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      Association of inflammation with atrial fibrillation in hyperthyroidism

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          Abstract

          Objectives

          The aim of this study was to evaluate the relationship between inflammation and development of atrial fibrillation (AF) in patients with hyperthyroidism.

          Methods

          A total of 65 patients with newly diagnosed hyperthyroidism, 35 of whom were in sinus rhythm and 30 of whom in AF. Thirty five age- and gender-matched patients in a control group were included in the study. Factors associated with the development of AF were evaluated by multivariate regression analysis.

          Results

          Factors associated with AF in multivariate analysis included high sensitivity C reactive protein (HsCRP) [odds ratio (OR): 11.19; 95% confidence interval (95% CI): 1.80-69.53; P = 0.003], free T4 (OR: 8.76; 95% CI: 2.09–36.7; P = 0.003), and left atrial diameter (OR: 1.25; 95% CI: 1.06–1.47; P = 0.008).

          Conclusions

          The results of the present study suggest that HsCRP, an indicator of inflammation, free T4 and left atrial diameter are associated with the development AF in patients with hyperthyroidism.

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          Echocardiographic assessment of left ventricular hypertrophy: comparison to necropsy findings.

          Richard Devereux, Daniel R. Alonso, Elizabeth M. Lutas … (1986)
          To determine the accuracy of echocardiographic left ventricular (LV) dimension and mass measurements for detection and quantification of LV hypertrophy, results of blindly read antemortem echocardiograms were compared with LV mass measurements made at necropsy in 55 patients. LV mass was calculated using M-mode LV measurements by Penn and American Society of Echocardiography (ASE) conventions and cube function and volume correction formulas in 52 patients. Penn-cube LV mass correlated closely with necropsy LV mass (r = 0.92, p less than 0.001) and overestimated it by only 6%; sensitivity in 18 patients with LV hypertrophy (necropsy LV mass more than 215 g) was 100% (18 of 18 patients) and specificity was 86% (29 of 34 patients). ASE-cube LV mass correlated similarly to necropsy LV mass (r = 0.90, p less than 0.001), but systematically overestimated it (by a mean of 25%); the overestimation could be corrected by the equation: LV mass = 0.80 (ASE-cube LV mass) + 0.6 g. Use of ASE measurements in the volume correction formula systematically underestimated necropsy LV mass (by a mean of 30%). In a subset of 9 patients, 3 of whom had technically inadequate M-mode echocardiograms, 2-dimensional echocardiographic (echo) LV mass by 2 methods was also significantly related to necropsy LV mass (r = 0.68, p less than 0.05 and r = 0.82, p less than 0.01). Among other indexes of LV anatomy, only measurement of myocardial cross-sectional area was acceptably accurate for quantitation of LV mass (r = 0.80, p less than 0.001) or diagnosis of LV hypertrophy (sensitivity = 72%, specificity = 94%).(ABSTRACT TRUNCATED AT 250 WORDS)
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            Structural correlate of atrial fibrillation in human patients.

            Sawa Kostin, Jutta Schaper, Z Szalay … (2002)
            We tested the hypothesis that structural remodeling of cellular connections, alterations in the expression of connexins (Cx), and an increase in fibrosis represent anatomic substrates of atrial fibrillation (AF). In 31 patients with AF undergoing a Maze procedure and 22 patients in sinus rhythm (SR), biopsies were taken intraoperatively from the right atrial (RA) free wall and appendages and investigated with immunoconfocal and electron microscopy. All patients with AF exhibited a concomitant lateralization of gap junctional proteins Cx43 and Cx40, and N-cadherin (the major mechanical junction protein), instead of being confined to the intercalated discs, as observed in SR. These results were confirmed by quantitative immunoconfocal analysis and electron microscopy. Among diverse junctional proteins, in AF, Cx40 was markedly heterogeneous in distribution. As compared with the SR group, Cx43 was significantly decreased in AF by 57% in RA appendages and by 56% in RA free wall. Cx40 was reduced by 54% in appendages, but had a tendency to be increased in the RA free wall. Collagen I was significantly higher in AF than in SR by 48% in RA appendages and by 69% in the RA free wall tissues. The structural correlate of AF comprises extensive concomitant remodeling of mechanical and electrical junctions, reduction of Cx43, heterogeneous distribution of Cx40 in terms of different amounts of Cx40 in different RA tissues or in spatially adjacent regions of atrial myocardium. These changes, together with augmentation of fibrosis, may underlie localized conduction abnormalities and contribute to initiation and self-perpetuation of re-entry pathways and AF.
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              Effects of thyroid hormone on the cardiovascular system.

