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

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dc.contributor.authorİrgi, T.
dc.contributor.authorBaycan, Ö.F.
dc.contributor.authorGüvenç, T.S.
dc.contributor.authorÖzcan, F.B.
dc.contributor.authorAtıcı, A.
dc.contributor.authorYılmaz, Y.
dc.contributor.authorÇalişkan M.
dc.date.accessioned2024-05-19T14:33:18Z
dc.date.available2024-05-19T14:33:18Z
dc.date.issued2024
dc.departmentİstinye Üniversitesien_US
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. © 2024 The Author(s)en_US
dc.identifier.doi10.1016/j.ahjo.2024.100393
dc.identifier.issn2666-6022
dc.identifier.scopus2-s2.0-85190270647en_US
dc.identifier.scopusqualityN/Aen_US
dc.identifier.urihttps://doi.org/10.1016/j.ahjo.2024.100393
dc.identifier.urihttps://hdl.handle.net/20.500.12713/4182
dc.identifier.volume41en_US
dc.indekslendigikaynakScopusen_US
dc.language.isoenen_US
dc.publisherElsevier Inc.en_US
dc.relation.ispartofAmerican Heart Journal Plus: Cardiology Research and Practiceen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.snmz20240519_kaen_US
dc.subjectAmyloidosisen_US
dc.subjectArteriopathyen_US
dc.subjectCarpal Tunnel Syndromeen_US
dc.subjectEndothelial Dysfunctionen_US
dc.subjectMicrovascular Dysfunctionen_US
dc.titleConcomitant amyloidosis is the primary cause of endothelial and coronary microvascular dysfunction in carpal tunnel syndromeen_US
dc.typeArticleen_US

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