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Article: Vascular protective effects of statin-related increase in serum 25-hydroxyvitamin D among high-risk cardiac patients

TitleVascular protective effects of statin-related increase in serum 25-hydroxyvitamin D among high-risk cardiac patients
Authors
Issue Date2015
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.jcardiovascularmedicine.com
Citation
Journal of Cardiovascular Medicine (Hagerstown), 2015, v. 16 n. 1, p. 51-58 How to Cite?
AbstractAIM: To investigate the protective effects of statin-related increase in serum 25-hydroxyvitamin D [25(OH)D] on vascular function among high-risk cardiovascular patients. METHODS: We studied 443 high-risk cardiovascular patients (coronary disease 83%, ischemic stroke 21%; mean age 68 ± 10 years; men 77%). Serum 25(OH)D was measured by ELISA assay. Carotid intima-media thickness (IMT) and brachial flow-mediated dilatation were measured by high-resolution vascular ultrasound. Circulating CD34KDR and CD133KDR endothelial progenitor cells (EPCs) were measured by flow cytometry. RESULTS: Three hundred and twenty-nine (74%) patients were statin users. Serum 25(OH)D was higher among statin users than nonusers (30.2 ± 12.8 versus 26.8 ± 8.5 ng/ml; P = 0.009), which remained significant after multivariable adjustment [B = +3.8, 95% confidence interval (CI) 0.6 to 6.9, P = 0.019). Serum 25(OH)D was associated with reduced carotid IMT (R = -0.11, P = 0.026), and increased circulating CD34KDR EPC (R = 0.13, P = 0.030) and CD133KDR EPC (R = 0.15, P = 0.012). Adjusted for potential confounders, serum 25(OH)D remained independently associated with reduced carotid IMT (B = -0.003, 95% CI -0.005 to 0.000, P = 0.017), and increased circulating CD34KDR EPC [B = 0.006, 95% CI 0.002 to 0.009, P = 0.001, log, unit (×10/ml)] and CD133KDR EPC [B = 0.004, 95% CI 0.001 to 0.008, P = 0.016, log, unit (×10/ml)]. Interaction test showed no multiplicative effect between statins and serum 25(OH)D on carotid IMT or EPCs. Serum 25(OH)D was negatively associated with HbA1c (B = -0.010, 95% CI -0.019 to -0.001, P = 0.035). There was no significant association between serum 25(OH)D and brachial flow-mediated dilatation (R = -0.045, P = 0.344). CONCLUSION: In patients with cardiovascular disease, statin use is associated with increased serum 25(OH)D, which is independently associated with reduced carotid atherosclerotic burden, increased circulating EPCs, and improved glycemic control. These may partially explain the pleotrophic effects of statins.
Persistent Identifierhttp://hdl.handle.net/10722/216024
ISSN
2015 Impact Factor: 1.658
2015 SCImago Journal Rankings: 0.309
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorChan, YH-
dc.contributor.authorLau, GKK-
dc.contributor.authorYiu, KH-
dc.contributor.authorLi, LSW-
dc.contributor.authorTam, S-
dc.contributor.authorLam, TH-
dc.contributor.authorLau, CP-
dc.contributor.authorSiu, DCW-
dc.contributor.authorCheung, BMY-
dc.contributor.authorTse, HF-
dc.date.accessioned2015-08-21T13:49:21Z-
dc.date.available2015-08-21T13:49:21Z-
dc.date.issued2015-
dc.identifier.citationJournal of Cardiovascular Medicine (Hagerstown), 2015, v. 16 n. 1, p. 51-58-
dc.identifier.issn1558-2027-
dc.identifier.urihttp://hdl.handle.net/10722/216024-
dc.description.abstractAIM: To investigate the protective effects of statin-related increase in serum 25-hydroxyvitamin D [25(OH)D] on vascular function among high-risk cardiovascular patients. METHODS: We studied 443 high-risk cardiovascular patients (coronary disease 83%, ischemic stroke 21%; mean age 68 ± 10 years; men 77%). Serum 25(OH)D was measured by ELISA assay. Carotid intima-media thickness (IMT) and brachial flow-mediated dilatation were measured by high-resolution vascular ultrasound. Circulating CD34KDR and CD133KDR endothelial progenitor cells (EPCs) were measured by flow cytometry. RESULTS: Three hundred and twenty-nine (74%) patients were statin users. Serum 25(OH)D was higher among statin users than nonusers (30.2 ± 12.8 versus 26.8 ± 8.5 ng/ml; P = 0.009), which remained significant after multivariable adjustment [B = +3.8, 95% confidence interval (CI) 0.6 to 6.9, P = 0.019). Serum 25(OH)D was associated with reduced carotid IMT (R = -0.11, P = 0.026), and increased circulating CD34KDR EPC (R = 0.13, P = 0.030) and CD133KDR EPC (R = 0.15, P = 0.012). Adjusted for potential confounders, serum 25(OH)D remained independently associated with reduced carotid IMT (B = -0.003, 95% CI -0.005 to 0.000, P = 0.017), and increased circulating CD34KDR EPC [B = 0.006, 95% CI 0.002 to 0.009, P = 0.001, log, unit (×10/ml)] and CD133KDR EPC [B = 0.004, 95% CI 0.001 to 0.008, P = 0.016, log, unit (×10/ml)]. Interaction test showed no multiplicative effect between statins and serum 25(OH)D on carotid IMT or EPCs. Serum 25(OH)D was negatively associated with HbA1c (B = -0.010, 95% CI -0.019 to -0.001, P = 0.035). There was no significant association between serum 25(OH)D and brachial flow-mediated dilatation (R = -0.045, P = 0.344). CONCLUSION: In patients with cardiovascular disease, statin use is associated with increased serum 25(OH)D, which is independently associated with reduced carotid atherosclerotic burden, increased circulating EPCs, and improved glycemic control. These may partially explain the pleotrophic effects of statins.-
dc.languageeng-
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.jcardiovascularmedicine.com-
dc.relation.ispartofJournal of Cardiovascular Medicine (Hagerstown)-
dc.titleVascular protective effects of statin-related increase in serum 25-hydroxyvitamin D among high-risk cardiac patients-
dc.typeArticle-
dc.identifier.emailLau, GKK: gkklau@hku.hk-
dc.identifier.emailYiu, KH: khkyiu@hku.hk-
dc.identifier.emailTam, S: stam@hkucc.hku.hk-
dc.identifier.emailLam, TH: hrmrlth@hkucc.hku.hk-
dc.identifier.emailLau, CP: cplau@hkucc.hku.hk-
dc.identifier.emailSiu, DCW: cwdsiu@hkucc.hku.hk-
dc.identifier.emailCheung, BMY: mycheung@hkucc.hku.hk-
dc.identifier.emailTse, HF: hftse@hkucc.hku.hk-
dc.identifier.authorityChan, YH=rp01313-
dc.identifier.authorityLau, GKK=rp01499-
dc.identifier.authorityYiu, KH=rp01490-
dc.identifier.authorityLam, TH=rp00326-
dc.identifier.authoritySiu, DCW=rp00534-
dc.identifier.authorityCheung, BMY=rp01321-
dc.identifier.authorityTse, HF=rp00428-
dc.identifier.doi10.2459/JCM.0000000000000026-
dc.identifier.pmid25436938-
dc.identifier.scopuseid_2-s2.0-84918563524-
dc.identifier.hkuros247186-
dc.identifier.hkuros243685-
dc.identifier.volume16-
dc.identifier.issue1-
dc.identifier.spage51-
dc.identifier.epage58-
dc.identifier.isiWOS:000345759600007-
dc.publisher.placeUnited States-

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