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In striated muscle, TTN is the largest protein and the third type of filament in addition to actin and myosin.<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">Coronary artery fistulas are a rare anomaly, and their association with hypertrophic cardiomyopathy (HCM) is even more unusual.<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> In this paper we present the case of a newborn with non-obstructive HCM and multiple fistulas.</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Case report</span><p id="par0015" class="elsevierStylePara elsevierViewall">The patient was a female newborn with a gestational age of 34 + 5 weeks and a prenatal diagnosis of interventricular communication (IVC), HCM, bradycardia, polyhydramnios, and dilatation of the third ventricle. Due to the pathological findings detected in a Doppler ultrasound and the suspected diagnosis of fetal anemia, an eutocic delivery was scheduled, following which the patient had to be admitted to the Neonatal Intensive Care Unit.</p><p id="par0020" class="elsevierStylePara elsevierViewall">On admission to this unit, the diagnosis of severe HCM was confirmed (diastolic interventricular septum of 8 mm and Z score of + 4.03). Dilatation of the right coronary system with multiple tracts draining into the apex of the right ventricle (RV) was also detected, in addition to a large fistula originating in the left coronary artery, with several tracts also draining into the RV. Evidence of diastolic steal was observed in the aortic arch and the ascending aorta, together with RV diastolic dysfunction and severe pulmonary hypertension (PHT). Both an electrocardiogram (ECG) and blood work showed signs of myocardial ischemia, with troponin levels of up to 2149 ng/L. In addition, the ECG revealed an alternation between a sinus node rhythm and a tendency to suffering from bradycardia.</p><p id="par0025" class="elsevierStylePara elsevierViewall">Following her admission to the unit, she developed arterial hypertension, metabolic acidosis, elevated lactic acid levels, and PHT, owing to which she required aggressive hemodynamic and respiratory support.</p><p id="par0030" class="elsevierStylePara elsevierViewall">At 12 days of life, she exhibited evidence of hemodynamic worsening, in addition to increased levels of troponins (155.2 ng/L), pro-brain natriuretic peptide (pro-BNP; 582,989 pg/mL), and lactic acid (>20 mmol/L), with the existence of biventricular dysfunction with a low cardiac output being confirmed in a follow-up echocardiogram. Considering these findings, limitation of therapeutic efforts was agreed upon with her relatives, and the patient eventually passed away at 14 days of life.</p><p id="par0035" class="elsevierStylePara elsevierViewall">Genetic testing included a cardiomyopathy panel and Pompe disease screening, both yielding normal results. A Trio Exome analysis (ExoNIM® NIMGenetics, Madrid, Spain) found two variants of the <span class="elsevierStyleItalic">TTN</span> gene: c.25564 G > A; p.(Asp8522Asn), missense mutation in exon 88, <span class="elsevierStyleItalic">in silico</span> prediction of 6/8 missense mutations in heterozygosis inherited from the father and c.74895A > C; p.(Gln24965His), missense mutation in exon 326, <span class="elsevierStyleItalic">in silico</span> prediction of 1/8 missense mutations inherited from the mother, which were initially categorized as variants of uncertain significance (VUS). The variant identified in heterozygosis in both the proband and her father was registered in the ClinVar databases (variation ID: 47332), with a conflict of interpretation of a VUS, and in the Human Gene Mutation Database (HGMD) (accession number: CM1516151) associated with dilated cardiomyopathy. The variant identified in heterozygosis in both the proband and the mother was registered in ClinVar (variation ID: 47332), with a conflict of interpretation between a VUS and a probably benign variant. Given the strong association between these variants and the clinical context, they can be attributed as the cause of the patient’s symptoms and classified as probably pathogenic.</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0010">Discussion and conclusions</span><p id="par0040" class="elsevierStylePara elsevierViewall">Salih myopathy is a rare entity, especially with such an early onset as in the case described herein. Coronary fistulas are often associated with severe cardiac complications secondary to coronary steal phenomena.<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> Its pathogenesis is attributed to the persistence of embryonic myocardial sinusoids originating from endothelial protrusions in the intertrabecular spaces.<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a> Solitary fistulas with hemodynamic involvement indicate a need for correction (surgery or catheterization).</p><p id="par0045" class="elsevierStylePara elsevierViewall">Salih myopathy is characterized by muscle weakness during the neonatal period or early infancy, as well as delayed motor development, contractures, scoliosis, and cardiac dysfunction.<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> As our patient died during the neonatal period, other clinical manifestations could not be examined.</p><p id="par0050" class="elsevierStylePara elsevierViewall">Titin, or TTN, has become an emerging target for genetic diagnosis, a diagnostic and prognostic biomarker, and a potential therapeutic target for cardiomyopathies.<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a> Genetic testing and the use of novel technologies, such as next generation sequencing (NGS), have an increasingly important role in the diagnosis and treatment of heart diseases, as they confirm the diagnosis, aid in the prognosis, and offer a more targeted treatment. The results of genetic tests in heart conditions are mostly probabilistic and should be interpreted considering all clinical information available. In the case of our patient, we assessed the phenotype to support our findings on the cause of her clinical picture.</p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0015">Funding</span><p id="par0055" class="elsevierStylePara elsevierViewall">We received no funding for the conduct of this research.</p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0020">Conflicts of interest</span><p id="par0060" class="elsevierStylePara elsevierViewall">The authors of this paper declare no conflicts of interest in relation to the conduct of this work.</p></span></span>" "textoCompletoSecciones" => array:1 [ "secciones" => array:5 [ 0 => array:2 [ "identificador" => "sec0005" "titulo" => "Case report" ] 1 => array:2 [ "identificador" => "sec0010" "titulo" => "Discussion and conclusions" ] 2 => array:2 [ "identificador" => "sec0015" "titulo" => "Funding" ] 3 => array:2 [ "identificador" => "sec0020" "titulo" => "Conflicts of interest" ] 4 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as: Martínez de Morentin Navarcorena AL, Izquierdo Álvarez S, Palanca Arias D. Miocardiopatía de presentación posnatal en una recién nacida con miopatía de Salih. Med Clin (Barc). 2021;157:499–500.</p>" ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0005" "bibliografiaReferencia" => array:5 [ 0 => array:3 [ "identificador" => "bib0005" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:1 [ "referenciaCompleta" => "Hackman P, Savarese M, Carmignac V, Udd B, Salih MA. Salih Myopathy. Early-Onset Myopathy with Fatal Cardiomyopathy. En: Adam MP, Ardinger HH, Pagon RA, et al., editors. 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