a weakened heart pump blood. Used primarily in very sick patients, it is often considered a bridge to heart transplantation.
  • One other device still being evaluated is a mesh-like device that wraps around the heart to reduce heart dilation and heart muscle stress. In a small study called ACORN, the device improved LVEF, stopped or reduced heart chamber dilation, improved NYHA class, and was associated with other benefits in heart failure patients who had it implanted.  This approach remains experimental.

Heart Transplantation

When medical and surgical treatments cease to be effective, a patient is said to have reached end-stage heart failure and may be a candidate for heart transplantation. A patient will have to be matched to a donor — that is, a person whose tissue is as similar as possible to the recipient — to reduce the risk of the body’s rejecting the donor heart. There is a balancing act required when choosing heart transplant candidates; the patient must be sick enough require a donor heart but healthy enough to survive the surgery and gain long-term benefit from the new heart.

According to the National Heart, Lung, and Blood Institute, survival rates for heart transplant patients have improved over the past decade or so. About 88% survive the first year following the surgery, 72% survive for 5 years, 50% for 10 years, and 16% for 20 years. However, given the limited availability of donor hearts, only about 2,000 heart transplants are performed annually in the U.S.

In transplant surgery, a patient is attached to a heart-lung machine, and the entire diseased heart is removed from the body and replaced with the donor heart. About 90% of heart transplant patients return to normal activities of daily living, although fewer than half return to work due to a variety of reasons.

Living With Heart Failure

Because there really isn’t a cure for heart failure, your best course of action is to stay as healthy as possible for as long as possible by following the advice and treatment plan provided by your doctor. Start by sticking with your medication schedule. If you experience side effects, talk to your doctor quickly.  Don’t stop a medication until your doctor says it’s OK; some drugs need to be halted over time and stopping them immediately may be dangerous. Also, let your doctor know if you have missed medication doses, failed to refill a prescription, or are having difficulties with the costs of your regimen.  Heart failure treatment is truly a partnership between the patient and the health care provider, and success is greatest when communication is open and forthright.  Treatment adjustments are based upon your response to therapy – if your doctor does not have the complete picture of what you are really doing, those treatment adjustments may end up being counter-productive, or even dangerous.  Also, always tell your cardiologist if you are prescribed any new medications by other doctors to avoid drug-drug interactions.

Be aware that respiratory infections, such as flu and pneumonia, can be very worrisome if you have heart failure. People with heart failure have a much greater risk of serious complications if they get the flu. Vaccines usually protect people from the flu, but the body’s immune response appears to be poorer in people with heart failure compared to healthy individuals. It is still very important that heart failure patients get a flu vaccination, but additional preventative steps might be needed to reduce exposure to the flu virus in patients with heart failure. During flu season, this might include reducing exposure to crowds of people, more frequent hand washing, and reduced exposure to individuals known to have the flu.

Also, make all necessary lifestyle changes to get and stay as healthy as possible.  Many of us prefer to relax rather than to be active, and apple pie rather than an apple, but when your life is on the line in terms of both its quality and quantity, then carrots and celery may look more appealing and a nightcap less so. Make your diet as healthy as possible and get as physically active as your doctor advises. And consistency is important; it’s not just a week’s worth of commitment but rather a long-term objective that enhances life and improves quality-of-life after a diagnosis of heart failure.

Understand that this disease requires a great deal of attention and coping, especially if symptoms worsen. The nature of the disease may cause depression in some people. It is natural and most certainly NOT a personal failure. Make your doctor aware of how you are feeling mentally as well as physically so that you receive further treatment or support as needed.  And realize your family may need support, too, in helping you deal with heart failure. It can be a challenge but for those who take on the challenges, the reward can be a longer and better life.


The best way to prevent heart failure is to live a healthy lifestyle. It’s a common theme that needs regular repeating since so many health problems are in essence self-inflicted through poor diet, lack of physical activity, smoking, and other lifestyle choices. More than 50% of the deaths and disability from heart disease and strokes could be cut by a combination of simple, cost-effective actions to reduce major risk factors such as high blood pressure, diabetes, obesity and smoking. How successful are these preventive measures: Optimal blood pressure control alone, for example, decreases the risk of new heart failure by approximately 50%.

