The Different Facets of Dyslipidemia and Hypertension in Atherosclerosis

Atherosclerosis is the narrowing of arteries due to the accumulation of macrophages overloaded with lipids resulting in foam cell formation, and these events occur preferentially at the branching points of arteries which are particularly susceptible to hyperlipidemic stress-induced inflammation and...

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Bibliographic Details
Published in:Current atherosclerosis reports 2016-12, Vol.18 (12), p.82-82, Article 82
Main Authors: Hurtubise, Jessica, McLellan, Krystie, Durr, Kevin, Onasanya, Oluwadara, Nwabuko, Daniel, Ndisang, Joseph Fomusi
Format: Article
Language:English
Subjects:
Angiology
Animals
Atherosclerosis - complications
Atherosclerosis - metabolism
Cardiology
Dyslipidemias - complications
Dyslipidemias - metabolism
Humans
Hypertension - complications
Hypertension - metabolism
Inflammation - metabolism
Lipid and Metabolic Effects of Gastrointestinal Surgery (R. Cohen
Lipoproteins - metabolism
Medicine
Medicine & Public Health
Oxidative Stress
Section Editor
Topical Collection on Lipid and Metabolic Effects of Gastrointestinal Surgery
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Summary:Atherosclerosis is the narrowing of arteries due to the accumulation of macrophages overloaded with lipids resulting in foam cell formation, and these events occur preferentially at the branching points of arteries which are particularly susceptible to hyperlipidemic stress-induced inflammation and oxidative stress. The different stages of atherogenesis rely on oxidative stress, endothelial dysfunction, and inflammation, and hypertension or dyslipidemia can independently trigger these stages. Dyslipidemia and hypertension are pathological conditions that damage the endothelium, triggering cell proliferation, vascular remodeling, apoptosis, and increased cellular permeability with increased adhesion molecules that bind monocytes and T lymphocytes to create a vicious cocktail of pathophysiological factors. Correspondingly, the factors are redirected by chemo-attractants and pro-inflammatory cytokines into the intima of the vasculature, where monocytes differentiate into macrophages taking up oxidized LDL uncontrollably to form foam cells and atherosclerotic lesions. Moreover, endothelial damage also causes loss of vasomotor activity, disproportionate vascular contractility, and elevation of blood pressure in dyslipidemic patients, while in hypertensive patients, further elevation of blood pressure occurs, creating a self-perpetuating vicious cycle that aggravates the development and progression of atherosclerotic lesions. This review offers an in-depth analysis of atherosclerosis and the related interplay between dyslipidemia/hypertension and critically appraises the current diagnosis, etiology, and therapeutic options.
ISSN:1523-3804
1534-6242
DOI:10.1007/s11883-016-0632-z