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as proposed and validated by Iacobellis et al&#46;<a class="elsevierStyleCrossRefs" href="#bib0065"><span class="elsevierStyleSup">3&#44;4</span></a> Echocardiographic EAT is a linear measurement at a single location and therefore may not reflect the variability of fat thickness or total EAT volume as measured by computed tomography&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall">Of note&#44; EAT has been shown to correlate with waist circumference and intra-abdominal and intracardiac fat&#44; and to serve as a good surrogate marker of visceral adiposity&#46;<a class="elsevierStyleCrossRefs" href="#bib0070"><span class="elsevierStyleSup">4&#8211;6</span></a></p><p id="par0025" class="elsevierStylePara elsevierViewall">Impaired myocardial performance as assessed echocardiographically by left ventricular global longitudinal strain<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">7</span></a> was recently associated with increased myocardial fat content and enhanced EAT volume&#46; EAT penetrates inside the human myocardium&#44; affecting its biological behavior&#44; which supports the concept that EAT and cardiac function are closely connected&#46;<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">8</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">Metformin&#44; which was developed from galegine&#44; an anti-diabetic compound derived from <span class="elsevierStyleItalic">Galega officinalis</span>&#44; is the first-line therapy to treat type 2 diabetic patients&#46;</p><p id="par0035" class="elsevierStylePara elsevierViewall">In this issue of the <span class="elsevierStyleItalic">Journal</span>&#44; Ziyrek et al&#46;<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">9</span></a> add interesting findings to the growing literature on cardiac adiposity and heart disease&#46; The authors demonstrated that metformin monotherapy significantly decreases EAT thickness and body mass index &#40;BMI&#41; after three months of therapy in newly diagnosed type 2 diabetes patients&#46;</p><p id="par0040" class="elsevierStylePara elsevierViewall">We read Ziyrek et al&#46;&#8217;s study with interest&#44; as it unveils new roles for metformin beyond its use as a first-line therapy for diabetes&#46; The authors did not assess cardiovascular outcomes and no other visceral fat depots were measured in this study&#46; Further work is needed to study and correlate the beneficial effects of metformin on EAT with possible positive cardiovascular outcomes in type 2 diabetic patients&#46;</p><p id="par0045" class="elsevierStylePara elsevierViewall">In addition&#44; diabetic patients in Ziyrek et al&#46;&#8217;s study were uncomplicated&#44; and the results may not be applicable to diabetic patients with macrovascular complications&#46; However&#44; their results may warrant further studies in complicated and&#47;or poorly controlled diabetic subjects&#46;</p><p id="par0050" class="elsevierStylePara elsevierViewall">Inflammation is the real culprit when it comes to triggering cardiovascular disease&#46; This prospective observational study should have measured inflammatory markers&#44; suggesting a mechanism of action and highlighting the importance of metformin in this context&#46;</p><p id="par0055" class="elsevierStylePara elsevierViewall">The main finding of the study was that metformin significantly reduces BMI and EAT thickness in newly diagnosed type 2 diabetic patients&#44; reinforcing the use of metformin as a first line therapy for type 2 diabetes&#46; Nevertheless&#44; further research is needed to determine whether type 2 diabetic patients with macrovascular disease treated with metformin can achieve similar reductions in EAT thickness and volume&#46; Also&#44; modifications of the EAT transcriptome may open new avenues of treatment for cardiometabolic diseases&#46; Indeed&#44; EAT may serve as a therapeutic target for medications modulating adipose tissue in patients with cardiovascular disease&#46;<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">10</span></a></p><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Funding</span><p id="par0065" class="elsevierStylePara elsevierViewall">This study was supported by Funda&#231;&#227;o para a Ci&#234;ncia e a Tecnologia &#40;Award IDs&#58; PTDC&#47;BIM-MET&#47;4447&#47;2014 and COMPETE&#58; POCI-01-0145-FEDER-016784&#41;&#46;</p></span><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0010">Conflicts of interest</span><p id="par0060" class="elsevierStylePara elsevierViewall">The author has no conflicts of interest to declare&#46;</p></span></span>"
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Editorial comment
Epicardial adipose tissue: An important therapeutic target
Tecido adiposo epicárdico: um alvo terapêutico importante
Cristina M. Sena
Institute of Physiology, iCBR, Faculty of Medicine, University of Coimbra, Coimbra, Portugal
