Skip to content
DraconiticResearch
Search Sources API
197,768 studies31 sourcesUpdated just now
Peer-reviewedCC BYMedicina (Kaunas, Lithuania)

Accelerated Atherosclerosis.

  • Alexandru-Cristian Nechita1,2
  • Dan-Cristian Popescu1,2,3
  • Mara Diaconu1,2,3
  • Adrian-Claudiu Popa1
  • Bogdan Marcu1
  • Vasilica Enache1,2
  1. 1Department of Cardiology, Clinical Emergency Hospital Sfântul Pantelimon, 021659 Bucharest, Romania.
  2. 2Faculty of Medicine, Carol Davila University of Medicine and Pharmacy, 020021 Bucharest, Romania.
  3. 3Faculty of Medicine, Transilvania University, 500036 Brasov, Romania.
Read full textPDFDOICite

Abstract

Accelerated atherosclerosis (AA) denotes a disproportionately early and rapid progression of arterial atheroma unpredictable by standard tools. Clinicians often rely on simplified frameworks for cardiovascular risk assessment, which may overlook genetic and pathological conditions associated with AA. Some of these are well established, others are considered future therapy targets. This review examines the conditions in which AA is most firmly established, including rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), antiphospholipid syndrome, chronic kidney disease (CKD), human immunodeficiency virus (HIV), diabetes mellitus, and psoriasis. We also examined the importance of genetic determinants of AA, with particular emphasis on clonal hematopoiesis of indeterminate potential (CHIP) and lipoprotein (a) (Lp(a)); contemporary imaging-based detection and monitoring; the diagnostic role of circulating non-coding microRNAs; and complementary protein biomarkers of residual inflammatory risk. After identifying biomarkers of increased cardiovascular risk and possible AA, clinicians should assess atherosclerotic disease directly using the available imaging techniques, most of which are non-invasive. The clinical consequences of AA are discussed and a comprehensive review of the therapeutic options is provided to offer a practical approach.

Related

  1. Sexually dimorphic transdifferentiation of endothelial cells in atherosclerosis
    Cheng Luo, Songmao Wang, Qing Rex Lyu +1
    Communications BiologyPeer-reviewedCC BY-NC-ND 4.0Full textImmunologyCrossref
  2. IRE1 deficiency in myeloid cells increases atherosclerosis in apoE−/− mice
    Xiaoning Zhao, Jianchang Zhou, Kuang-Yuh Chyu +4
    Scientific ReportsPeer-reviewedCC BY-NC-ND 4.0ImmunologyCrossref
  3. Genome-Wide Transcriptomics Uncovers a Lung-to-Aorta Inflammatory Program Driving Influenza-Induced Atherosclerosis Exacerbation
    Louis DeVito, John C. Notaro, Nicholas J. Constantinesco +3
    bioRxivPreprintAll rights reservedFull textImmunologybioRxivPMC
  4. Macrophage PIM1 Drives Atherosclerosis by Enhancing Foam Cell Formation Via CD36
    Mirza Ahmar Beg, Quoc Quang Luu, Wenjing Chen +5
    Arteriosclerosis Thrombosis and Vascular BiologyPeer-reviewedLicence not statedFull text5 citedImmunologyOpenAlex
  5. High-fat diet promotes exhaustion-associated T-cell remodeling across vascular and lymphoid tissues in atherosclerosis-prone mice
    P. Yarahmadi, Y. Xie, D. T. N. Huynh +4
    bioRxivPreprintAll rights reservedFull textImmunologybioRxiv

Cite

BibTeXRIS
BibTeX
@article{nechita2026accelerated,
  title = {{Accelerated Atherosclerosis.}},
  author = {Alexandru-Cristian Nechita and Dan-Cristian Popescu and Mara Diaconu and Adrian-Claudiu Popa and Bogdan Marcu and Vasilica Enache},
  journal = {Medicina (Kaunas, Lithuania)},
  year = {2026},
  month = sep,
  doi = {10.3390/medicina62101898},
  url = {https://europepmc.org/article/MED/42942429},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Accelerated Atherosclerosis.
AU  - Alexandru-Cristian Nechita
AU  - Dan-Cristian Popescu
AU  - Mara Diaconu
AU  - Adrian-Claudiu Popa
AU  - Bogdan Marcu
AU  - Vasilica Enache
PY  - 2026
DA  - 2026/09/30
JO  - Medicina (Kaunas, Lithuania)
DO  - 10.3390/medicina62101898
UR  - https://europepmc.org/article/MED/42942429
AB  - Accelerated atherosclerosis (AA) denotes a disproportionately early and rapid progression of arterial atheroma unpredictable by standard tools. Clinicians often rely on simplified frameworks for cardiovascular risk assessment, which may overlook genetic and pathological conditions associated with AA. Some of these are well established, others are considered future therapy targets. This review examines the conditions in which AA is most firmly established, including rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), antiphospholipid syndrome, chronic kidney disease (CKD), human immunodeficiency virus (HIV), diabetes mellitus, and psoriasis. We also examined the importance of genetic determinants of AA, with particular emphasis on clonal hematopoiesis of indeterminate potential (CHIP) and lipoprotein (a) (Lp(a)); contemporary imaging-based detection and monitoring; the diagnostic role of circulating non-coding microRNAs; and complementary protein biomarkers of residual inflammatory risk. After identifying biomarkers of increased cardiovascular risk and possible AA, clinicians should assess atherosclerotic disease directly using the available imaging techniques, most of which are non-invasive. The clinical consequences of AA are discussed and a comprehensive review of the therapeutic options is provided to offer a practical approach.
SN  - 1010-660X
SN  - 1648-9144
ER  -