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Dyslipidemias and Microcirculation
Abstract
Dyslipidemia is widely accepted as one of the major risk factors in cardiovascular disease mainly due to its contribution in the pathogenesis of atherosclerosis in medium-sized and large arteries. However, it has become increasingly accepted that high-cholesterol levels can also adversely affect the microvasculature prior to the development of overt atherosclerosis. Moreover, hypercholesterolemia has shown, in preclinical animal models, to exert detrimental effects beyond the vascular tree leading to larger infarcts and adverse cardiac remodeling post-myocardial infarction. At a functional level, hypercholesterolemia has shown to impair endotheliumdependent vasodilation because on defects on nitric oxide bioavailability. The pathogenic mechanisms underlying microvascular dysfunction involve an enhanced arginase activity, enhanced production of free radicals and the activation, recruitment and accumulation of leukocytes, primarily neutrophils, via their diffusion through postcapillary venules. In turn, recruited inflammatory cells and certain inflammatory mediators enhance platelet adhesion, overall inducing a proinflammatory and prothrombotic phenotype. Within the present review, we aim to discuss the existing evidence regarding the presence of dyslipidemia - particularly high low density lipoprotein-cholesterol levels - and the occurrence of microvascular dysfunction, the mechanism by which high cholesterol levels induce functional alterations in the microvascular bed and, finally comment on the impact of dislipidemia-induced microvascular dysfunction at the myocardial level.
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Small and dense LDL particles have an increased capacity to penetrate the arterial wall and are more readily oxidized compared with large and buoyant particles, contributing to atherosclerotic plaque progression.
“Small and dense LDL particles have an increased capacity to penetrate the arterial wall and are more readily oxidized compared with the large and buoyant particles,2 therefore contributing to atherosclerotic plaque progression.”
From Lactiplantibacillus plantarum strains KABP011, KABP012, and KABP013 modulate bile acids and cholesterol metabolism in humans (2024) · cites this paper as [2]
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Metadata
- Authors
- Padró, T., Vilahur, G., & Badimon, L.
- Affiliations
- Hospital de Sant Pau (ES)
- Cardiovascular ICCC- Program, Research Institute Hospital de la Santa Creu i Sant Pau, IIB-Sant Pau, Barcelona, Spain
- Corresponding author
- Padró, Teresa
- Venue
- Current Pharmaceutical Design
- Publisher
- Bentham Science Publishers Ltd.
- Published
- 2018-11-08
- Volume
- 24
- Issue
- 25
- Pages
- 2921-2926
- ISSN
- 1381-6128 (ISSN-L)
- OpenAlex
- W2889857190
- Cited by
- 43
- References
- 0
- Citations by year
- 2026: 2 · 2025: 13 · 2024: 3 · 2023: 9 · 2022: 4 · 2021: 7 · 2020: 5
- FWCI
- 2.07
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Current Pharmaceutical Design (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipoproteins and Cardiovascular Health
- Keywords
- dyslipidemia, hypercholesterolemia, microvascular dysfunction, LDL cholesterol, endothelial dysfunction, nitric oxide bioavailability, arginase, free radicals, neutrophil recruitment, postcapillary venules, platelet adhesion, pro-inflammatory phenotype, prothrombotic phenotype, myocardial infarction, cardiac remodeling, atherosclerosis, cardiovascular risk factors
- MeSH terms
- Animals, Humans, Microcirculation, Dyslipidemias
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