Case Presentation Pathophysiology Research Paper

Case Presentation Pathophysiology - Research Paper Example Coronary artery disease mostly occurs due to atheroma formation and its complications like thrombosis and rupture of atheroma. The arteries can also becomes diseased due to other conditions like polyarteritis, aortitis, connective tissue disorders, congenital anomalies like anamolous coronary artery origin, coronary artery malformation and fistula formation (Zevitz, 2006). Atheroma or atherosclerosis is the patchy focal deposition of plaques in the intima of the arttherosclerosis can affect any artery in the body and coronary arteries are at maximum risk for development of the disease (Maseri et al, 1992). Atherosclerosis begins to develop in the second or third decade of life. Thereafter it gradually progresses. Monocytes which circulate in the blood migrate into the intimal layer of the arteries. After reaching there, they take up low density lipoproteins after oxidization in the plasma. These are then known as lipid-laden foam cells (Zevitz, 2006). When these foam cells die, lipid s are released which develop fatty streaks on the intimal wall. This triggers migration and proliferation of the smooth muscles of the artery wall to form plaques. Over a period of time, collagen rich fibrous tissue surrounds the plague and forms mature fibrolipid plague. These plagues are dangerous because they can either rupture or create a fissure on the intima, allowing blood to enter the fissure. Entry of blood causes disruption of the arterial wall which leads to compromise of vessel lumen, thrombosis and also vasospasm, all of which contribute to decreased blood flow through the vessel. Rarely, the rupture of vessel can cause complete occlusion of the artery resulting in acute coronary artery syndrome (Zevitz, 2006). There are several risk factors which can cause ischemic heart disease, the most which is advanced age. This is because; as the age progresses, the size and the number of plaques increase. Other risk factors include male sex, family history of ischemic heart disea se, hypercholesterolemia, hyperlipidemia, smoking, obesity, hypertriglyceridemia, hyperfibrinogenemia, sedentary lifestyle, diabetes, hypertension, low levels of antioxidants, and poor eating habits (Zevitz, 2006). Ischemic heart disease can manifest as one or more of the following: angina, heart failure, myocardial infarction, arrhythmias and sudden death. Of these angina and myocardial infarction are common. Angina occurs due to imbalance between oxygen demand and blood supply to the heart muscle. The most common manifestation of angina is chest pain (Alaeddini and Shirani, 2006). Angina is caused due to chemical and mechanical stimulation of the sensory afferent nerve endings in the myocardium and coronary arteries. The main mediator of angina is adenosine (Alaeddini and Shirani, 2006). Whenever atherosclerotic plaque decreases the lumen by atleast 50 percent, angina manifests whenever there is increased oxygen demand. When more than 90 percent is blocked, angina manifests even i n rest (Alaeddini and Shirani, 2006). Investigations useful to diagnose angina are graded exercise stress test, stress echocardiography, myocardial perfusion scintigraphy tests, Coronary artery calcium scoring, electrocardiogram, stress electrocardiogram, ambulatory electrocardiogram, selective coronary angiography and intra-aortic balloon counter pulsation. Main treatments include nitroglycerine, betablockers, calcium channel blockers,