              Emiliano Palmieri, Serafino Fazio, Gaetano Lombardi … (2003)
              Increased or reduced action of thyroid hormone on certain molecular pathways in the heart and vasculature causes relevant cardiovascular derangements. It is well established that overt hyperthyroidism induces a hyperdynamic cardiovascular state (high cardiac output with low systemic vascular resistance), which is associated with a faster heart rate, enhanced left ventricular (LV) systolic and diastolic function, and increased prevalence of supraventricular tachyarrhythmias - namely, atrial fibrillation - whereas overt hypothyroidism is characterized by the opposite changes. However, whether changes in cardiac performance associated with overt thyroid dysfunction are due mainly to alterations of myocardial contractility or to loading conditions remains unclear. Extensive evidence indicates that the cardiovascular system responds to the minimal but persistent changes in circulating thyroid hormone levels, which are typical of individuals with subclinical thyroid dysfunction. Subclinical hyperthyroidism is associated with increased heart rate, atrial arrhythmias, increased LV mass, impaired ventricular relaxation, reduced exercise performance, and increased risk of cardiovascular mortality. Subclinical hypothyroidism is associated with impaired LV diastolic function and subtle systolic dysfunction and an enhanced risk for atherosclerosis and myocardial infarction. Because all cardiovascular abnormalities are reversed by restoration of euthyroidism ("subclinical hypothyroidism") or blunted by beta-blockade and L-thyroxine (L-T4) dose tailoring ("subclinical hyperthyroidism"), timely treatment is advisable in an attempt to avoid adverse cardiovascular effects. Interestingly, some data indicate that patients with acute and chronic cardiovascular disorders and those undergoing cardiac surgery may have altered peripheral thyroid hormone metabolism that, in turn, may contribute to altered cardiac function. Preliminary clinical investigations suggest that administration of thyroid hormone or its analogue 3,5-diiodothyropropionic acid greatly benefits these patients, highlighting the potential role of thyroid hormone treatment in patients with acute and chronic cardiovascular disease.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Geriatr Cardiol
                Journal ID (iso-abbrev): J Geriatr Cardiol
                Journal ID (publisher-id): JGC
                Title: Journal of Geriatric Cardiology : JGC
                Publisher: Science Press
                ISSN (Print): 1671-5411
                Publication date (Print): December 2012
                Volume: 9
                Issue: 4
                Pages: 344-348
                Affiliations
                [1 ]Department of Cardiology, Suleyman Demirel University, Kurtulus Mah 122. cad. Hatice Halici apt. no: 126, 32040 Isparta, Turkey
                [2 ]Department of Internal Medicine, Gulkent Hospital, Atatürk Blv, 10432, 32200 Sanayi Isparta, Turkey
                [3 ]Department of Cardiology, Gulkent Hospital, Atatürk Blv, 10432, 32200 Sanayi, Isparta, Turkey
                Author notes
                Correspondence to: Mehmet Ozaydin, MD, Professor, Department of Cardiology, Suleyman Demirel University, Kurtulus Mah, 122. cad. Hatice Halici apt. no: 126, 32040, Isparta, Turkey. E-mail: mehmetozaydin@ 123456hotmail.com Telephone:+90-532-413-9528 Fax:+90-246-232-6280
                Article
                Publisher ID: jgc-09-04-344
                DOI: 10.3724/SP.J.1263.2012.06251
                PMC ID: 3545250
                PubMed ID: 23341838
                SO-VID: 0c934a86-c911-4f52-a34b-aa3a95883480
                Copyright © Institute of Geriatric Cardiology
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported License, which allows readers to alter, transform, or build upon the article and then distribute the resulting work under the same or similar license to this one. The work must be attributed back to the original author and commercial use is not permitted without specific permission.

                History
                Date received : 25 June 2012
                Date revision received : 16 August 2012
                Date accepted : 19 October 2012
                Categories
                Subject: Research Articles

                ScienceOpen disciplines: Cardiovascular Medicine
                Keywords: atrial fibrillation,hyperthyroidism,inflammation
                Data availability:
                ScienceOpen disciplines: Cardiovascular Medicine
                Keywords: atrial fibrillation, hyperthyroidism, inflammation

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