Journal of Vascular Medicine & Surgery

Consequences of Endothelial Dysfunction and Lifestyle Habits that Influence Atherosclerosis Development

Lauren Jensen^* Department of Vascular Surgery, University of Vermont Medical Center, Burlington, USA
^*Correspondence: Lauren Jensen, Department of Vascular Surgery, University of Vermont Medical Center, Burlington, USA, Email:

Received: 22-Apr-2024, Manuscript No. JVMS-24-25909; Editor assigned: 26-Apr-2024, Pre QC No. JVMS-24-25909 (PQ); Reviewed: 10-May-2024, QC No. JVMS-24-25909; Revised: 17-May-2024, Manuscript No. JVMS-24-25909 (R); Published: 24-May-2024, DOI: 10.35248/2329-6925.24.12.557

Description

Atherosclerosis is a chronic disease characterized by the buildup of plaques within the arterial walls, leading to narrowing and hardening of the arteries. This condition is a major contributor to cardiovascular diseases, including heart attacks, strokes, and peripheral artery disease. Understanding the mechanisms, risk factors, and consequences of atherosclerosis is essential for effective prevention and management. Atherosclerosis begins with damage to the endothelial cells lining the arteries. This damage can be caused by various factors, including high blood pressure, high cholesterol, smoking, and inflammation. The damaged endothelium becomes more permeable to lipids, particularly Low-Density Lipoprotein (LDL) cholesterol. LDL cholesterol penetrates the arterial wall and undergoes oxidation, leading to the recruitment of monocytes from the bloodstream. These monocytes change into macrophages, which then become foam particles by consuming the oxidized LDL. The fatty streaks, which are the first obvious indications of atherosclerosis, are created by the buildup of foam cells. As the fatty streaks progress, they trigger a chronic inflammatory response. Smooth muscle cells migrate from the arterial media to the intima, where they proliferate and produce extracellular matrix, contributing to plaque stability. However, if the inflammatory response is intense, it can lead to plaque instability [1-3].

A fibrous covering surrounds the lipid-rich necrotic core of advanced atherosclerotic plaques. A thrombotic event may result from the seal becoming exposed to the bloodstream if it is highly susceptible to rupturing. If the artery is blocked by this thrombus, ischemic conditions like myocardial infarction or stroke may occur. Several modifiable and non-modifiable risk factors contribute to the development of atherosclerosis. High levels of LDL cholesterol and low levels of High-Density Lipoprotein (HDL) cholesterol increase the risk of plaque formation. Elevated blood pressure causes endothelial damage and promotes atherosclerosis [4,5]. Tobacco smoke contributes to endothelial dysfunction and promotes inflammatory processes. High blood sugar levels damage the endothelium and accelerate atherosclerotic changes. Excess body weight is associated with higher levels of LDL cholesterol and hypertension. Lack of physical activity is linked to several cardiovascular risk factors. A diet high in saturated fats, trans fats, and refined sugars promotes hyperlipidemia and obesity [6].

The risk of atherosclerosis increases with age and men are at higher risk than pre-menopausal women, although the risk equalizes after menopause. Family history of cardiovascular disease suggests a genetic component to atherosclerosis. Atherosclerosis can remain asymptomatic for many years until it causes significant arterial blockage or plaque rupture. The clinical manifestations depend on the location of the affected arteries. Atherosclerosis of the coronary arteries leads to reduced blood flow to the heart muscle, causing angina pectoris (chest pain) and, in severe cases, myocardial infarction (heart attack). Atherosclerosis of the carotid arteries or cerebral arteries can lead to Transient Ischemic Attacks (TIAs) or ischemic stroke [7-9].

Atherosclerosis of the peripheral arteries, particularly in the legs, causes intermittent claudication (pain in the legs during walking) and can lead to critical limb ischemia. The diagnosis of atherosclerosis involves a combination of clinical evaluation, imaging techniques, and laboratory tests. A thorough medical history and physical examination can reveal symptoms and signs suggestive of atherosclerosis, such as angina, claudication, or bruits (abnormal vascular sounds). Carotid ultrasound can detect plaques and measure the thickness of the arterial wall. Coronary angiography visualizes the coronary arteries and identifies stenosis. CT angiography provides detailed images of blood vessels and can detect calcium deposits. MRI angiography is useful for imaging blood vessels without using ionizing radiation. The management of atherosclerosis involves lifestyle modifications, pharmacological treatments, and in some cases, surgical interventions too [10,11]. The Mediterranean diet, rich in fruits, vegetables, whole grains, and healthy fats, is particularly beneficial for a healthy heart. Controlling blood sugar levels reduces the risk of atherosclerosis complications. During Percutaneous Coronary Intervention (PCI), a balloon catheter is used to widen the artery, and then a stent is usually inserted to maintain the artery open. Heart surgery that uses a transplant from another area of the body is to establish a bypass around the clogged coronary artery [12].

Conclusion

Atherosclerosis is a multifaceted disease with significant implications for cardiovascular health. Early detection, risk factor modification, and appropriate treatment can prevent its progression and reduce the incidence of life-threatening complications. There is a hope for better treatment and results for patients with atherosclerosis through ongoing research into the molecular causes of the disease and the creation of innovative medicines. For the purpose of improving public health generally and lowering the worldwide burden of cardiovascular illnesses, it is imperative to comprehend and treat atherosclerosis.

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