Heart Failure is a progressive heart disease when the muscle of the heart is weakened so that it cannot pump blood as it should; the blood backs up into the blood vessels around the lungs and the other parts of the body (NHS Choice, 2015). In heart failure, the heart is not able to maintain a normal range cardiac output to meet the metabolic needs of the body (Kemp and Conte, 2012). Heart failure is a major worldwide public health problem, it is the end stage of heart disease and it could lead to high mortality. At present, heart failure is usually associated with old age, given the dramatic increase in the population of older people (ACCF/AHA, 2013). In the USA, there are about 5.7 million adults who have heart failure, about half of the people die within 5 years of diagnosis, and it costs the nation an estimated $30.7 billion each year (ACCF/AHA, 2013).
Systolic heart failure results from the inability of the cardiac muscle to contract effectively from inadequate cardiac output. As the cardiac output drops, compensatory mechanisms to try to restore its function through takes place by ventricular remodeling. During this remodeling phase, the heart begins to develop changes in its size and becomes hypertrophic that results in a decreased ability of the heart to contract, decreased available oxygen, and available ATP. Secondly, this hypertrophic states increases preload that results
The research team hopes to use the numerical model they have designed to link modifications that take place at the cellular and tissue level when a heart fails to a numerically computed ECG. This, they wish, will assist to determine what it is that triggers ventricular fibrillation (VF), and to recognize the risk of VF.
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
Heart failure is a syndrome that involves dysfunction of the cardiac muscle that results in or increase the risk of developing manifestations of low cardiac output and/or pulmonary or systemic congestion (Grossman & Porth, 2014). The National Heart, Lung, and Blood Institute estimate that about 5.8 million people in the United States have heart failure. Even though heart failure can occur in any age group, it primarily affects older adults. Although morbidity and mortality rates from other cardiovascular diseases have decreased over the past several decades, the incidence of heart failure is increasing at an alarming rate. Approximately 400,000 to 700,000 people are diagnosed with heart failure each year (Grossman &
Stem cells have the ability to grow heart cells, which can further lead to new discoveries in medicine. A team of scientists researching stem cells “has grown the earliest form of human heart cells from embryonic stem cells and found a way to direct them into the three major cell types found in the human heart”. This demonstrates the morality of stem cells because they can develop into a helpful tool to grow heart cells. Furthermore, the experiment’s goal is that “[the] lab created cells could be used to grow new heart tissue or repair heart muscle damage” (Ogilvie, 1). If people continue to put their hope in the benefits of stem cell research, then eventually it will be able to not only just grow heart cells but the tissue itself.
A few individuals with coronary illness and diabetes have gotten trial medications taking into account foundational cells disconnected from grown-up tissue, frequently from bone marrow, with shifting degrees of achievement. These mesenchymal stem cells, or MSCs, can develop into a few tissues including muscle, bone, ligament and fat yet there is no ensure that they will develop into heart muscle. This will left us with the answer to many people around the world why and how stem cells are stored.
INTRODUCTION The heart is made of specialized tissue known as cardiac muscle. Cardiac muscle is made of myocardial cells which can be further divided into autorhythmic and contractile cells. The autorhythmic cells are composed of sinoatrial (SA) nodes and atrioventricular (AV) nodes. These nodes contain pacemaker cells that control heart rate by producing pacemaker potentials.
When an obstruction of a coronary vessel occurs, there is a possibility of myocardial necrosis. In adults the monocytes located in the cardiac tissue are not able to replicate. There are smooth muscle and endothelial cells which can replicate, but cause the formation of scar tissue. Using primitive stem cells, could be a way to regrow the tissue resulting from necrosis. Primitive stem cells are located on the organs usually of the fetus. They have functional plasticity in which they are able to move to different areas in the body when needed. In this experiment bone marrow was extracted from mice and then tested with the c-kit expression, which identifies certain proteins located in the bone marrow. A side population of cells. or SP cells, were used from the bone marrow and from these the cells RNA was used and tested using PCR (Polymerase Chain Reaction) and primers. The SP cells isolated earlier in the experiment were then injected into female mice and after two and a half months the coronary artery of the female mice was occluded. The hearts were then extracted after two weeks and the hearts of those mice that were still alive at that time were stained with x-gal. The x-gal showed that these SP cells migrated to the injured parts of the heart by using the circulatory system.
Meis1 is a key regulatory protein for cardiac differentiation during embryonic development and using siRNA against Mesi1 can increase the proliferation of cardiomyocytes about threefold . Additionally, siRNA administration against PLB, a key regulator of cardiac Ca2+ homeostasis, can improve cardiac function in heart failure. It was suggested from this study that down-regulation of PLB can enhance the activity of sarcoplasmic reticulum Ca2+ pump (SERCA2a) and therefore can improve the cardiac function [149-151]. Another strategy for heart regeneration is targeting the inflammatory reactions in infarcted area of myocardium. Reactive oxygen species (ROS) are the key factors in inflammatory reactions and provoking heart regeneration (i.e. cardiomyocytes apoptosis, fibroblast proliferation and myocyte hypertrophy). NADPH (Nicotinamide adenine dinucleotide phosphate) oxidase is a major source for superoxide production in infarcted myocardium that contains a catalytic subunit, Nox2
Opposed to performing heart transplants after a myocardial infarction, cell sheets can be attached to the existing cardiac muscle in order to repair the damaged tissue, sticking the sheet to the heart without sutures. The researcher’s extracted bone marrow from a pig, washed away all red blood cells with a solution, and used reverse transcription so RNA makes cDNA. These cells were placed in a petri dish until the cells floated to the top of the culture, they were then placed in a different culture set at 37 degrees Celsius where two more cell layers were added on top of them. The cell sheets were placed on 5 different pig hearts on the left ventricle either basal or apical side up, after 15-60min the sheets and heart tissue underneath were removed for analysis under a scanning electron microscope. The basal side adhered to the heart tissue better than the apical side, showing a solid connection with the heart tissue about 30 minutes after being inserted. During open heart surgery, the chest should remain open at least 30 minutes after inserting the cell sheet in order to confirm it has properly stuck to the heart tissue. This study is significant because it demonstrates progress toward effectively using cell sheets to treat the heart after myocardial infarction.
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
While contraction in skeletal muscle is triggered by motor neurons under central control, certain cardiac muscle variants exhibit autorhythmicity. This means that that they are capable of producing their own depolarizing electrical potential. The cardiomyocytes that are capable of producing their own electrical potentials are found in what is referred to as the electrical condition system of the heart. This system is comprised of specializes cardiomyocytes that are autorhythmic and are able to conduct electrical potentials rapidly. These specialized structures include the sinoatrial node, atrioventricular node and bundle, and Purkinje fibers.