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Subclinical Hypothyroidism

2014; Lippincott Williams & Wilkins; Volume: 7; Issue: 1 Linguagem: Inglês

10.1161/circep.113.001058

1941-3149

Francesca Esposito, Vincenzo Liguori, Gennaro Maresca, Annunziata Cerrone, Ovidio De Filippo, Bruno Trimarco, Antonio Rapacciuolo,

Cardiac Arrhythmias and Treatments

HomeCirculation: Arrhythmia and ElectrophysiologyVol. 7, No. 1Subclinical Hypothyroidism Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessResearch ArticlePDF/EPUBSubclinical HypothyroidismA Reversible Cause of Complete Loss of Ventricular Lead Capture Francesca Esposito, MD, Vincenzo Liguori, MD, PhD, Gennaro Maresca, MD, Annunziata Cerrone, BS, Ovidio De Filippo, BS, Bruno Trimarco, MD, PhD and Antonio Rapacciuolo, MD, PhD Francesca EspositoFrancesca Esposito From the Division of Cardiology, Federico II University of Naples, Naples, Italy. , Vincenzo LiguoriVincenzo Liguori From the Division of Cardiology, Federico II University of Naples, Naples, Italy. , Gennaro MarescaGennaro Maresca From the Division of Cardiology, Federico II University of Naples, Naples, Italy. , Annunziata CerroneAnnunziata Cerrone From the Division of Cardiology, Federico II University of Naples, Naples, Italy. , Ovidio De FilippoOvidio De Filippo From the Division of Cardiology, Federico II University of Naples, Naples, Italy. , Bruno TrimarcoBruno Trimarco From the Division of Cardiology, Federico II University of Naples, Naples, Italy. and Antonio RapacciuoloAntonio Rapacciuolo From the Division of Cardiology, Federico II University of Naples, Naples, Italy. Originally published1 Feb 2014https://doi.org/10.1161/CIRCEP.113.001058Circulation: Arrhythmia and Electrophysiology. 2014;7:182–184Case PresentationA 77-year-old male former smoker with hypertension, dyslipidemia, and diabetes mellitus was admitted to our institution for recurrent syncope. He had a history of previous non–Q-wave inferior myocardial infarction in 1980, which had never been investigated by coronary angiography. Echocardiogram showed left ventricular dilation, inferior akinesia, and hypokinesia of the remaining segments with severe left ventricular dysfunction (left ventricular ejection fraction, 30%). Twenty-four–hour Holter ECG recording revealed 3 episodes of self-terminating sustained ventricular tachycardia. The patient underwent a coronary angiography that evidenced multivessel disease with chronic total occlusion of the proximal right coronary artery and of the mid left circumflex artery and diffuse disease of the left anterior descending artery without critical stenosis. Collateral flow ran from left anterior descending artery to left circumflex artery via diagonal branches (Rentrop 2); mid-distal right coronary artery was supplied by homo- contralateral vessel circulation via left circumflex artery collateral channels (Rentrop 3). No revascularization therapy was performed because both mid-distal right coronary artery and left circumflex artery were supplied by valid collateral flow and the patient was asymptomatic for both angina and dyspnea (New York Heart Association class I). Optimal medical therapy was established, including angiotensin-converting enzyme inhibitors, β-blockers, loop diuretics, and mineralocorticoid receptor antagonists. Therefore, according to current guidelines, he underwent the implantation of a dual-chamber implantable cardioverter defibrillator (ICD). Through the standard left subclavian vein approach, we implanted a dual-coil passive fixation lead (Endotak Reliance G 0286, Boston Scientific Corporation) at the right ventricular apex and a J-shaped passive fixation lead (Isoflex Optim, 1944/52 cm, St Jude Medical) in the right atrial appendage. The leads were connected to a dual- chamber defibrillator (Fortify ST DR, St Jude Medical) which was implanted prepectorally. Postimplantation parameters of both atrial and ventricular leads were normal (P-wave amplitude, 2.5 mV; atrial threshold, 0.75 V×0.5 ms; atrial lead impedance, 650 Ω; R-wave amplitude, 7.2 mV; ventricular threshold, 0.5 V×0.5 ms; ventricular pacing lead impedance, 490 Ω; shock impedance, 44 Ω). One month later, the patient was readmitted for persistent atrial fibrillation. Successful conversion to sinus rhythm with intravenous amiodarone was performed, and at discharge, oral amiodarone was continued. Predischarge thyroid function was normal. At 6-month follow-up ICD interrogation, intrinsic R wave was 8.1 mV, pacing impedance was 512 Ω, and shock impedance was 40 Ω, but analysis of stimulation threshold revealed complete lack of ventricular capture (maximum output tested, 7.5 V×1.0 ms; Figure 1). Atrial lead parameters were normal. Blood tests evidenced subclinical hypothyroidism: thyroid-stimulating hormone, 35.20 μU/mL (normal range, 0.3–4.2 μU/mL); free triiodothyronine, 3.7 pg/mL (normal range, 2.0–4.4 pg/mL); and free thyroxine, 0.87 ng/dL (normal range, 0.9–1.7 ng/dL). A standard posterior–anterior and lateral chest radiograph was performed. Chest radiograph showed ventricular lead to be in standard position. Because the patient was not pacing dependent and amiodarone is known to raise pacing threshold, this drug was discontinued and ICD interrogation was scheduled at 1 month. ICD interrogation 1 month after amiodarone withdrawal evidenced persistent lack of ventricular capture (maximum output tested, 7.5 V×1.0 ms). The patient was admitted to hospital for ventricular lead revision. Because