Because heart failure often develops from other cardiovascular diseases, preventing those diseases in the first place will help prevent heart failure. Yet, there is no magic key to preventing heart failure. If you have no risk factors that predispose you to the disease, then keeping healthy overall should keep your heart that way. If you are at a higher than normal risk of heart failure, preventive measures mentioned here can greatly reduce your risk. Remember: big benefits come from simple changes to diet, activity, and overall lifestyle.


**Source: Cardiosource- American College of Cardiology.

Atrial Fibrillation


Atrial fibrillation (AF) is the most common heart rhythm disorder seen by doctors. It’s a big public health issue in terms of not only the sheer number of patients affected, but also by the fact that managing these specific arrhythmias (which is the medical name for heart rhythm problems) is expensive.

Also Known As: A Fib, AF, Atrial Fib, auricular fibrillation, supraventricular arrhythmia, supraventricular tachyarrhythmia


  • In the United States, more than 2.2 million people have atrial fibrillation (AF) including 9% of people over the age of 80.
  • About 15% to 20% of all strokes result from atrial fibrillation.
  • AF can arise from temporary (acute) causes such as alcohol consumption, heart attack, surgery, lung disease, or a metabolic disorder (such as an overactive thyroid gland).
  • AF can also be related to long-term (chronic) conditions such as high blood pressure, diabetes, or heart failure.
  • Obesity is an important risk factor for the development of AF and weight loss may decrease the risk associated with AF.
  • AF can be occasional (paroxysmal, which self terminates) or ongoing (persistent). If it does not respond to an electric current that is used to reset the heart’s rhythm back to its regular pattern (called cardioversion), it can progress to permanent AF.
  • The most common signs of AF are heart palpitations, chest pain, and shortness of breath.  AF can also be silent.
  • There are two approaches to treatment: heart rate control or heart rhythm control, with therapies ideally achieving both goals.. When medication is ineffective, AF treatments can include cardioversion, ablation therapy (that targets specific cells that are causing the AF), and open-heart or minimally-invasive surgery that also targets a specific area of the heart that is causing the problem.
  • Heart-healthy lifestyles can help prevent AF or make you better able to live with it.


The heart has an electrical system that controls both the speed and rhythm of each heartbeat. This electrical system is controlled by the autonomic nervous system, which also handles critical functions such as breathing and digestion – all those functions that need to happen automatically rather than under our conscious control.

When your heart beats, an electrical signal starts at the top of the heart in a group of cells called the sinus (or sinoatrial) node. This node, your heart’s natural pacemaker, is located in the right atrium, which is the upper right chamber of the heart. There are two atria (the right and left) and these function primarily as priming pumps for the two ventricles, the main squeezing chambers and workhorses of the heart.

The electrical signal from the sinus node travels through the right and left atrium to the atrioventricular (AV) node, a sort of relay station, where the electrical signal pauses before it spreads to the right and left ventricles.  As the signal travels from the sinus node toward the AV node, it causes the atria to contract and pump blood into the ventricles, ensuring optimal filling of these chambers.

When the electrical signal then spreads from the AV node to the ventricles, it causes those chambers to squeeze, pushing blood out of the heart and into the body.  This rhythmic, coordinated sequence of events ensures efficient heart function. A normal heart repeats this sequence automatically and without stopping, beating on average 60 to 100 times per minute.  And when the electrical system is functioning normally, we say the patient is in “normal sinus rhythm”.

An arrhythmia occurs when the heart’s electrical system malfunctions causing a failure in the synchronization that’s required for the heart to work properly. In the specific arrhythmia known as atrial fibrillation, electrical signals no longer start in the sinus node, but rather fire rapidly and haphazardly throughout the heart’s upper chambers.

These disorganized electrical impulses cause the atria to contract quickly and irregularly, resulting in rapid quivering of the upper chambers, which is medically known as fibrillation (hence, the name atrial fibrillation). These chaotic and rapid electrical signals also bombard the AV node, usually causing heart rate to rise.  As a result, the organized flow of blood within the heart becomes disrupted and heart rhythm becomes very irregular.  It can also become quite fast, occasionally reaching heart rates as high as 160 beats per minute at rest.

Up to one-third of patients with atrial fibrillation have asymptomatic or “silent” AF, which is more common in the elderly. Other people with AF experience symptoms such as palpitations, fainting, chest pain, or even heart failure.

If the heart’s atria are not contracting properly, blood can pool in the heart’s upper chambers. Such pooled blood can lead to the formation of blood clots within the atria, which in turn can cause strokes if the clots are carried into the blood stream and lodge in the arteries of the brain.

