Commentary - (2024) Volume 10, Issue 10
Received: 01-Oct-2024, Manuscript No. IPIC-24-21789; Editor assigned: 03-Oct-2024, Pre QC No. IPIC-24-21789 (PQ); Reviewed: 17-Oct-2024, QC No. IPIC-24-21789; Revised: 22-Oct-2024, Manuscript No. IPIC-24-21789 (R); Published: 29-Oct-2024, DOI: 10.36648/2471-8157.10.10.98
Atherosclerosis is a chronic, progressive condition that affects the arteries, posing a major risk to cardiovascular health worldwide. It is characterized by the buildup of plaque-a mixture of cholesterol, fatty substances, cellular waste, calcium, and fibrin-within the inner walls of arteries. Over time, this buildup narrows and hardens the arteries, restricting blood flow and increasing the risk of heart attacks, strokes, and other serious cardiovascular diseases. Despite being a slowdeveloping condition, atherosclerosis often progresses silently until significant artery blockage occurs. This article explores the underlying mechanisms, risk factors, complications, and management strategies of atherosclerosis. The development of atherosclerosis begins with damage to the endothelium, the thin layer of cells lining the arteries. Various factors, such as high blood pressure, smoking, or elevated cholesterol levels, can contribute to this damage. Once the endothelium is compromised, Low-Density Lipoprotein (LDL) cholesterol particles penetrate the arterial wall and accumulate, initiating an inflammatory response. White blood cells, particularly macrophages, are recruited to the site to engulf the cholesterol, creating foam cells. Over time, these foam cells accumulate and form fatty streaks, which are the early signs of plaque development. Smooth muscle cells from the arterial wall migrate to the plaque, producing fibrous tissue and calcium deposits. This process leads to the formation of a fibrous cap that hardens the plaque, contributing to the stiffening and narrowing of the artery, a process known as stenosis. As the plaque grows, it can either remain stable or become unstable. Unstable plaques are more dangerous because they can rupture, releasing their contents into the bloodstream. This rupture can trigger the formation of blood clots, which may fully obstruct the artery, causing an acute cardiovascular event such as a heart attack or stroke. High Cholesterol Levels: Elevated levels of LDL ("bad") cholesterol contribute significantly to plaque formation, while low levels of High Density Lipoprotein (HDL, or "good" cholesterol) reduce the clearance of LDL from the bloodstream. High blood pressure increases the force against arterial walls, which can damage the endothelium and accelerate the process of atherosclerosis. Tobacco smoke contains chemicals that damage blood vessels, promote the buildup of plaque, and reduce the oxygen content of blood, making it easier for plaque to form. High blood sugar levels contribute to the accumulation of LDL in the arterial walls and damage the endothelium, making diabetics more susceptible to atherosclerosis. Excess body fat, particularly visceral fat, is associated with elevated cholesterol levels, high blood pressure, and inflammation-all of which promote atherosclerosis. Sedentary behavior contributes to several risk factors for atherosclerosis, including obesity, high cholesterol, and hypertension. The risk of atherosclerosis increases with age, and men are generally at higher risk at younger ages compared to women, although post-menopausal women have a higher risk. Genetic factors play a role in the development of atherosclerosis, as individuals with a family history of cardiovascular disease are more likely to develop the condition. When atherosclerosis affects the coronary arteries, which supply blood to the heart, it can lead to chest pain (angina), heart attacks, or heart failure. Atherosclerosis can also affect the arteries that supply the kidneys, reducing their ability to filter waste from the blood.
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The author’s declared that they have no conflict of interest.
Citation: Martinez S (2024) Atherosclerosis: Understanding the Silent Threat to Cardiovascular Health. Interv Cardiol J. 10:98.
Copyright: © 2024 Martinez S. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
