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Article: Cardiac valvular calcification as a marker of atherosclerosis and arterial calcification in end-stage renal disease

TitleCardiac valvular calcification as a marker of atherosclerosis and arterial calcification in end-stage renal disease
Authors
Issue Date2005
PublisherAmerican Medical Association. The Journal's web site is located at http://www.archinternmed.com
Citation
Archives Of Internal Medicine, 2005, v. 165 n. 3, p. 327-332 How to Cite?
AbstractBackground: Patients with end-stage renal disease (ESRD) are at increased risk for tissue calcifications as a result of deranged mineral metabolism. We tested the hypothesis that valvular calcification is a marker of atherosclerosis in patients with ESRD. Methods: Echocardiography was performed in 92 patients undergoing peritoneal dialysis with no background atherosclerotic vascular complications to detect valvular calcification. We used B-mode ultrasonography to determine carotid artery intima-media thickness and the presence of plaque and calcification. Results: Compared with patients without valvular calcification (n=66), those with valvular calcification (n=26) had higher C-reactive protein levels (P=.01) and greater mean±SE carotid intima-media thickness (1.12±0.06 vs 0.88±0.04 mm; P=.003). Carotid artery calcification was present unilaterally and bilaterally in 4 patients (15%) and 17 patients (65%) with valvular calcification vs 11 (17%) and 14 (21%) without, respectively (P<.001). Carotid artery plaque was present unilaterally and bilaterally in 11 patients (12%) and 16 patients (65%) with valvular calcification vs 3 (17%) and 17 (24%) without, respectively (P=.001). Using multiple logistic regression analysis, every 1-mm increase in carotid intima-media thickness was independently associated with a 6.51-fold (95% confidence interval, 1.58-26.73; P=.009) increased risk of valvular calcification, and calcification and plaque in the carotid arteries were associated with a 7.18-fold (95% confidence interval, 2.39-21.51; P<.001) and a 5.00-fold (95% confidence interval, 1.77-14.13; P=.002) increased risk of valvular calcification, respectively. Conclusion: The associations among valvular calcification, inflammation, carotid atherosclerosis, and arterial calcification suggest that valvular calcification is a marker of atherosclerosis and arterial calcification in patients with ESRD.
Persistent Identifierhttp://hdl.handle.net/10722/162786
ISSN
2014 Impact Factor: 17.333
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWang, AYMen_US
dc.contributor.authorHo, SSYen_US
dc.contributor.authorWang, Men_US
dc.contributor.authorLiu, EKHen_US
dc.contributor.authorHo, Sen_US
dc.contributor.authorLi, PKTen_US
dc.contributor.authorLui, SFen_US
dc.contributor.authorSanderson, JEen_US
dc.date.accessioned2012-09-05T05:23:31Z-
dc.date.available2012-09-05T05:23:31Z-
dc.date.issued2005en_US
dc.identifier.citationArchives Of Internal Medicine, 2005, v. 165 n. 3, p. 327-332en_US
dc.identifier.issn0003-9926en_US
dc.identifier.urihttp://hdl.handle.net/10722/162786-
dc.description.abstractBackground: Patients with end-stage renal disease (ESRD) are at increased risk for tissue calcifications as a result of deranged mineral metabolism. We tested the hypothesis that valvular calcification is a marker of atherosclerosis in patients with ESRD. Methods: Echocardiography was performed in 92 patients undergoing peritoneal dialysis with no background atherosclerotic vascular complications to detect valvular calcification. We used B-mode ultrasonography to determine carotid artery intima-media thickness and the presence of plaque and calcification. Results: Compared with patients without valvular calcification (n=66), those with valvular calcification (n=26) had higher C-reactive protein levels (P=.01) and greater mean±SE carotid intima-media thickness (1.12±0.06 vs 0.88±0.04 mm; P=.003). Carotid artery calcification was present unilaterally and bilaterally in 4 patients (15%) and 17 patients (65%) with valvular calcification vs 11 (17%) and 14 (21%) without, respectively (P<.001). Carotid artery plaque was present unilaterally and bilaterally in 11 patients (12%) and 16 patients (65%) with valvular calcification vs 3 (17%) and 17 (24%) without, respectively (P=.001). Using multiple logistic regression analysis, every 1-mm increase in carotid intima-media thickness was independently associated with a 6.51-fold (95% confidence interval, 1.58-26.73; P=.009) increased risk of valvular calcification, and calcification and plaque in the carotid arteries were associated with a 7.18-fold (95% confidence interval, 2.39-21.51; P<.001) and a 5.00-fold (95% confidence interval, 1.77-14.13; P=.002) increased risk of valvular calcification, respectively. Conclusion: The associations among valvular calcification, inflammation, carotid atherosclerosis, and arterial calcification suggest that valvular calcification is a marker of atherosclerosis and arterial calcification in patients with ESRD.en_US
dc.languageengen_US
dc.publisherAmerican Medical Association. The Journal's web site is located at http://www.archinternmed.comen_US
dc.relation.ispartofArchives of Internal Medicineen_US
dc.subject.meshAnalysis Of Varianceen_US
dc.subject.meshArteriosclerosis - Diagnosis - Epidemiology - Etiologyen_US
dc.subject.meshBiological Markersen_US
dc.subject.meshCalcinosis - Epidemiology - Physiopathologyen_US
dc.subject.meshCarotid Arteries - Ultrasonographyen_US
dc.subject.meshEchocardiographyen_US
dc.subject.meshFemaleen_US
dc.subject.meshHeart Valve Diseases - Epidemiology - Physiopathologyen_US
dc.subject.meshHong Kong - Epidemiologyen_US
dc.subject.meshHumansen_US
dc.subject.meshKidney Failure, Chronic - Complications - Epidemiologyen_US
dc.subject.meshLogistic Modelsen_US
dc.subject.meshMaleen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshRisken_US
dc.titleCardiac valvular calcification as a marker of atherosclerosis and arterial calcification in end-stage renal diseaseen_US
dc.typeArticleen_US
dc.identifier.emailWang, M:meiwang@hkucc.hku.hken_US
dc.identifier.authorityWang, M=rp00281en_US
dc.description.naturelink_to_OA_fulltexten_US
dc.identifier.doi10.1001/archinte.165.3.327en_US
dc.identifier.pmid15710797-
dc.identifier.scopuseid_2-s2.0-13444270349en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-13444270349&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume165en_US
dc.identifier.issue3en_US
dc.identifier.spage327en_US
dc.identifier.epage332en_US
dc.identifier.isiWOS:000226952400013-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridWang, AYM=13606226000en_US
dc.identifier.scopusauthoridHo, SSY=36107985800en_US
dc.identifier.scopusauthoridWang, M=7406690398en_US
dc.identifier.scopusauthoridLiu, EKH=8672405800en_US
dc.identifier.scopusauthoridHo, S=7403717175en_US
dc.identifier.scopusauthoridLi, PKT=25928016800en_US
dc.identifier.scopusauthoridLui, SF=7102379144en_US
dc.identifier.scopusauthoridSanderson, JE=7202371250en_US
dc.identifier.issnl0003-9926-

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