File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Hemodynamic changes in hyperthyroidism-related pulmonary hypertension: A prospective echocardiographic study

TitleHemodynamic changes in hyperthyroidism-related pulmonary hypertension: A prospective echocardiographic study
Authors
Issue Date2007
PublisherThe Endocrine Society. The Journal's web site is located at http://jcem.endojournals.org
Citation
Journal Of Clinical Endocrinology And Metabolism, 2007, v. 92 n. 5, p. 1736-1742 How to Cite?
AbstractContext: Recent reports suggest an association between hyperthyroidism and pulmonary hypertension (PHT), although the potential mechanisms and clinical implications remain unclear. Objective: Our objective was to determine the prevalence of PHT related to hyperthyroidism and the associated hemodynamic changes and outcome. Methods and Results: We performed serial echocardiographic examinations in 75 consecutive patients with hyperthyroidism (43 ± 2 yr, 47 women) to estimate pulmonary artery systolic pressure (PASP), cardiac output (CO), total vascular resistance (TVR), and left ventricular (LV) filling pressure. Examinations were performed at baseline and 6 months after initiation of antithyroid treatment. Results were compared with 35 age- and sex-matched healthy controls. All hyperthyroid patients had normal LV systolic function, and 35 patients (47%) had PHT with PASP of at least 35 mm Hg. There were no significant differences in the clinical characteristics of hyperthyroid patients with or without PHT (all P > 0.05). Nonetheless, those with PHT had significantly higher CO, PASP, peak transmitral early diastolic flow velocity (E), and ratio of E to early diastolic mitral annular velocity (E′) compared with those without PHT and controls (all P < 0.05). Hyperthyroid patients with PHT also had significantly lower TVR than controls (P < 0.05). Among the 35 hyperthyroid patients with PHT, 25 (71%) had pulmonary arterial hypertension (PAH) with normal E/E′, and 10 (29%) had pulmonary venous hypertension (PVH) with elevated E/E′. Hyperthyroid patients with PAH had a significantly higher CO and a lower TVR compared with those with PVH. In contrast, hyperthyroid patients with PVH had lower E′ and a higher E/E′ ratio compared with those with PAH. These hemodynamic abnormalities and PHT were reversible in patients with PAH or PVH after restoration to a euthyroid state. Conclusion: In patients with hyperthyroidism and normal LV systolic function, up to 47% had PHT due to either PAH with increased CO (70%) or PVH with elevated LV filling pressure (30%). Most importantly, hyperthyroidism-related PHT was largely asymptomatic and reversible after restoration to a euthyroid state. Copyright © 2007 by The Endocrine Society.
Persistent Identifierhttp://hdl.handle.net/10722/76299
ISSN
2015 Impact Factor: 5.531
2015 SCImago Journal Rankings: 2.940
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorSiu, CWen_HK
dc.contributor.authorZhang, XHen_HK
dc.contributor.authorYung, Cen_HK
dc.contributor.authorKung, AWCen_HK
dc.contributor.authorLau, CPen_HK
dc.contributor.authorTse, HFen_HK
dc.date.accessioned2010-09-06T07:19:45Z-
dc.date.available2010-09-06T07:19:45Z-
dc.date.issued2007en_HK
dc.identifier.citationJournal Of Clinical Endocrinology And Metabolism, 2007, v. 92 n. 5, p. 1736-1742en_HK
dc.identifier.issn0021-972Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/76299-
dc.description.abstractContext: Recent reports suggest an association between hyperthyroidism and pulmonary hypertension (PHT), although the potential mechanisms and clinical implications remain unclear. Objective: Our objective was to determine the prevalence of PHT related to hyperthyroidism and the associated hemodynamic changes and outcome. Methods and Results: We performed serial echocardiographic examinations in 75 consecutive patients with hyperthyroidism (43 ± 2 yr, 47 women) to estimate pulmonary artery systolic pressure (PASP), cardiac output (CO), total vascular resistance (TVR), and left ventricular (LV) filling pressure. Examinations were performed at baseline and 6 months after initiation of antithyroid treatment. Results were