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Pathogenesis of Atherosclerosis: A Multifactorial Process

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Ischemic Heart Disease

Abstract

Atherosclerosis is an inflammatory and immunologically driven response of the vessel wall to chronic, multifactorial, repetitive injury. Endothelial cell dysfunction leads to increased oxidative stress, production of inflammatory cytokines, expression of adhesion molecules, and accumulation of oxidized LDL. Atherosclerotic plaques form as a consequence of endothelial damage, proliferation of modified smooth muscle cells, influx of monocytes and T lymphocytes, unregulated uptake of LDL cholesterol, foam cell formation, and connective tissue deposition. Inflammation is also important in the erosion or rupture of vulnerable plaques leading to clinical complications of atherosclerosis, including CAD or IHD. CAD is a genetically complex disease in which multiple genes influence the progression of atherosclerosis in populations, although CAD can develop due to single-gene mutations in lipid metabolism in some individuals.

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Abbreviations

(hs)-cTn:

High-sensitivity cardiac troponin

ACS:

Acute coronary syndromes

AMI:

Acute myocardial infarction

CAD:

Coronary artery disease

CHIP:

Clonal hematopoiesis of indeterminate potential

CHIP:

Clonal hematopoiesis of indeterminate potential

CMV:

Cytomegalovirus

CRP:

C-reactive protein

cTn:

Cardiac troponin

DAMP:

Danger-associated molecular patterns

EDRF:

Endothelium-derived relaxing factor

FH:

Familiar hypercholesterolemia

ICAM-1:

Intercellular adhesion molecule

IHD:

Ischemic heart disease

IL-18:

Interleukin-18

IL-1β:

Interleukin-1β

LD:

Linkage disequilibrium

LDL:

Low-density lipoprotein

MR:

Mendelian randomization

NF-κB:

Nuclear factor-kappa B

NO:

Nitric oxide

PAMP:

Pathogen-associated molecular patterns

PDGF:

Platelet-derived growth factor

PRP:

Pattern recognition receptors

TNF:

Tissue necrosis factor

UDMI:

Universal definition of myocardial infarction

VCAM-1:

Vascular cell adhesion molecule 1

VSMC:

Vascular smooth muscle cell

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Authors and Affiliations

  1. Department of Pathology and Laboratory Medicine, McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth), Houston, TX, USA

    L. Maximilian Buja

  2. Texas Heart Institute, Houston, TX, USA

    L. Maximilian Buja

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  1. Department of Adult Cardiac Surgery, Ospedale del cuore “G. Pasquinucci", Massa, Italy

    Giovanni Concistrè

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Buja, L.M. (2023). Pathogenesis of Atherosclerosis: A Multifactorial Process. In: Concistrè, G. (eds) Ischemic Heart Disease. Springer, Cham. https://doi.org/10.1007/978-3-031-25879-4_2

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