AF is a major risk factor for stroke (increasing stroke risk about 5-fold) with the absolute level of risk somewhat dependent on the number of additional risk factors for stroke in a given individual. Just like there can be silent AF, strokes can be “silent” too, but even these asymptomatic strokes may have significant ramifications. For example, elderly people with silent strokes have greater than double the risk of dementia and a steeper decline in global cognitive function compared to age-matched individuals without evidence of such strokes.

One particular high-risk variable: transient ischemic attacks (TIAs).  These are “warning strokes” that produce stroke-like symptoms but no lasting damage. A person who’s had one or more TIAs is almost 10 times more likely to have a stroke than someone of the same age and sex who hasn’t.  Therefore a history of TIA and AF is a combination that suggests a strong need for preventive therapy and stroke risk reduction.

Patterns of AF

Doctors tend to label AF by its pattern of occurrence. Episodes that last 7 days or less (often less than 24 hours) are called “paroxysmal AF” and they usually stop on their own.  However, when AF lasts longer than 7 days, it is considered “persistent” and may require treatment before the episode stops. When AF lasts longer than a year it is considered “permanent”.  If an individual has two or more AF episodes, whether the arrhythmia stops on its own or must be stopped via therapy, the condition is considered “recurrent AF”.


In the United States, about 2.2 million people have AF, and nearly 5 million are affected  in the European Union. This is the most common arrhythmia that doctors see in practice, and AF is the cause of about one-third of all hospitalizations related to cardiac rhythm problems. Overall, hospitalizations for AF have increased 66% in the last 20 years. This is due to various factors, including the aging of the population, a rise in chronic heart disease, and more frequent diagnosis through the use of ambulatory monitoring devices. The annual cost per patient is approximately $3,600, which may not seem like a lot, but given how many people are afflicted with AF, that comes to well over $7 billion per year in the United States and about $15.7 billion per year in the European Union.

About 15% to 20% of all strokes occur in someone with AF, which in hard numbers means that AF causes about 70,000 strokes each year just in the United States alone. Stroke risk increases with age. While AF is seen in only about 1% of the total U.S. adult population, it affects about 3.8% of those older than 60 years and 9.0% of those older than 80 years. Up to 40% of patients with heart failure also experience AF, and patients with this combination of heart problems are at particularly high risk for cardiac death.

Approximately 30% to 45% of cases of paroxysmal AF (when the AF lasts for 7 days or less) and 20% to 25% of cases of persistent AF (that lasts for more than 7 days) occur in young patients without any identifiable underlying disease. This is known as “lone AF.”


Risk factors

There are several well-established risk factors for AF, with coronary artery disease and heart failure being most frequently associated with atrial fibrillation. Rheumatic heart disease, which affects the valves of the heart, and congenital heart abnormalities (inherited heart defects) also increase the chance of AF.

Cardiac risk factors such as hypertension and diabetes can also play a role in damaging the atria of the heart, leading to AF.
There are a number of acute, temporary causes of AF as well as chronic conditions which lead to this rhythm abnormality.  For the most part, when the temporary condition ceases or is treated, AF usually resolves. In the presence of chronic conditions, treatment should target both the AF and the chronic problem that is contributing to the risk of AF-associated events.

Acute conditions

One acute condition associated with AF is excessive alcohol consumption. There is even a medical term for this: “holiday heart syndrome,” so named because the excessive consumption of alcohol that sometimes occurs with holiday celebrations is associated with a spike in the number of people presenting with AF.

Other acute conditions relate to medical factors such as surgery, lung disease, asthma attacks, extreme body stress due to conditions such as pneumonia, or the occurrence of a metabolic disorder, such as hyperthyroidism (overactive thyroid gland).  An inflammation of the lining of the heart can also cause the atria to fibrillate, and having a heart attack increases the risk of AF.

Many of these acute conditions can cause chemical imbalances that can lead to electrical imbalances in your heart, triggering AF. Once the necessary balance is restored – for example, pneumonia resolves or alcohol is eliminated – the AF usually disappears on its own.

Chronic conditions

A number of chronic or long-term conditions also can lead to AF. For the most part, these consist of existing heart problems, such as congenital heart defects, particularly atrial septal defect, or heart valve diseases such as those related to prior rheumatic fever. These conditions tend to results in atrial enlargement, which in effect stretches out the electrical “wiring” of those chambers, making short circuits and sparks (AF) more likely.  Additionally, AF may be associated with hypertrophic, dilated, or various other cardiomyopathies; these conditions also change the shape of the heart, interfering with the heart’s intricate electrical system.  Longstanding lung problems such as COPD (chronic obstructive lung disease), can also predispose to atrial fibrillation.