of lack of radiological evidence of ventricular lead dislodgment and a subclinical hypothyroidism of new onset, we decided to postpone ventricular lead revision until after hypothyroidism had been adequately treated. Therefore, levothyroxine (50 mg/day) was started. On the third day, thyroid-stimulating hormone level was reduced to 24.57 μU/mL, and ICD interrogation showed complete restoration of ventricular capture (ventricular pacing threshold was 0.75 V×0.5 ms; Figure 2). The patient was discharged on levothyroxine therapy. Three months after discharge, thyroid-stimulating hormone had returned within its reference range (3.3 μU/mL) and ventricular pacing threshold was 1.0 V×0.5 ms (Figure 3).Download figureDownload PowerPointFigure 1. Twelve-lead ECG showing lack of ventricular capture, despite pacing artifact (circle).Download figureDownload PowerPointFigure 2. ECG showing restoration of ventricular capture following levothyroxine administration.Download figureDownload PowerPointFigure 3. Ventricular pacing threshold vs time in relation to thyroid-stimulating hormone (TSH) levels. The figure highlights elevation of right ventricular threshold causing complete exit block, attributable to new onset subclinical hypothyroidism 6 months postimplantation. Short-term levothyroxine administration determines recovery of ventricular capture that persists 3 months after discharge, consistent with complete normalization of TSH levels.DiscussionThyroid disorders are known to exert a multitude of adverse effects on myocardium and cardiovascular system, such as bradycardia, atrioventricular block, and prolonged QT interval. Hypothyroidism causing myxedema cardiomyopathy has been reported as a cause of increased ventricular pacing threshold and complete exit block.1 A previous report by Patton et al describes an isolated atrial lead dysfunction in a young woman with overt hypothyroidism attributable to Graves disease completely reversed with thyroid hormone replacement.2 Subclinical hypothyroidism is characterized by abnormal lipid metabolism, cardiac dysfunction, and diastolic hypertension. It is associated with a significant risk of atherosclerosis and ischemic heart disease and increased cardiovascular mortality at follow-up.3 The management of subclinical thyroid dysfunction is controversial, and there is no sufficient evidence that treatment is beneficial. A consensus panel recommends treatment with levothyroxine for patients with serum thyroid-stimulating hormone levels >10 μU/mL, especially when associated to decreasing free thyroxine levels, because the rate of progression to overt hypothyroidism is 5%.4 This is the first demonstration that a complete loss of capture can be attributable to subclinical hypothyroidism. Immediate ventricular pacing threshold restoration with levothyroxine administration strongly supports the hypothesis that subclinical hypothyroidism was the cause of exit block.DisclosuresNone.FootnotesCorrespondence to Antonio Rapacciuolo, MD, PhD, Division of Cardiology, Federico II University of Naples, Via S. Pansini 5, 80131, Naples, Italy. E-mail [email protected]References1. Schlesinger Z, Rosenberg T, Stryjer D, Gilboa Y. Exit block in myxedema, treated effectively by thyroid hormone therapy.Pacing Clin Electrophysiol. 1980; 3:737–739.CrossrefMedlineGoogle Scholar2. Patton KK, Levy M, Viswanathan M. Atrial lead dysfunction: an unusual feature of hypothyroidism.Pacing Clin Electrophysiol. 2008; 31:1650–1652.CrossrefMedlineGoogle Scholar3. Singh S, Duggal J, Molnar J, Maldonado F, Barsano CP, Arora R. Impact of subclinical thyroid disorders on coronary heart disease, cardiovascular and all-cause mortality: a meta-analysis.Int J Cardiol. 2008; 125:41–48.CrossrefMedlineGoogle Scholar4. Surks MI, Ortiz E, Daniels GH, Sawin CT, Col NF, Cobin RH, Franklyn JA, Hershman JM, Burman KD, Denke MA, Gorman C, Cooper RS, Weissman NJ. Subclinical thyroid disease: scientific review and guidelines for diagnosis and management.JAMA. 2004; 291:228–238.CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Gorenek B, Boriani G, Dan G, Fauchier L, Fenelon G, Huang H, Kudaiberdieva G, Lip G, Mahajan R, Potpara T, Ramirez J, Vos M, Marin F, Blomstrom-Lundqvist C, Rinaldi A, Bongiorni M, Sciaraffia E, Nielsen J, Lewalter T, Zhang S, Gutiérrez O and Fuenmayor A (2018) European Heart Rhythm Association (EHRA) position paper on arrhythmia management and device therapies in endocrine disorders, endorsed by Asia Pacific Heart Rhythm Society (APHRS) and Latin American Heart Rhythm Society (LAHRS), EP Europace, 10.1093/europace/euy051, 20:6, (895-896), Online publication date: 1-Jun-2018. Sharma A, Vegh E, Orencole M, Miller A, Blendea D, Moore S, Lewis G, Singh J, Parks K and Heist E (2015) Association of Hypothyroidism With Adverse Events in Patients With Heart Failure Receiving Cardiac Resynchronization Therapy, The American Journal of Cardiology, 10.1016/j.amjcard.2015.01.559, 115:9, (1249-1253), Online publication date: 1-May-2015. February 2014Vol 7, Issue 1 Advertisement Article InformationMetrics © 2014 American Heart Association, Inc.https://doi.org/10.1161/CIRCEP.113.001058PMID: 24550411 Manuscript receivedSeptember 20, 2013Manuscript acceptedDecember 19, 2013Originally publishedFebruary 1, 2014 Keywordsamiodaronethyroid hormonesheart failurethyroid glandhypothyroidismPDF download Advertisement SubjectsCatheter Ablation and Implantable Cardioverter-DefibrillatorCongenital Heart DiseaseElectrocardiology (ECG)