• Clinical science

Atherosclerosis

Abstract

Atherosclerosis is the most common type of arteriosclerosis, or thickening and stiffening of the arterial wall. Major risk factors include smoking, diabetes mellitus, arterial hypertension, dyslipidemia, family history of early heart disease, and advanced age. The pathogenesis is a complicated process precipitated by endothelial damage, which leads to an invasion of inflammatory cells into the tunica intima and adhesion of platelets to the disrupted endothelium. Invading smooth muscle cells (SMCs) and macrophages take up cholesterol from oxidized low-density lipoprotein (LDL) in the vessel wall. They then become foam cells, which accumulate in early atherosclerotic lesions (fatty streaks), triggering the production of extracellular matrix (e.g., collagen). This leads to the formation of fibrous plaques (from cells, extracellular matrix, free cholesterol, and cellular debris), which may rupture and lead to thrombosis. Common sites of atherosclerosis include the abdominal aorta, coronary arteries, popliteal arteries, and carotid arteries. Depending on the location, atherosclerosis may lead to a variety of conditions, such as arterial aneurysms, dissection, coronary heart disease (CHD), peripheral artery disease (PAD), intestinal ischemia, subcortical vascular dementia (Binswanger's disease), thrombosis (e.g., acute coronary syndrome and stroke), and renovascular hypertension.

Definition

The terms “arteriosclerosis” and “atherosclerosis” are often used synonymously!


References:[1][2][3]

Epidemiology

  • Sex: >

References:[4]

Epidemiological data refers to the US, unless otherwise specified.

Etiology

The term metabolic syndrome refers to the presence of at least 3 of the following risk factors: obesity, elevated triglycerides, low high-density lipoprotein (HDL), diabetes mellitus, and arterial hypertension.
References:[5][4][6][7][8]

Pathophysiology

Pathogenesis of atherosclerosis

  1. Chronic stress on the endothelium
  2. Endothelial dysfunction, which leads to
  3. Inflammation of the vessel wall
  4. Macrophages and SMCs ingest cholesterol from oxidized LDL and transform into foam cells.

Common sites (in order of frequency)

Atherosclerotic diseases

References:[1][2][9][10][11]

Primary and secondary prevention of atherosclerosis

  • Lifestyle modifications
    • Weight reduction
    • Dietary modification
    • Moderate aerobic exercise
    • Smoking cessation
    • Moderate consumption of alcohol (about 1–2 glasses of wine or beer per day) presumably has a protective effect.
  • Medical treatment: Treat hypertension, diabetes and hyperlipidemia

The most significant therapeutic step patients with vascular disease can take is stopping smoking!
References:[12]

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last updated 12/13/2018
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