Two other common conditions that can lead to AF are obesity and sleep apnea.  In a study of more than 3,400 adult patients who never had atrial fibrillation, 14% ended up being diagnosed with AF after several years of follow-up. Beyond the typical risk factors mentioned above, the incidence of AF was strongly predicted both by obstructive sleep apnea and excess weight.

It turns out that obesity can actually change the size of the heart’s atria, with a graded increase in atrial size occurring as body weight increases from normal, to overweight, to obese. Weight loss has been shown to reduce atrial size, suggesting that weight reduction may decrease the risk of developing AF.

More than 25 million U.S. adults are estimated to have obstructive sleep apnea and the incidence of AF is about 5 times greater in people with apnea compared to people who do not have sleep apnea. Looking at it another way, between one third and one half of all patients with AF have sleep apnea.

Sleep apnea is a condition in which patients do not breathe normally or regularly during sleep. Instead, breathing pauses or becomes very shallow, with abnormal breathing episodes lasting a few seconds up to several minutes. These episodes can occur anywhere from 5 to 30 or more times per hour, disturbing restful sleep. This disrupted sleep can contribute to an increased risk of arrhythmias such as AF, although it is not clear whether this is due to biochemical alterations that occur when sleep is disrupted or other conditions that arise from sleep apnea.

Age and family history

AF tends to occur more frequently in older people, primarily because the older you are, the more likely you are to have heart disease or other health problems.

Although AF is often considered an electrical problem that is linked to underlying cardiac disease, that is not always the case. Approximately 30% to 45% of cases of paroxysmal AF and 20% to 25% of cases of persistent AF occur in younger patients who have no heart defects or disease (lone AF).  The cause of lone AF may not be known for quite some time, if at all.  When lone AF runs in a family, it is called familial AF. Your chances of developing AF are higher if your parents have or had it.


Probably the most recognizable sign of AF is heart palpitations, where your heart beats so fast that you think it is racing and/or you can feel it thumping or flopping in your chest. It may be accompanied by chest pain; lightheadedness or dizziness, especially if you are exerting yourself; weakness; or shortness of breath, including difficulty breathing when lying down. AF symptoms will vary depending on the degree of pulse irregularity and resultant heart rate, underlying functional status, how long the AF lasts, and individual patient factors.

Remember: one of the effects of AF may be formation of a blood clot in the atria. If this happens and the clot travels up to the brain, you may have a stroke. Sometimes a stroke is the first sign of underlying AF, especially if the symptoms have been light or nonexistent.

There is no set amount of time that marks an episode of AF – it may be very short and stop on its own or it may be prolonged and you find yourself in need of medical intervention. Over time, you may become more accustomed to the pattern of your AF, and what factors contribute to and relieve this arrhythmia.


First, your doctor will take a medical history from you looking for information on you and your family. The information from you will include questions that will: help your doctor understand your specific symptoms and how severe they may be; define your AF clinically (e.g., paroxysmal, persistent, or permanent); and reveal AF frequency, duration, precipitating factors, and how it terminated (if it did). If you received any treatment for the AF before seeing your doctor (if paramedics administered a drug or defibrillation therapy, for example), your doctor will want to review your response to such therapy. Finally, you will be examined to see if you have any heart disease that may be causing the AF or whether there may be a reversible condition, such as pneumonia, that triggered the AF.

Electrocardiograms and echocardiograms

You likely will have an electrocardiogram, known as an ECG or an EKG. This is a noninvasive test in which patches (called electrodes) are attached to your chest to detect and record the electrical activity of your heart. The electrical impulses travel by wires attached to the electrodes and are recorded as waves on a sheet of paper.  This test allows your physician to see how fast your heart is beating and whether the rhythm is regular or irregular. A number of heart irregularities and conditions are detectable with an ECG.  The tracing can even provide clues as to whether or not you have had a previous heart attack.

