The most common form, dilated cardiomyopathy (DCM), occurs when your heart muscle is too weak to pump blood efficiently. The muscles stretch and become thinner. This allows the chambers of your heart to expand. This is also known as enlarged heart.
How do you know if you have a weak heart?
The most common symptom of coronary artery disease is angina, or chest pain. ... Palpitations (irregular heart beats, or a "flip-flop" feeling in your chest) A faster heartbeat. Weakness or dizziness.
What does a weak heart mean?
The definition of heart failure is when the heart cannot pump efficiently enough for blood to circulate oxygen-rich blood throughout the body. When the heart becomes weak or when it becomes thickened and stiff, the heart muscle cannot keep up with its workload.
How long can you live with a weak heart?
While advancements have been made, 50% of patients will have an average life expectancy of five years. For those with advanced heart failure, up to 90% will pass away within one year. When asking how long can you live with congestive heart failure, those at a moderate stage will average ten years.
How do you strengthen a weak heart?
Just Making Exercise A Regular Part Of Your Lifestyle Can Result In:
- Strengthened heart and cardiovascular system.
- Improved circulation/oxygen use.
- Increased energy levels.
- Increased endurance.
- Lower blood pressure.
- Reduced stress.
- Improved muscle tone and strength.
- Improved balance and joint flexibility.
What is the first sign of heart failure?
Heart failure signs and symptoms may include: Shortness of breath (dyspnea) when you exert yourself or when you lie down. Fatigue and weakness. Swelling (edema) in your legs, ankles and feet.
Exercise Helps Repair Muscle Damage In Heart Failure Patients
- Date: November 8, 2007
Exercise increased the growth of new muscle cells and blood vessels in the weakened muscles of people with heart failure, according to two new studies.
"If you have heart failure, exercise training can improve your health status, increase your ability to exercise and reverse patterns of muscle damage that are common in heart failure," said Axel Linke, M.D., assistant professor of medicine at the University of Leipzig, Germany, and a co-author on both studies.
In chronic heart failure, the heart can't pump enough blood to other organs in the body.
"In addition to getting out of condition because it becomes difficult to exercise, people with heart failure have cellular-level changes in their muscles that make them weaker, more prone to fatigue, and in later stages results in actual muscle shrinkage," he said.
In one study (abstract 3797), researchers investigated whether exercise training could activate progenitor cells, a pool of immature cells in skeletal muscle that can divide into various mature cells as needed for muscle repair.
Compared with healthy people, those with heart failure have about a 50 percent reduction in the number of progenitor cells in their muscles, Linke said.
Researchers examined biopsies of the vastus lateralis, the largest quadricep muscle in the outer thigh, in 50 men, average age 56, with moderate to severe heart failure -- a level at which any exercise is uncomfortable. Researchers took the biopsies before and after a six-month period in which 25 men remained inactive and the other 25 participated in an individualized, physician-supervised endurance exercise program.
Study participants rode a stationary bicycle at least 30 minutes a day (usually divided into two sessions) at about half their peak exercise capacity.
At the end of the six-month study, levels of progenitor cells stayed the same in the inactive group but changed significantly in the exercisers:
Participants in the exercise program also felt better and increased their exercise capacity 20 percent during the six-month study, Linke said.
Whether exercise can induce similar changes in heart muscle is not known, researchers said.
"We also have c-kit+ cells in the heart but we don't know whether they are similar to those in skeletal muscle," Linke said.
In the second study (abstract 3796), researchers tracked endothelial progenitor cells that are created in bone marrow and circulate through the bloodstream. The cells help repair damaged blood vessel linings and spur new vessels to form in a process called vasculogenesis.
In heart failure, the linings of blood vessels are damaged, blood vessels in muscle do not dilate normally, and the number of small blood vessels (capillaries) in muscle tissue is reduced.
Researchers randomly assigned 37 men, average age 65, with severe heart failure to receive either 12 weeks of exercise training or to remain inactive. They took blood tests and biopsies of the quadricep muscle before and after the program. After 12 weeks, researchers found no changes in men assigned to the control group. In contrast, exercisers changed significantly:
More than 5 million people in the United States have heart failure. About 1 percent of people over age 65 start having heart failure annually.
