Dilated Cardiomyopathy

The prevalence of congestive heart failure is on the increase both in the United States and all over the world, and it is the leading cause of hospitalization in the elderly population. Congestive heart failure is a progressive disease generally seen in the elderly, which if not properly managed, can lead to repeated hospital admissions or death. Heart failure means that the heart muscle is weakened. A weakened heart muscle may not be strong enough to pump an adequate amount of blood out of its chambers. To compensate for its diminished pumping capacity, the heart may enlarge. Commonly, the heart's pumping inefficiency causes a buildup of blood in the

Apical hypertrophic cardiomyopathy is a disease that mainly affects the apex of the heart and does not cause any obstruction. [1] These abnormalities in the heart muscle can cause a wide variety of symptoms. As the heart becomes stiff it increases the pressure in the left ventricle which can push blood back into the lungs, causing shortness of breath in exercise. Chest pain can occur as there is not enough oxygen available to the cardiac muscle due to insufficient blood supply. Palpitations and lightheadedness, along with other conditions can occur as a result of HCM. In addition to these discomforting symptoms, the patient may develop an arrhythmias that often goes unnoticed. An arrhythmia takes place as the electrical conduction of the heart is disturbed by the abnormal scattering of myocytes. The two most common arrhythmias are atrial fibrillation causing palpitations, and ventricular tachycardia that can be life threatening causing sudden death. Both conditions can be controlled with medication. [4]

Systolic heart failure is characterized by enlarged ventricles that are unable to fully contract to pump enough blood into circulation to adequately perfuse tissues. The enlargement in ventricles is due to an increased end-systolic volume. If the heart is not able to sufficiently pump the expected volume of blood with each contraction, which in a normal healthy heart is 50-60%, there will be a residual volume left in the heart after every pump (Heart Healthy Women, 2012). With the next period of filling, the heart will receive the same amount of blood volume from the atria combined with that residual volume from the previous contraction. This causes the ventricles to have to dilate to accommodate this increase in volume. The dilation causes the walls of the ventricles to stretch and become thin and weak. Also the myocardium, the muscle layer of the heart, will stretch and not be able to adequately make a full and forceful enough contraction to push blood from the ventricles (Lehne, 2010).

CHF can be caused by many different reasons. Sometimes CHF can be a heart defect or can be caused by unhealthy lifestyles. “CHF is an ongoing condition in which the heart muscle is weakened and can’t pump as well as it normally does” (Congestive Heart Failure). When the heart becomes too weak to continue to pump blood throughout the body, it is called Congestive Heart Failure. When CHF first

As this disease progresses and the workload of the heart is consistently increased, ventricular hypertrophy occurs. At first, the hypertrophied heart muscles will increase contractility, thus increasing cardiac output; however, as hypertrophy of the ventricular myocardial cells continues, it begins to have poor contractility, requires more oxygen to perform, and has poor circulation from the coronary arteries. This can result in heart tissue ischemia and lead into cardiac dysrhythmias (Lewis et al. 2014, 768).

Contractility is the pumping of the heart muscle. It is measured as the ejection fraction. Contractility directly influences stroke volume. Increased contractility will increase stroke volume with any amount of preload. Diseases that disrupt myocyte activity reduce contractility. Myocardial infarction is the most common. Others include, but are not limited to, cardiomyopathies, degenerative valve disease, and myocarditis (Francis & Tang, 2003). Secondary causes of decreased contractility, such as myocardial ischemia and increased myocardial workload, contribute to neurohumoral , immune, and inflammatory changes and can cause ventricular remodeling. Ventricular remodeling occurs when the size, shape, and function of the affected chamber is distorted. Ventricular remodeling causes hypertrophy and dilation of the heart muscle and causes progressive myocyte contractile dysfunction over a period of time. When contractility is decreased, stroke

Congestive Heart Failure, also known as "cardiac decompensation, cardiac insufficiency, and cardiac incompetence," (Basic Nursing 1111) is an imbalance in pump function in which the heart is failing and unable to do its work pumping enough blood to meet the needs of the body's other organs. To some people, heart failure is defined as a sudden and complete stoppage of heart activity—i.e. that the heart just stops beating. This is an inaccuracy. Heart failure usually develops slowly, often over years, as the heart gradually loses its pumping ability and works less efficiently. CHF is a syndrome that affects individuals in different ways and to different degrees. It is usually a chronic disease. It gradually