If you do not have AF at the time of your ECG – for instance, if you have paroxysmal AF and the episode has abated – then you may be asked to wear a portable or “ambulatory” ECG monitor. One type, a Holter monitor, records your heart’s activity continuously for a 24- or 48-hour period. Other devices, called “event monitors”, record only when you press a button to indicate that you are feeling symptoms.  Event monitors can be worn for up to one month.
Another noninvasive test is an echocardiogram, known informally as an echo. If you have ever had or seen an ultrasound test used on pregnant women, then the technology and concept of an echo will be familiar to you. With an echo, sound waves are directed at your heart with a device called a transducer that is held on your chest. The sound waves bounce off your heart and are processed electronically to create a video of your heart as it beats.

Not only does an echo show the size and shape of your heart chambers, it also provides information on how well the chambers and valves are functioning or if there is evidence of previous heart damage. y. Clearly, echocardiography offers a great deal of insight into whether structural heart disease is present or if there are problems that could be causing or contributing to AF. The standard echo is also called a transthoracic echocardiogram (TTE), since the pictures are obtained by imaging through the chest wall, or thorax.

Another type of echo is the transesophageal echocardiogram (TEE), which uses a transducer at the end of a tube or probe inserted into the mouth and down the esophagus. This is done because the atria are deep in the chest and not always well imaged with a regular echo. The TEE is especially good at detecting possible clots in the atria. To ease the discomfort of a TEE, the patient is usually sedated and the back of the throat is numbed before the procedure.

Other tests

Your doctor also will order blood tests, primarily to measure thyroid function. Other blood tests may be ordered to evaluate kidney and liver function, mostly to see if there are any limitations with regards to the medications you might require. Additionally, you may have a chest X-ray to get a better assessment of your lungs, especially if there is any suspicion of pneumonia or other lung disease. Some physicians also may order exercise tests, especially if the AF is prolonged or considered permanent, to help determine whether your heart rate is under good control.

If necessary, you may undergo an electrophysiology study. Essentially, electrophysiology is the science of measuring the electrical potential of the body; for example, the electrical activity of the brain can be assessed by an electroencephalogram or EEG. Cardiac electrophysiology usually requires more invasive methods, such as inserting a special cardiac catheter that can record both ongoing electrical activity of the heart as well as responses to specific stimulation of the heart. Such tests help physicians look at a range of complex arrhythmias including AF, provide further insight into the potential causes of abnormal ECGs, assess your risk of developing AF or other heart rhythm problems in the future, and create a treatment plan if you do have AF. The electrophysiology study is not a routine test, and is not performed in all patients with AF.  Usually this type of evaluation is reserved for patients who have failed drug treatment and are being considered for ablation therapy (see below).


Atrial fibrillation can be tough to treat. Management of AF is designed to achieve several objectives:

  • Prevent blood clots from forming;
  • Control the heart rate, concentrating on how many times per minute the heart beats (rate control);
  • Restore the heart to a normal rhythm (rhythm control); this helps the heart’s chambers work together more efficiently, which also can improve rate control;
  • Treat underlying conditions that may be causing or worsening the AF, such as overactive thyroid function, other metabolic imbalances or various cardiac diseases.

There are different strategies to treat  AF, and the goal may be to achieve some or all of the above objectives.  Which approach is best for you will depend on various factors, including whether you are currently being treated for other heart or medical problems. Sometimes you will need a combination of treatments to effectively treat your AF.

Prevention of blood clots

The two most common drugs used to prevent blood clot formation (and thus reduce the risk of stroke) are warfarin and aspirin. Warfarin (commonly known as Coumadin) is more effective than aspirin for preventing stroke in this situation. However, warfarin has more side effects – such as potential bleeding problems – than aspirin. Aspirin is the standard treatment for patients without other risk factors for stroke who are also under 75 years of age. If you have only one moderate risk factor for stroke in addition to atrial fibrillation (such as hypertension, diabetes, or heart failure), either aspirin or warfarin may be considered to reduce stroke risk. If you have at least one high-risk factor (e.g., a previous stroke or TIA, age older than 75), you will likely receive warfarin.

Because warfarin is a powerful blood thinner, it requires intense monitoring. Such monitoring involves regular blood tests to measure INR.  INR stands for international normalized ratio and this test allows doctors to determine how thin the blood is.  For patients with atrial fibrillation, goal INR is usually 2.0 to 2.5.  The frequency of INR measurements varies from patient to patient and is driven by how stable the INR measurements are over time.

While aspirin and warfarin can be very effective in reducing the risk of stroke (and heart attack), they are associated with a small risk of serious side effects. Most of the side effects are bleeding related. Patients at higher risk for injury (those with balance issues, patients who abuse alcohol, and those who work in professions where falls are possible, etc.) may not be able to use warfarin, even if they would otherwise qualify for this therapy.