compared with 35 age- and sex-matched healthy controls. All hyperthyroid patients had normal LV systolic function, and 35 patients (47%) had PHT with PASP of at least 35 mm Hg. There were no significant differences in the clinical characteristics of hyperthyroid patients with or without PHT (all P > 0.05). Nonetheless, those with PHT had significantly higher CO, PASP, peak transmitral early diastolic flow velocity (E), and ratio of E to early diastolic mitral annular velocity (E′) compared with those without PHT and controls (all P < 0.05). Hyperthyroid patients with PHT also had significantly lower TVR than controls (P < 0.05). Among the 35 hyperthyroid patients with PHT, 25 (71%) had pulmonary arterial hypertension (PAH) with normal E/E′, and 10 (29%) had pulmonary venous hypertension (PVH) with elevated E/E′. Hyperthyroid patients with PAH had a significantly higher CO and a lower TVR compared with those with PVH. In contrast, hyperthyroid patients with PVH had lower E′ and a higher E/E′ ratio compared with those with PAH. These hemodynamic abnormalities and PHT were reversible in patients with PAH or PVH after restoration to a euthyroid state. Conclusion: In patients with hyperthyroidism and normal LV systolic function, up to 47% had PHT due to either PAH with increased CO (70%) or PVH with elevated LV filling pressure (30%). Most importantly, hyperthyroidism-related PHT was largely asymptomatic and reversible after restoration to a euthyroid state. Copyright © 2007 by The Endocrine Society.en_HK
dc.languageengen_HK
dc.publisherThe Endocrine Society. The Journal's web site is located at http://jcem.endojournals.orgen_HK
dc.relation.ispartofJournal of Clinical Endocrinology and Metabolismen_HK
dc.rightsJournal of Clinical Endocrinology and Metabolism. Copyright © The Endocrine Society.en_HK
dc.subject.meshAdulten_HK
dc.subject.meshAntithyroid Agents - therapeutic useen_HK
dc.subject.meshBlood Pressure - physiologyen_HK
dc.subject.meshCarbimazole - therapeutic useen_HK
dc.subject.meshCardiac Output - physiologyen_HK
dc.subject.meshEchocardiographyen_HK
dc.subject.meshEchocardiography, Doppleren_HK
dc.subject.meshFemaleen_HK
dc.subject.meshFollow-Up Studiesen_HK
dc.subject.meshHumansen_HK
dc.subject.meshHypertension, Pulmonary - etiology - physiopathology - ultrasonographyen_HK
dc.subject.meshHyperthyroidism - complications - physiopathology - ultrasonographyen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshPropylthiouracil - therapeutic useen_HK
dc.subject.meshProspective Studiesen_HK
dc.subject.meshTreatment Outcomeen_HK
dc.subject.meshVascular Resistance - physiologyen_HK
dc.subject.meshVentricular Function, Left - physiologyen_HK
dc.titleHemodynamic changes in hyperthyroidism-related pulmonary hypertension: A prospective echocardiographic studyen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0021-972X&volume=92&spage=1736&epage=42&date=2007&atitle=Hemodynamic+changes+in+hyperthyroidism-related+pulmonary+hypertension:+a+prospective+echocardiographic+studyen_HK
dc.identifier.emailSiu, CW:cwdsiu@hkucc.hku.hken_HK
dc.identifier.emailKung, AWC:awckung@hku.hken_HK
dc.identifier.emailTse, HF:hftse@hkucc.hku.hken_HK
dc.identifier.authoritySiu, CW=rp00534en_HK
dc.identifier.authorityKung, AWC=rp00368en_HK
dc.identifier.authorityTse, HF=rp00428en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1210/jc.2006-1877en_HK
dc.identifier.pmid17327384-
dc.identifier.scopuseid_2-s2.0-34249852339en_HK
dc.identifier.hkuros142049en_HK
dc.identifier.hkuros126521-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34249852339&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume92en_HK
dc.identifier.issue5en_HK
dc.identifier.spage1736en_HK
dc.identifier.epage1742en_HK
dc.identifier.isiWOS:000246221200029-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridSiu, CW=7006550690en_HK
dc.identifier.scopusauthoridZhang, XH=16425051500en_HK
dc.identifier.scopusauthoridYung, C=15770437000en_HK
dc.identifier.scopusauthoridKung, AWC=7102322339en_HK
dc.identifier.scopusauthoridLau, CP=7401968501en_HK
dc.identifier.scopusauthoridTse, HF=7006070805en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats