Peripheral Artery Disease Is A Prevalent Condition That Greatly Increases Risk Of Death From Myocardial Infarction

Intermittent claudication is a symptom of Peripheral Arterial Disease (PAD). PAD is the gradual narrowing or full or partial blockage of the arteries due to plague, which is also known as atherosclerosis. This blockage deprives the lower extremities form receiving adequate blood that contain oxygen and nutrients. Smoking, obesity, hyperlipidemia, hypertension, diabetes mellitus and familial preposition puts patient at a higher risk for PAD. The elderly are also at a higher risk for PAD due to their various illness. PAD can lead to strokes, chronic angina and myocardial infraction (MI). A nurse assessing a patient with PAD will notice bruit or aneurysm during assessment. This is the first stage of PAD which is also known as the asymptomatic

Stiffening of the artery has also been shown to have a high correlation with atherosclerosis [76].

Embolism from a cardiac source is the number one etiology of a PCA stroke, as embolism from a significant proximal

Atherosclerosis, the underlying cause of coronary heart disease which can affect any artery in the body, is essentially the narrowing of arteries due to excessive build up of cholesterol-rich lipids known as plaque (Insull 2009). Once the arteries become narrow, the flow of blood will be constricted, and the amount of blood, nutrients and oxygen that are able to reach the heart are reduced. As a consequence, the heart becomes increasingly hypoxic resulting in ineffective contraction. The aftermath of narrow arteries often poses serious consequences as it has a high probability of causing heart attack, angina, or even stroke (Marieb & Hoehn 2010; Insull 2009). Despite the fact that arteries will harden naturally as people age, the rate of plaque development is determined by the number of risk factors (Insull 2009). This essay will discuss and review the procedure in which the risk factors: hypertension, abnormal level of blood lipids, and smoking took to assist in the development of atherosclerosis.

Diastolic Heart Failure ejection fracture 70 % (October 2015), end-stage renal dialysis Monday, Wednesday, and Friday, paroxysmal atrial fibrillation (no anticoagulant therapy at home), Coronary Artery Disease, status post pacemaker, Diabetes Mellitus Type 2 with diabetic gastropathy, nephropathy, and neuropathy, hypertensive heart disease, chronic anemia, aortic sclerosis with mild to moderate stenosis and mitral regurgitation,

It is mainly as a result of one of these three problems: ST elevation myocardial infarction, unstable angina and lastly non ST elevation myocardial infarction with chest pain being the main symptom (Linton, 2012). There are five main pathophysiologic processes that contribute to the development of ACS: thrombus on pre-existing plaque, active obstruction from coronary spasm, progressive mechanical obstruction, infection and unstable angina due to oxygen supply to myocardial (Linton, 2012). ACS is mainly caused by thrombus formation on a pre-existing plaque and it can be demonstrated through angiography or autopsies (Marshall, 2010). A thrombus is formed from plasma coagulation and platelets. There are risk factors that contribute to ACS such as cigarette smoking, diabetes, hypertension and high blood cholesterol (Linton, 2012). Both men and women are at a risk of having a heart attack. However it is more common in men especially when having a family background of heart attack, being overweight and inactive (Scruth, Carter, Cheng, Rolley, & Page, 2012). Modifying and identifying the risk factors is important as it can prevent further heart problems.

Peripheral artery disease (PAD) is considered as a clinical manifestation of systemic atherosclerosis affecting primarily the blood supply to the lower extremities, but other noncardiac and non-intracranial arteries may also be involved. More than 200 million individuals worldwide are estimated to have diagnosed PAD and the prevalence continues to rise. In Europe and North America, an estimated 27 million people have PAD and around 413,000 annual hospital admissions are attributed to PAD. Due to an imbalance between the supply and demand for blood flow, patients with PAD most commonly experience exertional leg pain (intermittent claudication), which is triggered by ambulation and relieved by rest. The severity of the symptoms depends upon