Rate control

To slow heart rate, doctors usually rely on beta-blockers (such as metoprolol, propranolol, etc.), calcium channel blockers (verapamil, diltiazem, etc.), or digoxin. Other agents can be prescribed depending on your particular needs. Beta blockers and calcium channel blockers, although relatively safe, can lower blood pressure and slow the heart rate profoundly. That is why your doctor will carefully monitor the effects of whatever medication you are prescribed.

Rhythm control

Ideally, you want to get your heart to regain its normal rhythm, although this becomes more difficult the longer you have AF. To convert the heart to normal sinus rhythm, doctors may use cardioversion, which is defined as the conversion of one cardiac rhythm or electrical pattern to another. This can be accomplished with drug therapy or with medical procedures.

The medications used to treat AF, generally referred to as antiarrhythmics, are designed to suppress arrhythmias or pharmacologically convert an arrhythmia to a normal rhythm. The particular agent used to treat an episode of AF will depend on a number of variables, including the type of AF being treated (paroxysmal or persistent), patient age and other health issues which may be present. These drugs may be given by mouth or intravenously for faster delivery (although the latter is more likely if you have been hospitalized). If the antiarrhythmic medications produce the desired effect on an episode of AF (that is, you return to normal sinus rhythm), you may be given the same or similar medication to prevent repeat episodes of AF.  In some cases, you will need to take the medicine on a regular, ongoing basis; in others, you will take it as needed.

One potential side effect of medications that are used to control heart rhythm is that they may paradoxically cause different rhythm problems (“proarrhythmic effect”).  This is why some of these medications are only administered in a hospital setting and why your doctor will carefully monitor the effects of whatever medication you are prescribed. Ongoing research is evaluating newer agents that may improve on the effectiveness or safety of the currently available antiarrhythmic drugs. It is always wise to periodically check in with your doctor to see if any new medications are available that would be beneficial in your particular case.

Alternatives to drug therapy

When medications do not work, there are alternatives. Electrical cardioversion uses a jolt of electricity to your heart either through paddles or wired patches attached to your chest. This is a controlled, usually prescheduled procedure – not the type of emergency “defibrillation” depicted in film or on TV when a character’s heart has stopped. Defibrillation is done under light anesthesia in the hospital, and the patient usually goes home the day of the procedure.

Another option is catheter ablation, which targets and destroys small areas of cells in the heart thought to be the source of electrical malfunction. In this technique, a catheter is threaded into your heart and radio frequency energy in the form of radio waves is emitted to selectively cauterize the errant heart cells. This procedure usually improves heart function, exercise capacity, and quality of life.

The aim of catheter ablation is to “cure” AF, although that word may be misleading. Most studies which have looked at the outcome of ablation have followed patients for only 5- to 10-years. It’s unknown whether these “cured” patients may once again develop AF.

Not all patients undergoing ablation have their arrhythmia completely eliminated by the procedure.  Nevertheless, many such patients sill experience greatly improved heart rate control. The result of ablation may be that drug therapy that failed to control heart rate in the past may be effective once again. Between those patients experiencing an effective “cure” and those who see great improvement following ablation, the overall success rate of this procedure is about 70% to 80%. One important point: if ablation does not provide rhythm control, medications for that problem may remain necessary, as may the need for antithrombotic therapy to prevent blood clot formation. In some cases, implantation of a pacemaker will be recommended.
By the way, these ablation procedures may be repeated in some patients. As many as one-third of all patients end up getting a second procedure, which often proves effective for a year or more.

Another rhythm-control strategy is the Maze procedure, which often requires open heart surgery, because the clinician must make precise, small cuts (or possibly catheter burns) in specific places on the atria. The goal is to create a pattern of scar tissue – which does not conduct electricity – that effectively “walls off” the errantly firing heart tissue, preventing the AF from spreading to the rest of the heart. The procedure’s name comes from the pattern of incisions made in the atria – which look like a child’s maze.  Usually, the Maze procedure is only performed when open heart surgery is required for other reasons.

