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    "titulo" => "Congenital heart disease&#58; When simple becomes complex"
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Congenital heart disease &#40;CHD&#41; comprises a large range of cardiac defects&#44; repaired or unrepaired&#44; which determine the pathophysiological evolution and clinical presentation in adulthood&#46;<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">1</span></a> Pulmonary arterial hypertension &#40;PAH&#41;&#44; characterized by proliferative obstructive small vessel vasculopathy&#44; is not uncommon &#40;estimated prevalence 4&#46;2-28&#37;&#41; in adult CHD &#40;ACHD&#41; patients&#44; although other forms &#40;types 2&#44; 4 and 5&#44; see below&#41; of pulmonary hypertension &#40;PH&#41; may also develop&#46;<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">2</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">PAH-CHD is usually associated with the presence of a shunt and encompasses four clinical groups&#58; &#40;1&#41; Eisenmenger syndrome&#59; &#40;2&#41; PAH associated with predominant systemic-to-pulmonary shunt&#59; &#40;3&#41; PAH associated with a small defect&#59; and &#40;4&#41; PAH associated with a repaired defect&#44; with the latter two&#44; carrying the worst prognosis&#44; resembling idiopathic PAH&#46; Other forms of CHD may be associated with different types of PH&#44; namely&#58; &#40;1&#41; congenital left heart valvular disease&#44; congenital left ventricular outflow tract obstruction and congenital pulmonary vein stenosis &#40;type 2 PH&#41;&#59; &#40;2&#41; congenital peripheral pulmonary arterial stenosis &#40;type 4 PH&#41;&#59; and &#40;3&#41; segmental PH &#40;type 5 PH&#41;&#46;<a class="elsevierStyleCrossRefs" href="#bib0025"><span class="elsevierStyleSup">1&#8211;4</span></a> Furthermore&#44; PH may also develop due to comorbid acquired left heart disease&#46; The highly heterogeneous anatomical and functional milieu and dynamic competing mechanisms make PH classification&#44; interpretation and management challenging in ACHD patients&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">In this issue of the <span class="elsevierStyleItalic">Journal</span>&#44; Asmarats et al&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">4</span></a> report a rare case of severe PH and heart failure induced by systemic-to-pulmonary shunting through a right sinus of Valsalva aneurysm &#40;SVA&#41; ruptured into the right ventricle in a patient with a restrictive perimembranous ventricular septal defect&#46; The patient was successfully treated by percutaneous SVA closure after assessment of PH reversibility with occlusion testing&#46; Regarding the clinical case&#44; despite the possible presence of PAH associated with a small VSD&#44; the most probable cause of PH in this clinical setting was subacute pressure and volume overload imposed on the pulmonary circulation without elevation of pulmonary vascular resistance&#46; The present case reveals the complexity and the somewhat unpredictable course of a simple congenital defect&#44; creating a clinical dilemma concerning the etiology&#44; duration and management of PH&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall">The key messages that can be drawn from this case are&#58;<ul class="elsevierStyleList" id="lis0005"><li class="elsevierStyleListItem" id="lsti0005"><span class="elsevierStyleLabel">&#8211;</span><p id="par0025" class="elsevierStylePara elsevierViewall">All patients with ACHD should be seen at least once in a specialized clinic&#44; as even mild defects can develop serious complications&#46;</p></li><li class="elsevierStyleListItem" id="lsti0010"><span class="elsevierStyleLabel">&#8211;</span><p id="par0030" class="elsevierStylePara elsevierViewall">An unknown percentage of patients with small VSDs develop problems later in life&#44; including SVA&#44; aortic regurgitation&#44; double-chambered right ventricle&#44; or endocarditis&#44; and require life-long follow-up &#40;intervals depending on the associated lesions&#41;&#46;</p></li><li class="elsevierStyleListItem" id="lsti0015"><span class="elsevierStyleLabel">&#8211;</span><p id="par0035" class="elsevierStylePara elsevierViewall">Any change in clinical status in patients with ACHD should prompt a comprehensive assessment&#46;</p></li><li class="elsevierStyleListItem" id="lsti0020"><span class="elsevierStyleLabel">&#8211;</span><p id="par0040" class="elsevierStylePara elsevierViewall">PH in the context of CHD may have several overlapping etiologies&#44; and thorough assessment and elucidation of the pathophysiological mechanism are of paramount importance for appropriate management&#44; with emphasis on the role of careful invasive hemodynamic assessment and interpretation&#46;</p></li><li class="elsevierStyleListItem" id="lsti0025"><span class="elsevierStyleLabel">&#8211;</span><p id="par0045" class="elsevierStylePara elsevierViewall">All patients with PH and unrepaired CHD should undergo thorough assessment of the etiology&#44; mechanism and reversibility of pulmonary vascular disease before it is deemed unrepairable&#46;</p></li><li class="elsevierStyleListItem" id="lsti0030"><span class="elsevierStyleLabel">&#8211;</span><p id="par0050" class="elsevierStylePara elsevierViewall">Percutaneous shunt closure is a valid therapeutic option in appropriately selected patients&#46;</p></li></ul></p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Conflicts of interest</span><p id="par0055" class="elsevierStylePara elsevierViewall">The author has no conflicts of interest to declare&#46;</p></span></span>"
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