![]() Some plaques can rupture and lead to exposure of tissue factor, which culminates in thrombosis. For a lesion to cause angina at rest, it must be at least 90% stenosed. ![]() However, symptoms would abate at rest as the oxygen requirement comes down. As time passes, the lesion can become hemodynamically significant enough that not enough blood would reach the myocardial tissue at the time of increased demands, and angina symptoms would occur. If it becomes stable, a fibrous cap will form, and the lesion will become calcified over time. Over time, this plaque could grow in size or become stable if no further insult occurs to the endothelium. ![]() ![]() This process leads to the formation of subendothelial plaque. Growth factors released activate smooth muscles, which also take up oxidized LDL particles and collagen and deposit along with activated macrophages and increase the population of foam cells. T cells get activated, which releases cytokines only to aid in the pathologic process. These macrophages take up oxidized low-density lipoprotein (LDL) particles, and foam cells are formed. When a vascular insult occurs, the intima layer breaks, and monocytes migrate into the subendothelial space where they become macrophages. The first step in the process is the formation of a "fatty streak." Fatty streak is formed by subendothelial deposition of lipid-laden macrophages, also called foam cells. Plaque is a build-up of fatty material that narrows the vessel lumen and impedes the blood flow. The hallmark of the pathophysiology of CAD is the development of atherosclerotic plaque. High sensitivity CRP (hsCRP) is thought to be the best predictor of coronary artery disease in some studies although uses for it in a practical setting are controversial. Markers of inflammation are also strong risk factors for coronary artery disease. An individual's 10-year risk of atherosclerotic cardiovascular disease can be calculated using the ASCVD equation available online on the American Heart Association portal. Increased low-density lipoproteins (LDL) increased the risk for CAD and elevated high-density lipoproteins (HDL) decrease the incidence of CAD. Hypercholesterolemia remains an important modifiable risk factor for CAD. The male gender is more predisposed than the female gender. In 2016, the prevalence of smoking among the United States among adults was found to be at 15.5 %. Smoking remains the number one cause of cardiovascular diseases. In the US, better primary care in the middle and higher socioeconomic groups has pushed the incidence towards the later part of life. In the Western world, a faster-paced lifestyle has led people to eat more fast foods and unhealthy meals which has led to an increased prevalence of ischemic heart diseases. Modifiable risk factors include smoking, obesity, lipid levels, and psychosocial variables. Non-modifiable factors include gender, age, family history, and genetics. Etiologic factors can be broadly categorized into non-modifiable and modifiable factors. Coronary artery disease is a multifactorial phenomenon.
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