Rate versus rhythm control

The best-case scenario occurs when a treatment provides both effective rate and rhythm control. However, when treatment is not effective or it loses effectiveness over time, there has been a great deal of argument as to which approach is better: rhythm control or rate control. One common approach is to initially target rhythm control with the thought that restoration of normal sinus rhythm will lower the risk of stroke; reduce symptoms; improve exercise tolerance, quality of life, and even survival; and perhaps permit discontinuation of long-term warfarin therapy. Unfortunately, AF is not always responsive to antiarrhythmic therapy. Moreover, these drugs have been known to have serious side effects. That’s why it makes sense to opt for rate-control strategies in some patients, especially given that rate-control drugs are usually much less toxic than antiarrhythmic therapy.
Some researchers have compared the two strategies to see if either presents a survival advantage over the other. In the Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) trial involving 4,060 patients with advanced heart disease, there was no significant difference in terms of mortality rates between patients assigned to rate-control therapy and those receiving rhythm-control therapy. However, the rhythm-control group was hospitalized more often and experienced more adverse drug effects than those undergoing rate-control therapy.

A more recent study, the Atrial Fibrillation with Congestive Heart Failure (AF-CHF) study, involved an even sicker population of patients. Again, rhythm-control was no better than rate control in preventing deaths from cardiovascular causes.  Because of the greater spectrum of side effects seen with rhythm control, the investigators concluded that rate control should be the first approach in similar patients with advanced heart failure.

As far as which approach is best for you needs to be determined in the context of your overall health situation.  Your personal physician is in the best position to advise you in regards to these considerations.

Overall, the presence of AF does not preclude an active life. The disorder is usually controllable with treatment and many people with atrial fibrillation do very well. However, AF tends to become a chronic condition and may come back even with initially successful treatment.


As previously noted, there is an increased risk of stroke in people with AF and the risk is even greater in the presence of other types of heart disease. Persistent and especially permanent AF also leaves individuals susceptible to other cardiac diseases, especially heart failure, and an overall increased risk of dying. In fact, the death rate of patients with AF is about double that of people with normal sinus rhythm.

Because AF results in less efficient heart pumping, this rhythm can also affect quality of life, making it more difficult to handle even routine physical activities. In some patients, the AF is completely asymptomatic, having no effect on general sense of well being or activity levels.


Always take antiarrhythmic drugs exactly as directed. These drugs work best when they are at constant levels in the blood. To help keep levels constant, take your medicine as directed; do not miss any doses and never take larger or more frequent doses. Don’t stop taking antiarrhythmic drugs without checking first with your physician, because stopping some of these drugs suddenly could lead to serious side effects. If taking medicine at night interferes with sleep, or if it is difficult to remember to take your medicine during the day, check with a health care professional for suggestions.

When you visit your doctor or an emergency room (whether for an AF-related problem or not), bring a detailed list of all your prescription drugs with you.   Having a complete picture of all your medications is critical in any health care setting, but it is especially important if you are taking antiarrhythmics. Also, keep all medical appointments; don’t assume that because you’re feeling better it is not necessary to visit your doctor. Precise updates on your condition are required to make sure that the treatment strategy is right (and safe) for you. Keeping regular doctor’s appointments is particularly critical if you are taking anticoagulants or blood-thinning medications. If you experience medication side effects or symptoms of AF, be sure to share that with your doctor.

Besides making sure you follow all directions related to your prescription medications, beware of over-the-counter medicines – those that do not require a prescription – including nutritional supplements and cold and allergy medicines.  Some of these widely available drugs may contain stimulants or have other properties that can trigger arrhythmias and/or interact with your prescription medications in ways that can lessen their effectiveness or make the prescription drug much more powerful, increasing the likelihood of a serious side effect or other adverse event.

Limiting alcohol consumption is important, too, especially if alcohol triggers your AF. Reducing intake of caffeinated beverages may also be recommended since caffeine has stimulating properties that could be harmful in people with AF.


Left untreated, AF causes the atrial chambers to weaken and stretch out. This makes it even harder for the atria to contract properly, which leads to even more blood pooling in the atria, and a greater risk of stroke and heart failure. Treating AF correctly is the best way to reduce stroke risk.

If you are at risk of developing AF (based on family history, for example) you can help prevent AF. This requires action that can prevent or control the major risk factors for AF, such as coronary artery disease, hypertension, excess weight and diabetes. By avoiding these risk factors, you can significantly reduce your chances of experiencing AF during your lifetime.

This requires adopting a heart-healthy lifestyle, which means weight loss if you are overweight, changing to a heart-healthy diet, becoming more physically active, and making sure that hypertension or other conditions that can lead to heart disease are treated and well managed.


**Source: Cardiosource- American College of Cardiology.


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