Essay On Myeloperoxidase

Cardiovascular diseases has affected large number of population worldwide and in developed countries it is responsible for half of all deaths, coronary artery disease (CAD) alone is responsible for 1 of every 4.7 deaths in the United States (Eichner et al., 2002).

Clearly differentiate the pathophysiology of angina and myocardial infarction, including signs and symptoms. (5 marks)

The present report argues that the 3 identified sources, are published in high-ranked journals and based on sufficient patient population, thereby constituting a strong research evidence for addressing the established research question.

Angina is associated with clinical events that can affect prognosis, for example Von Arnim et al

Representatives from Thrombolysis in Myocardial Infarction (TIMI), Duke Clinical Research Institute (DCRI), and Merck & Co., Inc.

Clinical trials have shown that statins, inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A reducatse can reduce cardiovascular evenrts (^1). Statins reduce the rate of cardiovascular events by lowering LDL levels “bad cholesterol”. Guidelines used for prevention of cardiovascular disease have

Data Source: Sources included Medline, Embase, Cochrane Library, Scopus and Non-Indexed Citations from inception through January 2016.

4.2 Clinical implications – disease severity, identifying high risk people, disease duration. Objective marker for diagnosis, treatment response

In these trial, 331 patients with advanced MTC were randomly assigned to vandetanib versus placebo with crossover was allowed after progression in the placebo arm. PFS was significantly superior in vandetanib arm versus placebo arm with HR of 0.35. Also, a statistically significant higher RR and better disease control rate were observed in vandetanib arm versus placebo arm (45 vs. 13 %). Initially, no overall survival benefit was seen, and this may be due to cross over from placebo to vandetanib arm upon disease progression. The AEs were generally tolerable, but 12 % of patients stopped the drug due to intolerability.

“Each year, an estimated 785,000 American have a first acute myocardial infarction” (Dunlay, et al, 2012, p 11). Understanding the disease process of MI, providing quality collaborative care, and instituting treatment of comorbid conditions can significantly reduce the incidence of re-hospitalization for these patients.

Several THA PROM clinical scores have been described, validated and compared (Alviar et al. 2011; Collins & Roos 2012; Hinman et al. 2014; Kemp et al. 2013; Klassbo, Larsson & Mannevik 2003; Soderman, Malchau & Herberts 2001; Thorborg et al. 2015; Ware, Kosinski & Keller 1996). Each assessment tool has its relative strengths and benefits, as well as its weaknesses. No single assessment tool has reported consistent superiority over another, and the choice of which one to use normally comes down to patient population, the pathology being investigated, investigator preference and resource management (Alviar et al. 2011; Collins & Roos 2012; Hinman et al. 2014; Kemp et al. 2013; Soderman, Malchau & Herberts 2001)

The CDC estimates that roughly 610,000 Americans die each year from an acute myocardial infarction and is the number one cause of death amongst men and women.1 Myocardial infarction (MI) stems from the occlusion of one or more coronary arteries, resulting in hypoxia and eventual death of the myocytes downstream.2 As oxygenated blood leaves the left ventricle traveling into the aorta, the left and right coronary arteries branch off almost immediately. These coronary arteries and their branches provide oxygen and nutrients to the epicardium and myocardium.3 Gradual depositions of fatty streaks in the arteries progress to unstable fibrofatty plaques that cause luminal narrowing.2 The etiology of an acute MI occurs when an atherosclerotic plaque breaks free inside a coronary artery, initiating a thrombotic event referred to as atherothrombosis4. This leads to the partial or total occlusion of a coronary artery, and can occur in a proximal or distal segment of the artery5. The location of this occlusion is often evident from patient’s symptoms and is used to determine course of treatment.5

You post is one that I can especially relate to working in an emergency room. Our hospital is considered the dedicated MI and Trauma center in our area. Patients presenting with MI or a " heart attack" are experiencing a lack of sufficient oxygen, or ischemia to the myocardial muscle causing intense pain or pressure primarily to the chest. During the reading, I was able to get a better understanding of the cascading events the lack of sufficient oxygen, to oxygen rich areas cause of the tissues and on a cellular level. The development of toxins, oxidative enzymes (cytochromes) cause inflammation, insufficient ATP production, and constriction (Holowaty, Miller, Rohan, & To, 1999, p. 56-57). Patient suffering from true myocardial infarct are

Atherosclerosis is classified as a chronic, progressive, and multifactorial disease of moderate and large sized arteries categorised by intimal lesions called atheroma plaques that pushes into the vessel lumens. Atherosclerosis leading to coronary artery is the main cause of coronary artery disease (CAD). It is vital to appreciate the central mechanisms of atherogenesis in order to understand the adverse clinical results of Coronary Artery Disease and their ensuing management. The progression of atheroma consist of several cellular and molecular events with endothelial dysfunction, leucocyte recruitment and dispedesis, LDL transcytosis, LDL oxidation, recruitment and proliferation of smooth muscle cells, synthesis of extracellular matrix proteins, build-up of foamy macrophages as well as interplay of different cytokines. (Bisht et al, 2012).

All studies except one reported ST as a clinical outcome. The definitions used for ST are shown in table 1. There were 22 ST events in LISA during 18,145 person-months follow up as opposed to 28 events in control group over 97,145 person-months follow up. Therefore, LISA was associated with significantly increased risk of ST events (IRR = 4.81; 95% CI 2.68-8.62) after the follow up imaging (Figure 2). There was no heterogeneity among the studies (I2 = 0%) and no subgroup difference among IVUS and OCT studies, although OCT studies did not report ST in any group. The results of random effect model (Figure 2) and Poisson regression models were consistent with the primary analysis ( IRR = 4.77 (random); 95% CI 2.68-8.50) as shown in figure 2S in Supplement. When analysis was restricted to studies reporting Academic Research Consortium defined definitive or probable ST, the LISA was still associated with higher risk of late