File Download
  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Arterial stiffness and endothelial function in patients with β-thalassemia major

TitleArterial stiffness and endothelial function in patients with β-thalassemia major
Authors
Issue Date2002
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://circ.ahajournals.org
Citation
Circulation, 2002, v. 106 n. 20, p. 2561-2566 How to Cite?
AbstractBackground - Increased iron store has been linked to risk of cardiovascular disease. Structural alterations of arteries in β-thalassemia major patients and in vitro functional disturbance of vascular endothelial cells by thalassemic serum have been described. We sought to determine whether arterial stiffness and endothelial function are altered in vivo. Methods and Results - Thirty thalassemia patients (16 male) aged 22.2±7.4 years were recruited. Left ventricular (LV) mass and function were assessed echocardiographically. Carotid and brachioradial artery stiffness was assessed by stiffness index and pulse-wave velocity (PWV), respectively. Brachial artery endothelial function was assessed by vascular response to reactive hyperemia (flow-mediated dilation [FMD]) and sublingual glyceryl trinitrate. These indexes were compared with those of 30 age- and sex-matched controls. None of the patients had LV systolic or diastolic dysfunction. When compared with controls, patients had greater absolute (113.8±38.0 versus 109.0±32.6 g, P=0.04) and indexed (82.4±17.5 versus 66.7±12.7 g/m2, P<0.001) LV mass, carotid artery stiffness index (8.1±3.5 versus 5.5±1.6, P<0.001), and brachioradial PWV (8.9±2.4 versus 7.9±1.7 m/s, P=0.03). Their FMD was impaired (3.5±3.3% versus 8.8±3.9%, P<0.001), whereas glyceryl trinitrate-mediated dilation was preserved (17.9±7.6% versus 16.3±6.1%, P=0.40). Both stiffness index and PWV correlated inversely with magnitude of FMD (r= -0.40, P=0.03; r= -0.41, P=0.03) and positively with indexed LV mass (r=0.50, P=0.005; r=0.40, P=0.027). Nonetheless, no significant correlation existed between ferritin level and carotid stiffness, PWV, or FMD. Conclusions - Increased arterial stiffness, endothelial dysfunction, and LV hypertrophy occur in patients with β-thalassemia major, which may result in reduction of mechanical efficiency of the heart.
Persistent Identifierhttp://hdl.handle.net/10722/170322
ISSN
2015 Impact Factor: 17.047
2015 SCImago Journal Rankings: 7.853
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorCheung, YFen_US
dc.contributor.authorChan, GCFen_US
dc.contributor.authorHa, SYen_US
dc.date.accessioned2012-10-30T06:07:29Z-
dc.date.available2012-10-30T06:07:29Z-
dc.date.issued2002en_US
dc.identifier.citationCirculation, 2002, v. 106 n. 20, p. 2561-2566en_US
dc.identifier.issn0009-7322en_US
dc.identifier.urihttp://hdl.handle.net/10722/170322-
dc.description.abstractBackground - Increased iron store has been linked to risk of cardiovascular disease. Structural alterations of arteries in β-thalassemia major patients and in vitro functional disturbance of vascular endothelial cells by thalassemic serum have been described. We sought to determine whether arterial stiffness and endothelial function are altered in vivo. Methods and Results - Thirty thalassemia patients (16 male) aged 22.2±7.4 years were recruited. Left ventricular (LV) mass and function were assessed echocardiographically. Carotid and brachioradial artery stiffness was assessed by stiffness index and pulse-wave velocity (PWV), respectively. Brachial artery endothelial function was assessed by vascular response to reactive hyperemia (flow-mediated dilation [FMD]) and sublingual glyceryl trinitrate. These indexes were compared with those of 30 age- and sex-matched controls. None of the patients had LV systolic or diastolic dysfunction. When compared with controls, patients had greater absolute (113.8±38.0 versus 109.0±32.6 g, P=0.04) and indexed (82.4±17.5 versus 66.7±12.7 g/m2, P<0.001) LV mass, carotid artery stiffness index (8.1±3.5 versus 5.5±1.6, P<0.001), and brachioradial PWV (8.9±2.4 versus 7.9±1.7 m/s, P=0.03). Their FMD was impaired (3.5±3.3% versus 8.8±3.9%, P<0.001), whereas glyceryl trinitrate-mediated dilation was preserved (17.9±7.6% versus 16.3±6.1%, P=0.40). Both stiffness index and PWV correlated inversely with magnitude of FMD (r= -0.40, P=0.03; r= -0.41, P=0.03) and positively with indexed LV mass (r=0.50, P=0.005; r=0.40, P=0.027). Nonetheless, no significant correlation existed between ferritin level and carotid stiffness, PWV, or FMD. Conclusions - Increased arterial stiffness, endothelial dysfunction, and LV hypertrophy occur in patients with β-thalassemia major, which may result in reduction of mechanical efficiency of the heart.en_US
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://circ.ahajournals.orgen_US
dc.relation.ispartofCirculationen_US
dc.rightsCirculation. Copyright © Lippincott Williams & Wilkins.-
dc.subject.meshAdulten_US
dc.subject.meshArteries - Physiopathologyen_US
dc.subject.meshBrachial Artery - Cytology - Physiopathologyen_US
dc.subject.meshCarotid Arteries - Physiopathologyen_US
dc.subject.meshComplianceen_US
dc.subject.meshEchocardiographyen_US
dc.subject.meshEndothelium, Vascular - Physiopathologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshFerritins - Blooden_US
dc.subject.meshHumansen_US
dc.subject.meshMaleen_US
dc.subject.meshVasodilationen_US
dc.subject.meshVentricular Function, Leften_US
dc.subject.meshVentricular Remodelingen_US
dc.subject.meshBeta-Thalassemia - Blood - Physiopathology - Ultrasonographyen_US
dc.titleArterial stiffness and endothelial function in patients with β-thalassemia majoren_US
dc.typeArticleen_US
dc.identifier.emailCheung, YF:xfcheung@hku.hken_US
dc.identifier.emailChan, GCF:gcfchan@hkucc.hku.hken_US
dc.identifier.authorityCheung, YF=rp00382en_US
dc.identifier.authorityChan, GCF=rp00431en_US
dc.description.naturelink_to_OA_fulltexten_US
dc.identifier.doi10.1161/01.CIR.0000037225.92759.A7en_US
dc.identifier.pmid12427652-
dc.identifier.scopuseid_2-s2.0-0037069422en_US
dc.identifier.hkuros74967-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0037069422&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume106en_US
dc.identifier.issue20en_US
dc.identifier.spage2561en_US
dc.identifier.epage2566en_US
dc.identifier.isiWOS:000179339300024-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridCheung, YF=7202111067en_US
dc.identifier.scopusauthoridChan, GCF=16160154400en_US
dc.identifier.scopusauthoridHa, SY=7202501115en_US

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats