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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">In their study published in this issue of the <span class="elsevierStyleItalic">Journal</span>&#44;<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">1</span></a> Oliveira et al&#46; elegantly described a family of patients with left ventricular non-compaction &#40;LVNC&#41;&#44; illustrating the challenges in clinical practice regarding etiological investigation and risk stratification of sudden cardiac death in these patients&#46;</p><p id="par0010" class="elsevierStylePara elsevierViewall">A family history of LVNC has been described in about 30&#37; of cases<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">2</span></a> and a pathogenic mutation has been found in nearly one-third&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">3</span></a> Although LVNC is a genetically heterogeneous cardiomyopathy&#44; sarcomere mutations represent more than half of the known genetic causes&#44; especially in adults&#44; and <span class="elsevierStyleItalic">MYH7</span> is one of the most commonly mutated genes&#46;<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">2</span></a> Nevertheless&#44; the causal relation between genetic variants and the LVNC phenotype remains to be ascertained in the majority of cases&#46; This case report underlines the importance of a specialized cardiomyopathy team in the systematic genetic and clinical screening of family relatives and the interpretation of the clinical significance of genetic variants in LVNC&#46; Moreover&#44; the previous report of this <span class="elsevierStyleItalic">MYH7</span> mutation in a case of hypertrophic cardiomyopathy further supports the notion that the same mutation may be associated with different cardiomyopathy phenotypes&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">The etiopathogenesis of LVNC is largely unknown&#46; Recently&#44; cellular models&#44; such as induced pluripotent stem cell lines derived from LVNC patients&#44; have been developed and may prove useful to clarify the molecular&#44; genetic&#44; and functional aspects of the condition&#46;<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">4</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall">Risk stratification of sudden cardiac death in LVNC is also a complex matter&#44; particularly in the primary prevention setting&#44; given the lack of robust evidence supporting clinical practice&#46; Although the optimal risk stratification strategy is not clear&#44; it will probably lie in a multiparametric assessment&#44; in which left ventricular function appears to play a major role&#44; as patients with reduced left ventricular systolic function have been found to be at a 4&#46;6-fold higher risk for major adverse cardiac events &#40;MACE&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">5</span></a> The role of genetic testing for risk stratification in LVNC is still a matter of debate and a deeper understanding of genotype-phenotype correlations in LVNC is necessary&#46; The identification of pathogenic mutations has been associated with a higher risk of MACE&#46; However&#44; it is noteworthy that sarcomere mutations have been associated with a lower risk of such events compared to other genetic causes&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">3</span></a> By contrast&#44; other studies have not found genetic variants to be predictors of the risk of MACE&#46;<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">5</span></a> Therefore&#44; as illustrated in the case presented by Oliveira et al&#46;&#44;<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">1</span></a> decisions on cardioverter-defibrillator implantation may be complex in current clinical practice and individualized clinical judgment by a specialized cardiomyopathy team is pivotal for accurate patient risk stratification&#46;</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Conflicts of interest</span><p id="par0025" class="elsevierStylePara elsevierViewall">The author has no conflicts of interest to declare&#46;</p></span></span>"
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Editorial comment
Left ventricular non-compaction: Challenges in the etiopathogenesis and risk stratification of sudden cardiac death in clinical practice
Não compactação ventricular esquerda: desafios na etiopatogénese e na estratificação de risco de morte súbita na prática clínica
Nuno Marquesa,b
a ABC-RI - Algarve Biomedical Center Research Institute, Faro, Portugal
b Faculdade de Medicina e Ciências Biomédicas da Universidade do Algarve, Faro, Portugal
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    "titulo" => "Left ventricular non-compaction&#58; Challenges in the etiopathogenesis and risk stratification of sudden cardiac death in clinical practice"
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">In their study published in this issue of the <span class="elsevierStyleItalic">Journal</span>&#44;<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">1</span></a> Oliveira et al&#46; elegantly described a family of patients with left ventricular non-compaction &#40;LVNC&#41;&#44; illustrating the challenges in clinical practice regarding etiological investigation and risk stratification of sudden cardiac death in these patients&#46;</p><p id="par0010" class="elsevierStylePara elsevierViewall">A family history of LVNC has been described in about 30&#37; of cases<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">2</span></a> and a pathogenic mutation has been found in nearly one-third&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">3</span></a> Although LVNC is a genetically heterogeneous cardiomyopathy&#44; sarcomere mutations represent more than half of the known genetic causes&#44; especially in adults&#44; and <span class="elsevierStyleItalic">MYH7</span> is one of the most commonly mutated genes&#46;<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">2</span></a> Nevertheless&#44; the causal relation between genetic variants and the LVNC phenotype remains to be ascertained in the majority of cases&#46; This case report underlines the importance of a specialized cardiomyopathy team in the systematic genetic and clinical screening of family relatives and the interpretation of the clinical significance of genetic variants in LVNC&#46; Moreover&#44; the previous report of this <span class="elsevierStyleItalic">MYH7</span> mutation in a case of hypertrophic cardiomyopathy further supports the notion that the same mutation may be associated with different cardiomyopathy phenotypes&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">The etiopathogenesis of LVNC is largely unknown&#46; Recently&#44; cellular models&#44; such as induced pluripotent stem cell lines derived from LVNC patients&#44; have been developed and may prove useful to clarify the molecular&#44; genetic&#44; and functional aspects of the condition&#46;<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">4</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall">Risk stratification of sudden cardiac death in LVNC is also a complex matter&#44; particularly in the primary prevention setting&#44; given the lack of robust evidence supporting clinical practice&#46; Although the optimal risk stratification strategy is not clear&#44; it will probably lie in a multiparametric assessment&#44; in which left ventricular function appears to play a major role&#44; as patients with reduced left ventricular systolic function have been found to be at a 4&#46;6-fold higher risk for major adverse cardiac events &#40;MACE&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">5</span></a> The role of genetic testing for risk stratification in LVNC is still a matter of debate and a deeper understanding of genotype-phenotype correlations in LVNC is necessary&#46; The identification of pathogenic mutations has been associated with a higher risk of MACE&#46; However&#44; it is noteworthy that sarcomere mutations have been associated with a lower risk of such events compared to other genetic causes&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">3</span></a> By contrast&#44; other studies have not found genetic variants to be predictors of the risk of MACE&#46;<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">5</span></a> Therefore&#44; as illustrated in the case presented by Oliveira et al&#46;&#44;<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">1</span></a> decisions on cardioverter-defibrillator implantation may be complex in current clinical practice and individualized clinical judgment by a specialized cardiomyopathy team is pivotal for accurate patient risk stratification&#46;</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Conflicts of interest</span><p id="par0025" class="elsevierStylePara elsevierViewall">The author has no conflicts of interest to declare&#46;</p></span></span>"
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