Congestive Heart Failure is when the heart's pumping power is weaker than normal. It does not mean the heart has stopped working. The blood moves through the heart and body at a slower rate, and pressure in the heart increases. This means; the heart cannot pump enough oxygen and nutrients to meet the body's needs. The chambers of the heart respond by stretching to hold more blood to pump through the body or by becoming more stiff and thickened. This only keeps the blood moving for a short while. The heart muscle walls weaken and are unable to pump as strongly. This makes the kidneys respond by causing the body to retain fluid and sodium. When the body builds up with fluids, it becomes congested. Many conditions can cause heart

Congestive heart failure is an older name for heart failure. Congestive heart failure takes place when the heart is unable to maintain an adequate circulation of blood in the bodily tissues or to pump out the venous blood returned to it by the veins (Merriam-Webster). The heart is split into two distinct pumping structures, the right side of the heart and the left side of the heart. Appropriate cardiac performance involves each ventricle to extract even quantities of blood over intervals. If the volume of blood reimbursed to the heart develops more than both ventricles can manage, the heart can no longer be an efficient pump.

Stem cells have made significant promise to help people understand and treat a broad range of injuries, diseases, and other health-related issues. This type of treatment has saved the lives of many people with leukemia and can also be used for tissue grafts to treat conditions with the skin, bone and surface of the eye ("Nine Things to Know about Stem Cell Treatments"). Dilated cardiomyopathy (DMC) is a disease characterized by expansion of the left ventricular chamber and it is usually associated with systolic dysfunction. The presentations of the condition include heart failure, myocardial infarction, and arrhythmia and as a refractory life-threatening condition which can cause heart failure, transplantation remains the ultimate therapy for

The major causes of diastolic heart failure are hypertension-induced myocardial hypertrophy and myocardial ischemia-induced ventricular transformation (coronary artery disease). Hypertrophy and ischemia cause a decreased ability of the myocytes to actively pump calcium from the cytosol, resulting in impaired relaxation. Some of the other causes are aortic valvular disease and cardiomyopathies. Diabetes can also lead to diastolic heart failure (Huether and McCune 2012). Other risk factors for this disease are chronic kidney disease, obstructive sleep apnea, and older age. There are two types of the heart failure: systolic heart failure and diastolic heart failure. In systolic heart failure, the left ventricle has difficulty contracting and ejecting blood into the circulation, which causes reduced left ventricular fraction. On the other hand, diastolic heart failure has a slow and delayed relaxation and increased chamber rigidity, which then causes inadequate filling of blood and

Cardiac hypertrophy is the enlargement of the lower, ventricular walls of the heart. Most commonly occurring in the left ventricular side, cardiac hypertrophy can occur on one side or both. Characterized by abnormal heart muscle growth it can be a healthy response to pregnancy or exercise. However, an increase in heart size could also be a sign of hypertension, diabetes, muscular dystrophy, obesity, or cardiomyopathy. Hypertrophy of the heart can be adaptive or maladaptive, therefore the growth may not lead to an increase in cardiac output.

When the ventricles are contracting at a rate greater than one hundred beats per minute, the heart becomes inefficient. Blood cannot properly fill the ventricular chambers before it is forced out. This decreases the amount of oxygenated blood circulating through the body.

The goal of medical management is to minimized myocardial damage, preserve myocardial function, and prevent complications. These goals are achieved by reperfusing the area by emergency use of Percutaneous Transluminal Coronary Angioplasty (PTCA) or thrombolytic medication. Minimizing myocardial damage is also accomplished by reducing myocardial oxygen demand and increasing oxygen supply with medications, oxygen administration, and bed rest.

It is well established that cardiomyopathy can be recapitulated by experimental immunization with cardiac myosin plus an adjuvant or with the administration of antibodies against troponin I and the β1-adrenergic receptor (33, 28, 34, 35). Similarly, we provide evidence that autoimmunity against specific M2AChR epitopes (M2AChR-el2 and M2AChR-il3) may play a causal role in DCM. Therefore, BALB/c mice were DNA-immunized using a gene gun with plasmids encoding partial epitopes to induce potentially harmful anti-M2AChR-el2 and anti-M2AChR-il3 antibodies and establish cardiomyopathy. All mice progressively developed left ventricle dilation and dysfunction detected by echocardiography analyses (approximately 10-20 weeks post-immunization). Next, we mimicked the presence of autoantibodies