Concomitant amyloidosis is the primary cause of endothelial and coronary microvascular dysfunction in carpal tunnel syndrome

dc.contributor.authorIrgi, Tugce
dc.contributor.authorBaycan, Ömer Faruk
dc.contributor.authorGuvenc, Tolga Sinan
dc.contributor.authorOzcan, Fatma Betul
dc.contributor.authorAtıcı, Adem
dc.contributor.authorYılmaz, Yusuf
dc.contributor.authorÇalışkan, Mustafa
dc.date.accessioned2025-05-10T19:48:19Z
dc.date.issued2024
dc.departmentİstanbul Medeniyet Üniversitesi
dc.description.abstractStudy objectives: Patients with carpal tunnel syndrome (CTS) show manifestations of arterial abnormalities, including carotid intimal thickening and increased vascular stiffness. As carpal tunnel syndrome is associated with amyloidosis, we hypothesized that previously observed abnormalities can largely be related with concomitant amyloidosis rather than CTS itself. Design: Prospective observational study. Setting: Medeniyet University Goztepe Hospital Participants: 61 patients with CTS (of whom 32 had biopsy-proven amyloidosis) and 36 healthy controls. Interventions: Subjects underwent ultrasound examinations for the measurement of coronary flow velocity reserve (CFVR), flow-mediated vasodilatation (FMD) and carotid intimal-media thickness (CIMT). Main outcome measures Comparison of CFVR, FMD and CIMT in CTS patients with or without amyloidosis. Results: Patients with either CTS or CTS with concomitant amyloidosis (CTS-A) had significantly lower FMD (9.7 % +/- 4.0 % in CTS and 10.3 % +/- 4.6 % in CTS-A groups, p < 0.05 for both) and CFVR (2.4 (2.1-2.8) in CTS and 1.8 (1.6-2.1) in CTS-A groups, p < 0.001 for both) as compared to controls, while CIMT was only increased in CTS-A group (0.70 (0.60-0.80), p < 0.001). The reduction in CFVR was solely related to an increased basal flow velocity in CTS patients while there was also a reduced hyperemic flow velocity in patients with CTS-A. Conclusion: Most arterial phenomena in CTS patients could be attributable to concomitant amyloidosis, although endothelial dysfunction was present even in patients with CTS without amyloidosis.
dc.identifier.doi10.1016/j.ahjo.2024.100393
dc.identifier.issn2666-6022
dc.identifier.pmid38655035
dc.identifier.scopus2-s2.0-85190270647
dc.identifier.scopusqualityQ3
dc.identifier.urihttps://doi.org/10.1016/j.ahjo.2024.100393
dc.identifier.urihttps://hdl.handle.net/20.500.14730/11677
dc.identifier.volume41
dc.identifier.wosWOS:001230098200001
dc.identifier.wosqualityN/A
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherElsevier
dc.relation.ispartofAmerican Heart Journal Plus: Cardiology Research and Practice
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.snmzKA_WOS_20250302
dc.subjectAmyloidosis
dc.subjectArteriopathy
dc.subjectCarpal tunnel syndrome
dc.subjectEndothelial dysfunction
dc.subjectMicrovascular dysfunction
dc.titleConcomitant amyloidosis is the primary cause of endothelial and coronary microvascular dysfunction in carpal tunnel syndrome
dc.typeArticle

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