Myocardial Inactivation of Thyroid Hormones in Patients with Aortic Stenosis

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dc.contributorSistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSP
dc.contributor.authorPAOLINO, Bruno S.
dc.contributor.authorPOMERANTZEFF, Pablo M.
dc.contributor.authorDALLAN, Luis Alberto O.
dc.contributor.authorGAIOTTO, Fabio A.
dc.contributor.authorPREITE, Nailliw Z.
dc.contributor.authorLATRONICO, Ana Claudia
dc.contributor.authorNICOLAU, Jose Carlos
dc.contributor.authorBIANCO, Antonio C.
dc.contributor.authorGIRALDEZ, Roberto R. C. V.
dc.date.accessioned2017-06-09T15:31:35Z
dc.date.available2017-06-09T15:31:35Z
dc.date.issued2017
dc.description.abstractObjective: The human heart expresses the type 2 deiodinase (D2) that activates thyroxine (T4) to triiodothyronine (T3). At the same time, the inactivating type 3 deiodinase (D3) has been found in a rat model of right ventricular hypertrophy. It is not known whether the human myocardium metabolizes thyroid hormone. This study examined myocardial thyroid hormone metabolism in patients with aortic valve stenosis (AS) undergoing aortic valve replacement and in patients with coronary artery disease (CAD) undergoing coronary artery bypass grafting surgery. Methods: Myocardial thyroid hormone metabolism was assessed by analyzing the difference in serum thyroid hormone levels between the aortic root (incoming blood) and the coronary sinus (outgoing blood) of patients undergoing cardiac surgery. A total of 23 patients with AS and 35 patients with CAD were included. Patients received a pre-surgical echocardiogram, and pre-, during and post-surgical thyroid hormone serum levels were collected in the myocardial and peripheral circulations. Results: Patients with AS exhibited the expected left ventricle (LV) hypertrophy (i.e., 20-30% increase in LV posterior wall and interventricular septum thickness and similar to 10% increase in AS in LV diastolic diameter). Immediately before cardiopulmonary bypass, blood flowing through the AS myocardium exhibited a 4.6% reduction in T3 and 6.9% increase in rT3 levels, decreasing the serum T3/rT3 ratio by 9.6%. T4 and thyrotropin serum levels remained similar between the aortic root and coronary sinus. In contrast, no myocardial thyroid hormone metabolism was observed in CAD patients. Notably, the AS myocardium lost the ability to inactivate thyroid hormone after cardiopulmonary bypass, possibly due to myocardial stunning. Conclusions: There is accelerated thyroid hormone inactivation in the AS myocardium, which is likely the result of D3 expression. No evidence to suggest thyroid hormone activation in the myocardium was obtained in the present study.
dc.description.indexMEDLINE
dc.description.sponsorshipNIDDK NIH HHS
dc.identifier.citationTHYROID, v.27, n.5, p.738-745, 2017
dc.identifier.doi10.1089/thy.2016.0514
dc.identifier.eissn1557-9077
dc.identifier.issn1050-7256
dc.identifier.urihttps://observatorio.fm.usp.br/handle/OPI/20009
dc.language.isoeng
dc.publisherMARY ANN LIEBERT, INC
dc.relation.ispartofThyroid
dc.rightsrestrictedAccess
dc.rights.holderCopyright MARY ANN LIEBERT, INC
dc.subjecteuthyroid sick syndrome
dc.subjectdeiodinases
dc.subjectthyroid hormones
dc.subjectaortic stenosis
dc.subjectheart surgery
dc.subject.othertype-2 iodothyronine deiodinase
dc.subject.othercardiac-specific thyrotoxicosis
dc.subject.othercardiopulmonary bypass
dc.subject.othersurgery
dc.subject.othercardiomyopathy
dc.subject.otherdysfunction
dc.subject.otheramiodarone
dc.subject.otherexpression
dc.subject.otherinduction
dc.subject.othertherapy
dc.subject.wosEndocrinology & Metabolism
dc.titleMyocardial Inactivation of Thyroid Hormones in Patients with Aortic Stenosis
dc.typearticle
dc.type.categoryoriginal article
dc.type.versionpublishedVersion
dspace.entity.typePublication
hcfmusp.affiliation.countryEstados Unidos
hcfmusp.affiliation.countryisous
hcfmusp.author.externalPREITE, Nailliw Z.:Rush Univ, Med Ctr, Dept Internal Med, Div Endocrinol & Metab, Chicago, IL 60612 USA
hcfmusp.author.externalBIANCO, Antonio C.:Rush Univ, Med Ctr, Dept Internal Med, Div Endocrinol & Metab, Chicago, IL 60612 USA
hcfmusp.citation.scopus8
hcfmusp.contributor.author-fmusphcBRUNO DE SOUZA PAOLINO
hcfmusp.contributor.author-fmusphcPABLO MARIA ALBERTO POMERANTZEFF
hcfmusp.contributor.author-fmusphcLUIS ALBERTO OLIVEIRA DALLAN
hcfmusp.contributor.author-fmusphcFABIO ANTONIO GAIOTTO
hcfmusp.contributor.author-fmusphcANA CLAUDIA LATRONICO XAVIER
hcfmusp.contributor.author-fmusphcJOSE CARLOS NICOLAU
hcfmusp.contributor.author-fmusphcROBERTO ROCHA CORREA VEIGA GIRALDEZ
hcfmusp.description.beginpage738
hcfmusp.description.endpage745
hcfmusp.description.issue5
hcfmusp.description.volume27
hcfmusp.origemWOS
hcfmusp.origem.pubmed28095748
hcfmusp.origem.scopus2-s2.0-85018287375
hcfmusp.origem.wosWOS:000400657900017
hcfmusp.publisher.cityNEW ROCHELLE
hcfmusp.publisher.countryUSA
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