Atherosclerosis -Cardiovascular Disease - Essay Example

ATHEROSCLEROSIS INTRODUCTION: Cardiovascular disease is a broad term that encompasses various diseases affecting the heart as well as blood vessels. The diseases affecting the heart include ischemic heart disease, hypertensive heart disease, valvular heart disease, rheumatic heart disease, and congenital heart disease. The diseases that affect the blood vessels are arteriosclerosis, hypertensive vascular disease, aneurysms and dissections, and various inflammatory diseases. Together, these diseases account for 17.1 million mortalities every year (WHO) Atherosclerosis, the most common and significant type of arteriosclerosis, affects the intimal layer of the blood vessels. Previously thought to be a chronic progressive disease, atherosclerosis is now proved to develop in periodic active and quiescent phases. The pathogenesis of the disease is the result of complex interplay among several factors, that together lead to the hardening and thickening of the vessel wall due to the deposition of fibro fatty material (Cheema 2006). This ultimately results in obstruction of the lumen. Response-to-injury theory and lipid hypothesis (Zurgil et al 1999) explain the primary mechanism: Injury to the vessel wall, caused by elevated cholesterol (LDL), free radicals, toxins or any infectious agents, leads to the inflammatory response. Circulating monocytes infiltrate the affected area of the intima and form activated tissue macrophages, which engulf the cholesterol and other offending lipids and turn into foam cells, which are characteristic of atherosclerosis (Packard et al 2008). The pathogenesis of the disease comprises of six stages, starting from macrophage foam cells, which progress to a fatty streaks, these are the earliest lesions of atherosclerosis. As the condition advances to stage 3, the lipids start accumulating extracellularly (preatheroma) and progresses to form a core of lipid called atheroma. Stage five is characterized by the accumulation of fibrotic layer over the lipid core forming fibrous plaques. Surface defects, hemorrhagic hematomas, and thrombi are encountered as the disease reaches the stage six of complex lesions (Kumar et al 2005). (The Merck manual of medical information home edition 2004 - How Atherosclerosis develops) LABORATORY DIAGNOSIS: Since the pathogenesis of atherosclerosis is complex and influenced by multiple factors, the laboratory diagnosis procedures to identify the cause of the disease and then the treatment are equally vast (British Atherosclerosis society 2005). The basic step to diagnose any vascular injury leading to atherosclerosis at any stage is a detailed history. It will reveal the patients background, life style and risk factors. Sedentary living with lack of physical activity and adequate exercise, and risk factors like family history, smoking, hypertension, all add up to increase the chances of the development of atherosclerosis (Hackam et al 2003). The physical examination shows the findings consistent with atherosclerosis only when the disease has advanced enough to produce systemic effects. Hyperlipidemia is evident on surface in the form of xanthomas (Xanthomata). Blockade of coronary arteries, due to atherosclerosis, leads to tachycardia and appreciable fourth heart sound. Cerebrovascular block expresses itself as the focal neurologic symptoms and diminished carotid pulse and artery bruits, which indicate poor blood flow due to plaque buildup (Lee et al 2008). In case of diminished organ perfusion due to atherosclerotic thrombi, the respective organ undergoes ischemia and then gangrene or necrotic death. Atheroembolism is the complication of atherosclerosis resulting from the embolization of an atheroma. It can be appreciated as livedo reticularis, cyanosis, progressing to gangrene and ulceration. The diagnosis is confirmed through laboratory investigations. Routine laboratory investigations include a complete blood count (CBC), along with sedimentation rate, blood lipid profile showing total and high-density lipoprotein (HDL) cholesterol, a VDRL test, urinalysis, a urine culture with colony count and sensitivity, and ankle/ brachial index. Imaging studies for the diagnosis of atherosclerosis comprise of coronary angiography, ultrasonography, and intravascular ultrasonography (IVUS), chest x-ray, CT scan and MRI report, advanced PET scans. Stress testing and flat plate of the abdomen for kidney size also support the diagnosis. Elevated blood LDL (bad cholesterol) and low HDL (good cholesterol) is considered as high risk factor for atherosclerosis. According to national cholesterol education program and American heart association, the desirable level of total blood cholesterol has been approved as less than 200 mg/dl, with LDL cholesterol level less than 100 mg/dl and HDL level 40 mg/dl or above. Borderline is reached when the total cholesterol rises above 200mg/dl to between 201- 240 mg/dl. Total cholesterol level beyond 240 mg/dl constitutes high risk for the development of atherosclerosis. HDL/ LDL ratio is a very consistent marker to determine the risk. Target ratio is above 0.3, the ideal being 0.4. Blood glucose and glycosylated hemoglobin, i.e. hemoglobin A1c is measured in patients of diabetes mellitus (Jagla et al 2001). Desirable Lipid Levels in Adults Lipid Goal (mg/dL)* Total cholesterol Less than 200 mg/dL Low-density lipoprotein (LDL) cholesterol Less than 100 mg/dL High-density lipoprotein (HDL) cholesterol More than 40 mg/dL Triglycerides Less than 150 mg/dL *mg/dL = milligrams per deciliter of blood. (The Merck manual of medical information home edition 2004 – Desirable Lipid Levels In Adults) Ultrasonography plays an important diagnostic role. The two standard tests are brachial artery reactivity and carotid artery intima thickness. Brachial artery reactivity checks the endothelial integrity of even the small vessels like brachial artery. An intact vessel dilates in response to increased blood flow, while an atherosclerosed vessel does not. Carotid artery intima thickness is a reliable, noninvasive technique to asses the thickening of the intimal layer of common and internal carotid arteries (De Groote et al 2008). Intravascular ultrasound (IVUS) involves the insertion of a catheter in the vessel to analyze the thickness and acoustic properties of the intima. It also helps in identifying recent disruptions in the vascular wall. Coronary angiography is one of the most important diagnostic approaches. An iodinated contrast agent is injected through a catheter at the Ostia of coronary arteries and the visualizations are appreciated through fluoroscopic x-ray examination of the heart (Hartung et al 2007). A limitation to this procedure is that only the patent vessels can be visualized as iodide contrast flows through them. Areas blocked by atherosclerotic plaques remain imperfused and so the extent of damage can not be assessed accurately. CT scans allow excellent visualization of the vessels (Schroeder et al 2004). Attempts are being made at reducing the amount of radiation used while performing the diagnostic procedure to minimize the risks. If results prove to be promising, CT scans can be very useful to detect asymptomatic patients without harming them. Similarly, magnetic resonance imaging (MRI) is the noninvasive procedure that allows the visualization of the vessels to appreciate vessel wall characteristics and plaque formation (Moran et al 2008). Ankle/ Brachial index is the simple test that involves measuring the blood pressure in the ankle and then in the arm, and compare the two to appreciate the flow of blood. REFLECTION: The aforementioned detail about atherosclerosis and its pathogenesis add to my knowledge the very basics of the pathologic condition, ranging from its risk factors, through developmental course and morbidity, to the ways of prevention. Now, after knowing the pathogenesis and progression of the disease through each stage, I can directly relate to the diagnostic approach involved for the intervention at any particular stage, whether it is an early stage or an advanced one. Above findings prove atherosclerosis to be one of the leading causes of morbidity and mortality around the globe. Ranging from genetic predisposition to the varied life style that each affected individual practices, and the multiple environmental factors that directly or indirectly affect the circulation of blood as the person enters the ongoing cascade in which, one damage leads to another, ultimately resulting in the ischemic death or infarction. Thanks to the ever advancing research and latest diagnostic techniques, it is now possible to detect the disease at early stages and prevent further damage by adapting a better, healthier lifestyle and managing the risk factors (Curtiss 2009). Prognosis depends upon various factors, which include number of the vascular beds involved, extent of obstruction to the flow as well as systemic load of the disease. Plaque rupture and thrombi formation, sometimes advancing to embolization are critical events (Stoll et al 2006, Tang et al 2008). Risk assessment and measures to avoid such complications are imperative. Nevertheless, despite the efforts to control the condition, atherosclerosis still continues to affect a major portion of population because of its extensive multifactorial foundations, and needs to be combatted vigilantly on various grounds. REFERENCES: BRITISH ATHEROSCLEROSIS SOCIETY. (2005). Report on the spring meeting of the British Atherosclerosis Society. CHEEMA, S. K. (2006). Biochemistry of atherosclerosis. Advances in biochemistry in health disease, v. 1. New York, NY, Springer. http://dx.doi.org/10.1007/0-387-36279-3. CURTISS LK. (2009). Reversing atherosclerosis? The New England Journal of Medicine. 360, 1144-6. DE GROOT E, VAN LEUVEN SI, DUIVENVOORDEN R, MEUWESE MC, AKDIM F, BOTS ML, & KASTELEIN JJ. (2008). Measurement of carotid intima-media thickness to assess progression and regression of atherosclerosis. Nature Clinical Practice. Cardiovascular Medicine. 5, 280-8. HACKAM DG, & ANAND SS. (2003). 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