Co-authors of both studies are Volker Adams, Ph.D., presenter; Sandra Erbs, M.D.; Robert Höllriegel, M.D.; Ephraim B. Beck, M.D.; Stephan Gielen, M.D.; Sven Möbius-Winkler, M.D.; Rainer Hambrecht, M.D.; and Gerhard Schuler, M.D.
In chronic heart failure, the heart can't pump enough blood to other organs in the body.
These studies were reported at the American Heart Association's Scientific Sessions 2007. The German Heart Foundation funded the studies.
In chronic heart failure, the heart can't pump enough blood to other organs in the body.
"In addition to getting out of condition because it becomes difficult to exercise, people with heart failure have cellular-level changes in their muscles that make them weaker, more prone to fatigue, and in later stages results in actual muscle shrinkage," he said.
In one study (abstract 3797), researchers investigated whether exercise training could activate progenitor cells, a pool of immature cells in skeletal muscle that can divide into various mature cells as needed for muscle repair.
Compared with healthy people, those with heart failure have about a 50 percent reduction in the number of progenitor cells in their muscles, Linke said.
Researchers examined biopsies of the vastus lateralis, the largest quadricep muscle in the outer thigh, in 50 men, average age 56, with moderate to severe heart failure -- a level at which any exercise is uncomfortable. Researchers took the biopsies before and after a six-month period in which 25 men remained inactive and the other 25 participated in an individualized, physician-supervised endurance exercise program.
Study participants rode a stationary bicycle at least 30 minutes a day (usually divided into two sessions) at about half their peak exercise capacity.
At the end of the six-month study, levels of progenitor cells stayed the same in the inactive group but changed significantly in the exercisers:
- Total number of progenitor cells (identified by c-kit+ protein marker on the cell surface) increased by 109 percent.
- Progenitor cells differentiating into muscle cells (identified by c-kit/MEF2+ marker) increased by 166 percent.
- Progenitor cells actively dividing to form new cells and repair muscle damage (identified by c-kit/Ki67+ protein marker) significantly increased six-fold.
Participants in the exercise program also felt better and increased their exercise capacity 20 percent during the six-month study, Linke said.
Whether exercise can induce similar changes in heart muscle is not known, researchers said.
"We also have c-kit+ cells in the heart but we don't know whether they are similar to those in skeletal muscle," Linke said.
In the second study (abstract 3796), researchers tracked endothelial progenitor cells that are created in bone marrow and circulate through the bloodstream. The cells help repair damaged blood vessel linings and spur new vessels to form in a process called vasculogenesis.
In heart failure, the linings of blood vessels are damaged, blood vessels in muscle do not dilate normally, and the number of small blood vessels (capillaries) in muscle tissue is reduced.
Researchers randomly assigned 37 men, average age 65, with severe heart failure to receive either 12 weeks of exercise training or to remain inactive. They took blood tests and biopsies of the quadricep muscle before and after the program. After 12 weeks, researchers found no changes in men assigned to the control group. In contrast, exercisers changed significantly:
- Circulating progenitor cells (identified by CD34+ marker) increased 47 percent.
- Circulating progenitor cells beginning to mature into endothelial cells (identified by CD34/KDR+ marker) significantly increased 199 percent.
- Functional activity of the circulating progenitor cells (measured by migratory capacity) significantly increased 149 percent.
- The density of capillaries in skeletal tissue significantly increased 17 percent.
More than 5 million people in the United States have heart failure. About 1 percent of people over age 65 start having heart failure annually.
Co-authors of both studies are Volker Adams, Ph.D., presenter; Sandra Erbs, M.D.; Robert Höllriegel, M.D.; Ephraim B. Beck, M.D.; Stephan Gielen, M.D.; Sven Möbius-Winkler, M.D.; Rainer Hambrecht, M.D.; and Gerhard Schuler, M.D.
In chronic heart failure, the heart can't pump enough blood to other organs in the body.
These studies were reported at the American Heart Association's Scientific Sessions 2007. The German Heart Foundation funded the studies.
Story Source:
Materials provided by American Heart Association.
Materials provided by American Heart Association.
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