A Brief Note On Myocardial Infarction Of The United States

Cardiovascular disease is a global health problem causing nearly 1 in 3 deaths every year. Many of these deaths are due to coronary heart disease. Myocardial infarction (MI) is a major manifestation of coronary heart disease. In 1959, the World Health Organization defined MI as a combination of 2 of 3 characteristics: typical symptoms, enzyme rise, and a typical electrocardiographic (Patil, 2011).

In order for the heart to keep functioning normally, it needs a constant blood supply carrying Oxygen and nutrients to fit the demands of the working myocardial cell. When the blood supply coming from the coronaries to the myocardium cannot fit those demands, a condition called Myocardial Ischemia takes place. If that imbalance between supply and demand persists, a certain cascade of cellular, inflammatory and biochemical events lead to the irreversible death of myocardial cells, resulting in a Myocardial Infarct (MI).

In other tissues, IL-10 is identified as a critical counterbalance to proinflammatory cytokine synthesis (10). It acts to terminate the inflammatory response and limit inflammation-induced tissue pathology by deactivating macrophages and silencing their synthesis of TNF-, IL-6, IL-1, IL-8, and an array of other proinflammatory cytokines and chemokines (11, 12), as well as inducing synthesis of the soluble TNF- receptor antagonist, soluble TNFRII (13). IL-10 is expressed abundantly in a gestational stage-dependent manner in the maternal uterine decidua and placental tissues in mice (14 –17) and in humans (18 –21). In vitro studies demonstrate the ability of IL-10 to down-regulate synthesis of TNF-, IL-6, and PG in human chorion, decidual, and placental cells (22– 25). The potential importance of this cytokine in limiting adverse inflammatory responses in the gestational tissues is suggested by findings of decreased IL-10 expression in preterm labor (26, 27). In rats, exogenously administered IL-10 can attenuate fetal loss and growth restriction induced by LPS (28) and abrogate preterm birth and fetal growth impairment elicited by in utero infection with Escherichia coli (29). Furthermore, treatment of rats with IL-10 can reduce the extent of severe fetal brain injury often evident after uterine bacterial infection

Over the past 30 years, high cholesterol has been identified as a modifiable risk factor with LDL screening remaining an important tool in the identification and target of at risk patients for CV death (Kones, 2011). However, LDL alone is insufficient to identify all individuals as 50% of cardiac events occur in the setting of normal LDL levels (Kannel, 1995; Braunwald, 1997) suggesting the influence of other risk factors. In effort to better identify individuals at risk, inflammatory mediators

CVD [27]. In this response, macrophages play an important role, through the production of proinflammatory

Myocardial infarction is a common health threat that is seen in the healthcare field. A Myocardial infarction happens when the heart has a lack of blood supply caused by a blocked blood vessel. If the heart is not getting adequate blood and oxygen this can damage the heart and cause a myocardial infarction. Blockage is usually caused by plaque that builds up and then occludes the vessel (Craig, J., 2011). It is important as healthcare professionals to understand risk factors, signs and symptoms, and ways to prevent heart attacks. The purpose of this paper will be to educate on modifiable risk factors, ways patients can detect signs of a heart attack, and ways to prevent an attack from happening.

The macrophage is one of the white cells. From the white blood cell called monocytes, the macrophages are produced. It is a cell responsible for engulfing, digesting a cellular debris and is able to locate the foreign substances and cancer cells. In order to get rid of the unwanted invaders the phagocytosis destroys and cleans the body. The macrophage is aware of which cell is to keep and which do not belong to the body.

Human Cardiac Fibroblasts (HCFs) are the most prevalent cell type in the heart, comprising 60-70% of all cells. They play a central role in the maintenance of the ECM in the normal heart and the synthesis of growth factors and cytokines. Under pathological conditions, cardiac fibroblasts are involved in scar formation following myocardial infarction, cardiac fibrosis, and cardiac hypertrophy.

Cardiology Division, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, 55 Fruit Street, Boston, MA, 02114, USA.

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 [145]. 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

The usage of cardiac-derived cells are considered as the most potential autologous cell source for cardiac repair as in a research done by Tang et al. (2013), there is a reduction in the size of the scar but has no significant improvement in cardiac functions as measured using left ventricular ejection function (LVEF).

Myocardial infarction in most cases is usually experienced in the setting of coronary artery disease. A sequence of events is followed

PCI causes mechanical damage, induces immune response and cascade inflammatory response, stimulates the proliferation of vascular smooth muscle cells and deposition of extracellular matrix, leading to neointimal thickening and restenosis. platelets, neutrophils, and monocytes play a central role in the initial inflammatory response after PCI，studies showed that Mac-1 and platelet mediated leukocyte adhesion play an important role in vascular inflammation and restenosis after coronary stent implantation. Platelets and fibrin are deposited on the vascular walls of the endothelium, and by a series of cell adhesion molecules they collect white blood cells into the damaged blood vessels. The initial platelet leukocyte binding and rolling through leukocyte receptor P- selectin glycoprotein ligand -1 (PSGL-1) and P- protein binding to platelet mediated, when the leukocyte integrin Mac-1 (CD11b / CD18) combined with platelet glycoprotein Ib alpha 53 or platelet glycoprotein IIb / IIIa binding protein fiber the original, leukocyte rolling stop and firmly attached to the adherent

Some researchers believe that exogenous stem cells may also stimulate proliferation of endogenous cardiac precursors or stem cells through neovascularization or paracrine signaling actions. Other state that exogenous stem cells may lead to cardiac repair via fusion of donor cells with host cardiomyocytes.20 Other suggest that, the effects of stem cells are mediated by altering mechanical properties to strengthen the MI scar, thereby preventing deterioration in cardiac function, inflammation and diminished vascular supply causes many cells to die within seven days after transplantation16, 17

Heart is the first organ that develops and functions in mammalian embryo (Moorman et al., 2003). In mouse, it was reported to starting differentiation at E7.25 embryo. Twenty four hours later, a primitive heart tube was formed from the precardiac mesoderm, and start beating at E8 in mouse compared to about 3 weeks of gestation in human (Brand, 2003; Sissman, 1970). In mice, Roche et al., (2013) reported that the heart is considered a unique structure as it is derived from a four distinct pools of progenitors: the cardiac crescent, the second heart field (SHF), the proepicardial organ, and the cardiac neural crest. These progenitors were tracked into the different cell types namely, cardiomyocytes, fibroblasts, smooth muscle cells, endothelial cells, and the conduction system described in adult heart (Roche, Czubryt, & Wigle, 2013).