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Cardiovascular disease is the leading cause of death in Portugal&#44; accounting for one third of all deaths&#46;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">1</span></a> The rising prevalence of cardiovascular risk factors such as obesity and type 2 diabetes is concerning&#44; in Portugal as elsewhere in the world&#46;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">1</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">In the modern era of obesity and diabetes pandemics&#44; adipose tissue is in the spotlight&#46; Epicardial adipose tissue &#40;EAT&#41; is the visceral fat depot of the heart<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">2</span></a> and is of interest for cardiovascular diagnostics and therapeutics&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">EAT can be measured with standard echocardiography&#44; as proposed and validated by Iacobellis et al&#46;<a class="elsevierStyleCrossRefs" href="#bib0065"><span class="elsevierStyleSup">3&#44;4</span></a> Echocardiographic EAT is a linear measurement at a single location and therefore may not reflect the variability of fat thickness or total EAT volume as measured by computed tomography&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall">Of note&#44; EAT has been shown to correlate with waist circumference and intra-abdominal and intracardiac fat&#44; and to serve as a good surrogate marker of visceral adiposity&#46;<a class="elsevierStyleCrossRefs" href="#bib0070"><span class="elsevierStyleSup">4&#8211;6</span></a></p><p id="par0025" class="elsevierStylePara elsevierViewall">Impaired myocardial performance as assessed echocardiographically by left ventricular global longitudinal strain<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">7</span></a> was recently associated with increased myocardial fat content and enhanced EAT volume&#46; EAT penetrates inside the human myocardium&#44; affecting its biological behavior&#44; which supports the concept that EAT and cardiac function are closely connected&#46;<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">8</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">Metformin&#44; which was developed from galegine&#44; an anti-diabetic compound derived from <span class="elsevierStyleItalic">Galega officinalis</span>&#44; is the first-line therapy to treat type 2 diabetic patients&#46;</p><p id="par0035" class="elsevierStylePara elsevierViewall">In this issue of the <span class="elsevierStyleItalic">Journal</span>&#44; Ziyrek et al&#46;<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">9</span></a> add interesting findings to the growing literature on cardiac adiposity and heart disease&#46; The authors demonstrated that metformin monotherapy significantly decreases EAT thickness and body mass index &#40;BMI&#41; after three months of therapy in newly diagnosed type 2 diabetes patients&#46;</p><p id="par0040" class="elsevierStylePara elsevierViewall">We read Ziyrek et al&#46;&#8217;s study with interest&#44; as it unveils new roles for metformin beyond its use as a first-line therapy for diabetes&#46; The authors did not assess cardiovascular outcomes and no other visceral fat depots were measured in this study&#46; Further work is needed to study and correlate the beneficial effects of metformin on EAT with possible positive cardiovascular outcomes in type 2 diabetic patients&#46;</p><p id="par0045" class="elsevierStylePara elsevierViewall">In addition&#44; diabetic patients in Ziyrek et al&#46;&#8217;s study were uncomplicated&#44; and the results may not be applicable to diabetic patients with macrovascular complications&#46; However&#44; their results may warrant further studies in complicated and&#47;or poorly controlled diabetic subjects&#46;</p><p id="par0050" class="elsevierStylePara elsevierViewall">Inflammation is the real culprit when it comes to triggering cardiovascular disease&#46; This prospective observational study should have measured inflammatory markers&#44; suggesting a mechanism of action and highlighting the importance of metformin in this context&#46;</p><p id="par0055" class="elsevierStylePara elsevierViewall">The main finding of the study was that metformin significantly reduces BMI and EAT thickness in newly diagnosed type 2 diabetic patients&#44; reinforcing the use of metformin as a first line therapy for type 2 diabetes&#46; Nevertheless&#44; further research is needed to determine whether type 2 diabetic patients with macrovascular disease treated with metformin can achieve similar reductions in EAT thickness and volume&#46; Also&#44; modifications of the EAT transcriptome may open new avenues of treatment for cardiometabolic diseases&#46; Indeed&#44; EAT may serve as a therapeutic target for medications modulating adipose tissue in patients with cardiovascular disease&#46;<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">10</span></a></p><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Funding</span><p id="par0065" class="elsevierStylePara elsevierViewall">This study was supported by Funda&#231;&#227;o para a Ci&#234;ncia e a Tecnologia &#40;Award IDs&#58; PTDC&#47;BIM-MET&#47;4447&#47;2014 and COMPETE&#58; POCI-01-0145-FEDER-016784&#41;&#46;</p></span><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0010">Conflicts of interest</span><p id="par0060" class="elsevierStylePara elsevierViewall">The author has no conflicts of interest to declare&#46;</p></span></span>"
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Revista Portuguesa de Cardiologia (English edition)
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