Thursday, March 22, 2012

Warning - This Post is a Snoozer

If you’re like me, the more you know about something the better.  I always want to know what, why, where, and how.  And somehow this helps me.  I had an echocardiogram last week and found out that, despite the device installation, my ejection fraction is still just 15-20%.  It may just take more time.  Also, the medication that I had asked my cardiologist to reduce must now be put back at the higher dosage.  I guess I don’t have a medical degree after all. 
I feel great most of the time; I work full time and seriously do anything I want.  I am focused on living life to the fullest.  Losing weight and exercising more are still squarely on my target.  I am happier than I’ve ever been.
The following information was copied from a US News article written in conjunction with the Mayo Clinic.  Even though this article is from 2008, I learned a few new things.  It is a long read but you’ll find it interesting if you have dilated cardiomyopathy:
Cardiomyopathy is a general term used to describe a diverse group of diseases of the heart muscle. For most people with cardiomyopathy, their hearts don't function normally because the heart has become enlarged, abnormally thick, abnormally rigid, or unable to transmit electrical impulses in a normal fashion. These changes in the heart muscle correspond to the four principal types of cardiomyopathy—dilated cardiomyopathy, hypertrophic cardiomyopathy, restrictive cardiomyopathy, and arrhythmogenic right ventricular cardiomyopathy. Included in each of these categories are several dozen types of cardiomyopathy that are distinguished from one another based upon their individual cause.
Coronary artery disease, inflammatory diseases, viral or bacterial infections, chronic alcoholism, and metabolic and blood disorders are some of the more common conditions that can lead to cardiomyopathy. Genetic mutations, including some that run in families, can also cause cardiomyopathy. However, many forms of cardiomyopathy have no apparent cause; these are said to be idiopathic. Although it can affect people of all ages, sometimes even at birth, certain types of cardiomyopathy are more likely to occur in specific age groups, in men more than women, or in people of certain ethnic groups.
Many people can live long, healthy lives not even realizing that they have cardiomyopathy because they have no symptoms. For others, cardiomyopathy leads to serious complications including heart failure, abnormal heart rhythms, or sudden death. Cardiomyopathy is a leading cause for heart transplants and the most common identifiable cause of sudden death in young athletes. If the symptoms of heart failure develop, the outlook for people with cardiomyopathy can be discouraging—only one out of every three patients survives more than five years following the onset of heart failure. However, the symptoms and complications of many forms of cardiomyopathy can be effectively controlled using medication, surgery, and/or simple lifestyle changes.

The structure of the heart is analogous to a two-story house with four rooms or chambers. On the main floor are the two largest rooms, the left and right ventricles. The ventricles are the main pumping chambers of the heart. In a healthy heart, the left ventricle is the stronger pumping chamber. The wall between these two rooms is called the ventricular septum. Upstairs, there are two smaller rooms, the left and right atria. The atria function primarily as receiving chambers for blood, but they also help out slightly with pumping. The wall between the two atria is called the atrial septum.
The valves of the heart function like one-way doors that help control the direction of blood flow; this keeps the heart working efficiently. The four valves in the heart are the tricuspid, mitral, pulmonary, and aortic valves. Proper functioning of the mitral valve, which connects the left atrium to the left ventricle, can be important for people suffering from heart failure associated with dilated cardiomyopathy. The mitral valve keeps the blood flowing into the left ventricle, where it is pumped out of the heart and circulated throughout the body.
The pulmonary and the aortic arteries are the main pathways for blood in and around the heart. The pulmonary artery shunts blood from the right ventricle to the lungs. The pulmonary veins channel blood from the lungs back to the heart into the left ventricle. The aorta channels blood from the heart to the body. The coronary arteries, which branch off the aorta, distribute blood to the heart itself.

