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              "en" => "<p id="spar0045" class="elsevierStyleSimplePara elsevierViewall">Cardiac magnetic resonance imaging of two patients with hypertrophic cardiomyopathy included in the study showing late gadolinium enhancement &#40;LGE&#41; and the respective bull&#39;s eyes marking location and extent of LGE&#46; &#40;A&#41; Patient with a pathogenic mutation in <span class="elsevierStyleItalic">TNNI3</span>&#59; LGE was documented in four segments &#8211; basal inferior&#44; basal inferolateral&#44; mid anterior and distal septal&#59; &#40;B&#41; patient with no pathogenic mutation found on genetic testing&#59; LGE was documented in five segments &#8211; basal and mid inferoseptal&#44; basal and mid inferolateral&#44; and basal anteroseptal&#46;</p>"
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    "titulo" => "Arrhythmogenic risk of late gadolinium enhancement in patients with hypertrophic cardiomyopathy&#58; Burden and location&#63;"
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Hypertrophic cardiomyopathy &#40;HCM&#41; is a common genetic disease&#44; and is one of the leading causes of sudden cardiac death &#40;SCD&#41;&#44; particularly in young athletes&#46;<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">1</span></a> Myocardial fibrosis and scar formation are frequently observed in patients with HCM&#46;<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">2</span></a> Quantitative late gadolinium enhancement &#40;LGE&#41; has emerged as a tool for risk stratification in HCM&#44; as the presence and extent of LGE have been associated with increased risk of SCD&#46; Quantitative LGE &#40;through the use of various threshold methods&#41; and semi-quantitative methods have been proposed to quantify the extent of LGE&#46;<a class="elsevierStyleCrossRefs" href="#bib0100"><span class="elsevierStyleSup">3&#8211;5</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">In HCM&#44; LGE is most commonly observed in the septal wall&#44; usually but not always limited to hypertrophied segments in a variety of patterns that are not related to vascular territories&#46; This is in contrast to ischemic cardiomyopathy&#44; in which the subendocardial area related to the culprit artery is most frequently affected&#46;<a class="elsevierStyleCrossRefs" href="#bib0100"><span class="elsevierStyleSup">3&#44;6&#44;7</span></a> Histopathological analysis results from postmortem or post-surgical samples in HCM patients have shown that LGE areas are indicative of myocardial scarring or interstitial fibrosis&#44; and so the proposed mechanism has been hypothesized to be related to microvascular ischemia rather than stenosis of epicardial coronary arteries&#46;<a class="elsevierStyleCrossRefs" href="#bib0125"><span class="elsevierStyleSup">8&#44;9</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">In this issue of the <span class="elsevierStyleItalic">Journal</span>&#44; Barbosa and colleagues observe that the location of LGE&#44; in addition to its extent&#44; are important features associated with increased risk of ventricular arrhythmias in HCM patients&#46; They hypothesize that areas of increased mechanical stress are more prone to LGE development&#44; and that such areas may play an arrhythmogenic role&#46;<a class="elsevierStyleCrossRef" href="#bib0135"><span class="elsevierStyleSup">10</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall">There is a paucity of evidence linking LGE location and increased arrhythmogenic risk in HCM patients&#46; The exception is LGE that is isolated to the right ventricular insertion point&#46; This has been shown not to be correlated with SCD&#44; as here it in fact represents areas of expanded extracellular space rather than replacement fibrosis&#46;<a class="elsevierStyleCrossRef" href="#bib0140"><span class="elsevierStyleSup">11</span></a> Amano et al&#46;<a class="elsevierStyleCrossRef" href="#bib0145"><span class="elsevierStyleSup">12</span></a> have shown that in addition to the total number of LGE segments&#44; the presence of LGE in non-septal segments may also be related to arrhythmias and could add important information beyond fibrosis extent&#46; Nojiri et al&#46;<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">3</span></a> showed that the basal anteroseptal&#44; mid anteroseptal&#44; mid inferoseptal and apical septal segments&#44; in that order&#44; are the segments most often involved in HCM patients with preserved left ventricular ejection fraction&#44; and also that mid-wall area involvement is more prevalent than subepicardial or subendocardial involvement&#46; Based on the study&#39;s findings&#44; and dividing the heart into 18 segments and 3 layers&#44; they defined a scoring model up to 48 points and proposed that a higher score &#40;i&#46;e&#46; higher LGE&#41; is correlated with a higher rate of cardiac events including heart failure or ventricular tachycardia&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">Of interest&#44; Basso et al&#46;<a class="elsevierStyleCrossRef" href="#bib0150"><span class="elsevierStyleSup">13</span></a> showed that in patients with mitral valve prolapse&#44; LGE at the papillary muscles and basal inferior segment were associated with arrhythmia&#46; They hypothesized that mechanical stretch by the prolapsing leaflet &#40;and the subsequent development of LGE in the aforementioned segments&#41; could act as a trigger of electrical instability&#46; Maurer et al&#46;<a class="elsevierStyleCrossRef" href="#bib0155"><span class="elsevierStyleSup">14</span></a> suggested that there is an association between increased myocardial wall stress and increased metabolic demand&#44; mostly in locations corresponding to the basal inferior and lateral segments&#46; Excitation-contraction coupling plays an important role in cardiac physiology&#46; In addition&#44; mechanical stress could be a trigger for electrical activity and instability&#44; termed mechano-electrical feedback&#44; as in commotio cordis&#44; which is more pronounced in non-uniform cardiac muscle&#46;<a class="elsevierStyleCrossRefs" href="#bib0160"><span class="elsevierStyleSup">15&#44;16</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">The association between the location of LGE in HCM patients and clinical risk factors and subsequent premature cardiac death demonstrated by Barbosa et al&#46;<a class="elsevierStyleCrossRef" href="#bib0135"><span class="elsevierStyleSup">10</span></a> represents an important first step&#46; Nevertheless&#44; there is a wide range and overlap in the extent of LGE within patient subgroups&#46; Due to the small number of patients &#40;n&#61;61&#41; and of events &#40;n&#61;15&#41; in their study&#44; it is difficult to independently attribute the increased arrhythmogenic risk to the location of LGE&#44; rather than to the presence &#40;or more likely&#44; the overall burden&#41; of LGE&#46; It is also important to remember that using two or more clinical risk factors has just 45&#37; sensitivity and 23&#37; positive predictive value to predict sudden cardiac death in HCM patients&#46;<a class="elsevierStyleCrossRef" href="#bib0170"><span class="elsevierStyleSup">17</span></a> However&#44; the important data presented by Barbosa et al&#46; indicate that further research into the prognostic value of LGE location in HCM patients is warranted&#46;</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Conflicts of interest</span><p id="par0035" class="elsevierStylePara elsevierViewall">The author has no conflicts of interest to declare&#46;</p></span></span>"
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