Polyarteritis Nodosa is an autoimmune disease caused by immune deposition in the wall of small to medium sized muscular arteries.13 This process promotes infiltration with polymorphic leukocytes and liberation of necrotizing enzymes, leading to thrombosis, tissue ischemia, fibrosis, and ultimately tissue scarring. PAN may affect virtually every organ system and has a wide constellation of clinical manifestations (Table 1).14 Establishing the diagnosis of PAN is very difficult as there are no laboratory abnormalities specific for PAN. Acute phase reactants, such as erythrocyte sedimentation rate and C-reactive protein, are commonly increased.14 Chronic anemia is also frequently present.14 Histopathological evidence of vascular inflammation

First, I would like to emphasize the value of accurately diagnose a patient with PAD. Diagnosing a patient with PAD should not be taken for granted due to substantial reasons: Patients may suffer from complications related to PAD, including periodic disability of walking, critical limb ischemia, arterial insufficiency ulcers, frequent hospitalization, coronary revascularization and amputation (Hirsch et al., 2006). These contribute to the poor general well-being and causing a greater rate of depression (McDermott et al., 2003; Regensteiner et al., 2008). Patients with PAD are likely to

A major proportion of AMI occur in plaques that have not revealed clinically prior to the infarction, that is have not initiated adequate degree of luminal obstruction results angina, which obfuscates screening and interventional primary preventive procedures (38,44,45). Plaque distraction is the core remarkable reason of AMI. The procedure there the fibrous cap of a plaque ruptures plus reveal the blood for primary pro-thrombotic yields and following thrombus development is convoluted (39,44). Lessened collagen synthesis or amplified mortification of extracellular matrix all subsidize to this course. A lesser degree of smooth muscle cells (with attendant declined matrix production) as well as a extreme degree of lipids, inflammatory cells

Atherosclerosis is a disease dealing with the heart. This disease causes hardening, narrowing, or even blockage of the arteries, which makes the arteries thicken. Fat, calcium and plaque buildup are all components of atherosclerosis. The accumulations of calcium, fat, and plaque buildup quietly and slowly block the arteries, putting blood flow at an extremely high risk. Atherosclerosis is typically the reason for heart attacks, strokes, and peripheral vascular disease. These diseases with each other are called cardiovascular disease.1

When investigating the true cost of smoking cigarettes there is an overwhelming amount of research into the multiple effects smoking has on health. The smoke inhaled when smoking a cigarette contains 4,000 compounds which often leave toxic traces in the lungs and other organs. This is one of the biggest contributing factors as to why smokers visit the GP and hospital more often, have lower survival rate after surgery and take longer to heal wounds compared with non-smokers. The inhalation of the smoke is also known to cause around 60 carcinogens, which can harm every organ in the body, especially the heart. Cardiovascular diseases like atherosclerosis and coronary heart disease make up 10% of all heart related diseases caused by smoking. The tobacco smoke inhaled can seriously damage blood vessels increasing your chance of developing atherosclerosis. Atherosclerosis is caused by a thick substance called plaque which accumulates in the coronary arteries. As

Peripheral artery disease and cancer are prevalent conditions that often coexist. Thromboembolic complications are the

Cigarette smoking plays a key role in all the phases of atherosclerosis from endothelial dysfunction to acute clinical events, the latter being largely thrombotic. Both active and passive (environmental) cigarette smoking predisposes to cardiovascular events. Whether or not there is a distinct direct dose-dependent correlation between cigarette smoking and cardiovascular disease is debatable, as some recent experimental clinical studies have shown a non-linear relation between them. The exact toxic contents of cigarette smoke and the

Smoking creates toxins in the blood. This greatly contributes to the development of atherosclerosis. Atherosclerosis is a condition in which fatty material is deposited along the walls of the arteries. This fatty material thickens, hardens, and can eventually block the arteries if not treated. Clots may also form around the plaque deposits. Smoking raises the levels of proteins that cause the blood to clot and also increases platelet production, making the blood stickier which further creates risk for clots. This also interferes with the blood flow and poses an added danger if they were to break off and travel through the body causeing assorted health problems such as heart attack, stroke, or gangrene.