In general, the right side of the heart is responsible for pumping blood to the lungs. In a healthy heart, oxygen-depleted blood enters the heart at the right atrium, where it is pumped down into the right ventricle. When the right ventricle fills, the heart contracts strongly and pumps the blood through the pulmonary valve into the pulmonary artery, which carries the blood to the lungs. The pulmonary valve keeps the blood moving toward the lungs, preventing it from mixing with oxygen-rich blood.
In the lungs, the carbon dioxide in the blood is exchanged for oxygen. The oxygenated blood leaves the lungs and returns to the heart via the pulmonary veins, re-entering the heart at the left atrium. Exiting the left atrium through the mitral valve, the blood flows into the left ventricle. When the left ventricle fills with blood, the heart contracts strongly, pumping blood out through the aortic valve into the aorta to circulate oxygen to the rest of the body.
Ejection Fraction and Cardiomyopathy:
The primary pumping action of the heart is like a spring that contracts and relaxes. When the heart is relaxed, the ventricles simultaneously fill with blood. When the heart contracts, the ventricles eject a portion of the blood they contain to either the lungs (via the pulmonary artery from the right ventricle) or the rest of the body (via the aorta from the left ventricle). That exact portion of blood pumped out of the ventricles is called the ejection fraction. In a healthy heart, the ejection fraction is greater than 55-60 percent. If the ejection fraction falls below 55 percent, the heart is no longer able to circulate an adequate amount of blood to the body at a normal heart rate. A decrease in the volume of blood circulating throughout the body can cause a cascade of changes in the body's metabolism.
Like a spring, if a ventricle is continually overextended or stiff, it no longer functions properly. An overextended ventricle can lose the ability to contract, reducing the ejection fraction. The inverse problem can also occur where the ventricle is abnormally stiff. In this scenario, the ventricle no longer relaxes enough to fill adequately with blood. As a result, the volume of blood ejected from the heart is abnormally low because less blood has entered the heart.
Dilated cardiomyopathy, a common form of cardiomyopathy, is characterized by an overall enlargement or stretching of the heart muscle accompanied by a decrease in the heart's ability to contract. Dilated cardiomyopathy usually begins with stretching of the left ventricle; in some cases, the right ventricle may become affected as well. Dilated cardiomyopathy can lead to heart failure, a decrease in the heart's ability to contract and pump blood out into the arteries of the body. Other complications include disturbances in the heart's electrical system known as arrhythmias, blood clots forming within the heart, and sudden death, any of which can occur at any stage of the disease.
Although it can occur in infants and the elderly, dilated cardiomyopathy occurs most frequently between the ages of 20 and 60. It is three times more common in men than women and more common in African-Americans than Caucasians.
The progression of dilated cardiomyopathy can be rapid; some studies have found that 50 percent of deaths due to dilated cardiomyopathy occur within two years of diagnosis, although the risk of dying within one year for all patients with heart failure symptoms is about 12 percent. In general, the worse the symptoms, the worse the outlook. For example, a patient with mild breathlessness during significant exertion may have a 5 percent chance of dying within a year, while a person who has these symptoms while sitting in a chair may have a 30-50 percent risk of dying within a year.
When cardiomyopathy is caused by coronary artery disease (CAD) it is known as ischemic cardiomyopathy, the most common type of cardiomyopathy. People with ischemic cardiomyopathy often develop the same signs and symptoms as those with other forms of dilated cardiomyopathy. However, with ischemic cardiomyopathy, the symptoms are caused by narrowed or blocked coronary blood vessels restricting blood flow and oxygen to the heart tissue, which damages the heart muscle. Even though the signs and symptoms are the same, ischemic cardiomyopathy has traditionally been considered separate from dilated cardiomyopathy because coronary artery disease typically causes localized damage to the heart as opposed to the generalized damage of all heart cells associated with dilated cardiomyopathy. More importantly, the damage to heart muscle associated with ischemic cardiomyopathy can be reversed in some patients by opening the blockages caused by CAD. For this reason, almost all patients with a new diagnosis of dilated cardiomyopathy undergo a coronary angiogram to evaluate the condition of their coronary arteries.
Dilated cardiomyopathies can be caused by many other conditions or the cause may never be identified. In the United States, dilated cardiomyopathies other than ischemic cardiomyopathy account for 50,000 hospitalizations and over 10,000 deaths annually—and these statistics are on the rise. Other common types of dilated cardiomyopathy include:
Inflammatory cardiomyopathy can develop as the result of viral, bacterial, or autoimmune infection as well as myocardial inflammatory disease. Some of the infectious and inflammatory conditions that have been linked to inflammatory dilated cardiomyopathy are lymphocytic and giant cell myocarditis, Lyme disease, HIV, mumps, influenza, Epstein-Barr, and hepatitis B and C.
Familial (genetic) cardiomyopathy accounts for roughly 20 percent of all cases of dilated cardiomyopathy where no other cause can be identified. The details of the genetic link are not well understood but it's clear there is a genetic predisposition to developing dilated cardiomyopathy in some families. As such, evaluation of all first-degree relatives to rule out a "silent" familial cardiomyopathy is recommended for people whose dilated cardiomyopathy cannot be attributed to a specific cause.
Alcoholic cardiomyopathy usually begins to develop after about 10 years of heavy alcohol consumption.
Toxic cardiomyopathy may develop after exposure to certain toxins including cocaine, methamphetamines and some chemotherapy drugs.
Peripartum cardiomyopathy can develop in women during the last trimester of pregnancy or within five months after childbirth. Women often recover completely from peripartum cardiomyopathy, but it may recur with future pregnancies.
Valvular cardiomyopathy can develop when the workload on the heart in increased due to a malfunctioning heart valve.
Tachycardia-induced cardiomyopathy, caused by chronic rapid heart rate, is important to identify because the symptoms of heart failure can be reversed in these people by treating the arrhythmia.

The change in the heart muscle associated with the principal types of cardiomyopathy is the result of the interplay of a variety of factors. Genetic mutations in the cells of the heart muscle, other diseases, environmental and lifestyle factors, and the body's own survival mechanism can contribute to the development of cardiomyopathy.

Dilated cardiomyopathy can be thought of as a compensatory reaction of the heart to a weakened heart muscle. The cause of the weakening may be unknown or it may be associated with many different risk factors including viral infections, exposure to toxins and drugs, or coronary artery disease, as in ischemic cardiomyopathy.
In people with dilated cardiomyopathy, the heart enlarges to compensate for the inability of a weakened muscle to eject the amount of blood needed by the body. Stretching helps compensate for the weakened muscle in two ways. First, the overall volume of the heart is increased, thereby increasing the volume of blood ejected into the circulatory system. This action is analogous to a person squeezing a flexible plastic bottle. A strong person might be able to squirt out 50 percent of the contents of the bottle with each squeeze. If the person's grip is weakened and he is only able to eject 25 percent of the contents, only half as much liquid will exit the bottle. However, if the person had a bottle that holds twice as much, 25 percent of that bottle would be twice as much volume. In dilated cardiomyopathy, the heart is acting like the plastic squeeze bottle, dilating its chambers to try to maintain the amount of blood pumped to the tissues of the body by a heart whose ejection fraction is diminishing.
Stretching the heart muscle can also increase the strength of the contraction. Starling's Law, a basic principle involving the function of the heart, describes this phenomenon: the more the heart muscle stretches, the greater the force of its squeeze. The heart functions much like a spring whose coils are overstretched and then released to snap back into shape. If this action continues repeatedly, the heart will eventually lose the ability to regain its original shape, like an overstretched spring.
The heart can also compensate by beating faster. Although beating faster can improve circulation temporarily—normal hearts do this during exercise—a chronic increase in heart rate (tachycardia) can lead to dilated cardiomyopathy or serious arrhythmias.
The kidneys may also try to compensate for the decreased circulation by increasing the volume of blood and fluid in the circulatory system. Ironically, this compensatory mechanism exacerbates the situation by causing swelling in the legs and abdomen, and fluid accumulation in the lungs.
All of these compensatory mechanisms—dilating, stretching, beating faster, retaining fluid—evolved to keep the blood pumping to the body on a short-term basis following an injury or dehydration. In the long term, though, the heart responds like a spring that's been overextended; eventually, it can no longer return to its shape and function effectively. Then the dilated heart becomes more of a dam than a pump, with blood pooling inside an enlarged heart that is no longer capable of circulating blood. The most effective treatments for dilated cardiomyopathy focus on blocking these compensatory responses.

Risk Factors:

Medical research continues to reveal how different risk factors interact to influence a person's health and lifespan. Understanding your risks allows you to develop a strategy and make lifestyle choices accordingly. Your decisions then balance the value you place on your health with the risks that may compromise your health in the future. An increased risk does not mean the disease is inevitable; risk refers to the possibility that a disease could occur in the future.

The risk factors for dilated cardiomyopathy include both lifestyle choices as well as genetic traits. Many of the risk factors are actually other diseases. Uncommon bacterial or viral infections, rare blood disorders, and other inflammatory diseases can lead to dilated cardiomyopathy in some people.

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