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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">We read with interest the article published by Hern&#225;ndez V&#225;zquez et al&#46;<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">1</span></a> on partial anomalous pulmonary venous connection with pulmonary hypertension&#44; and we would like to put forward some thoughts that may be of interest&#46;</p><p id="par0010" class="elsevierStylePara elsevierViewall">Firstly&#44; significant pulmonary arterial hypertension &#40;PAH&#41;<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">2</span></a> rarely develops in association with heart defects with left-to-right shunt and volume overload&#44; such as partial anomalous pulmonary venous connection or drainage &#40;PAPVD&#41; and interatrial communication &#40;IAC&#41;&#44; in contrast to what the authors appear to claim in their discussion&#46; PAPVD patients usually have normal pulmonary blood pressure&#44; unless they have 2 pulmonary veins with abnormal return&#44; or else sinus venous ICA with a pulmonary to systemic blood flow ratio of 1&#46;5&#58;1 &#40;Qp&#58;Qs&#62;1&#46;5&#58;1&#41;&#46; Even in this situation&#44; severe PAH is very rarely observed &#40;less than 5&#37;&#41;&#44; and is more related to genetic predisposition &#40;as in primary PAH&#41; than to the extent of the shunt itself&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">3</span></a> In contrast&#44; when the left-to-right shunt is associated with volume and pressure overload &#40;interventricular communication&#44; patent ductus arteriosus&#44; aortopulmonary window or common arterial trunk&#41;&#44; PAH frequently becomes severe if the defect is large and left uncorrected during the first year of life&#46; Thus&#44; shunts resulting in volume overload are more typically found in asymptomatic or practically asymptomatic patients with right cavity dilation and mild or moderately increased pulmonary pressure&#44; while systemic or suprasystemic pulmonary pressures with shunt reversal are found in shunts with both volume and pressure overload &#40;Eisenmenger&#39;s syndrome&#41;&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">Secondly&#44; in PAPVD patients with significant PAH&#44; other etiologies must be ruled out&#46; These include respiratory disease&#44; obstructive sleep apnea&#44; connective tissue disease&#44; chronic thromboembolism&#44; portal hypertension&#44; human immunodeficiency virus&#44; use of appetite suppressants or toxic substances&#44; and left heart disease&#46; In the latter&#44; patients with multiple cardiovascular risk factors&#44; as discussed in the article&#44; or coronary heart disease &#40;not specified by the authors&#41; may develop left ventricular diastolic dysfunction and secondary pulmonary arterial hypertension&#44; even in the absence of evidence of heart failure&#46;<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">4</span></a> Special precautions must be taken in these cases&#44; since PAPVD can add to left atrial decompression and total correction of the defect may lead to a sudden increase in pulmonary venous pressure and the development of pulmonary edema&#46;<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">5</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall">Finally&#44; before PAPVD or IAC correction is attempted&#44; pulmonary vascular and systemic resistances and pressures must be identified&#44; in order to prevent converting an Eisenmenger&#39;s syndrome into a disease with a similar course as that of primary PAH&#44; with its correspondingly poorer prognosis&#46;<a class="elsevierStyleCrossRefs" href="#bib0040"><span class="elsevierStyleSup">3&#44;5</span></a></p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Funding</span><p id="par0025" class="elsevierStylePara elsevierViewall">None of the authors received funding&#46;</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0010">Authorship</span><p id="par0030" class="elsevierStylePara elsevierViewall">All authors participated in the interpretation of the data&#44; writing of the article and final approval of the version for publication&#46;</p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0015">Conflict of Interest</span><p id="par0035" class="elsevierStylePara elsevierViewall">The authors declare that they had no conflict of interests&#46;</p></span></span>"
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Letter to the Editor
Pulmonary Arterial Hypertension in Congenital Heart Defects With Left-To-Right Shunt
Hipertensión arterial pulmonar en cardiopatías congénitas con cortocircuito izquierda-derecha
Efrén Martínez-Quintanaa,
Corresponding author
efrencardio@gmail.com

Corresponding author.
, Fayna Rodríguez-Gonzálezb
a Servicio de Cardiología, Complejo Hospitalario Universitario Insular-Materno Infantil, Las Palmas de Gran Canaria, Spain
b Servicio de Oftalmología, Hospital Universitario de Gran Canaria Dr. Negrín, Las Palmas de Gran Canaria, Spain
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">We read with interest the article published by Hern&#225;ndez V&#225;zquez et al&#46;<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">1</span></a> on partial anomalous pulmonary venous connection with pulmonary hypertension&#44; and we would like to put forward some thoughts that may be of interest&#46;</p><p id="par0010" class="elsevierStylePara elsevierViewall">Firstly&#44; significant pulmonary arterial hypertension &#40;PAH&#41;<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">2</span></a> rarely develops in association with heart defects with left-to-right shunt and volume overload&#44; such as partial anomalous pulmonary venous connection or drainage &#40;PAPVD&#41; and interatrial communication &#40;IAC&#41;&#44; in contrast to what the authors appear to claim in their discussion&#46; PAPVD patients usually have normal pulmonary blood pressure&#44; unless they have 2 pulmonary veins with abnormal return&#44; or else sinus venous ICA with a pulmonary to systemic blood flow ratio of 1&#46;5&#58;1 &#40;Qp&#58;Qs&#62;1&#46;5&#58;1&#41;&#46; Even in this situation&#44; severe PAH is very rarely observed &#40;less than 5&#37;&#41;&#44; and is more related to genetic predisposition &#40;as in primary PAH&#41; than to the extent of the shunt itself&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">3</span></a> In contrast&#44; when the left-to-right shunt is associated with volume and pressure overload &#40;interventricular communication&#44; patent ductus arteriosus&#44; aortopulmonary window or common arterial trunk&#41;&#44; PAH frequently becomes severe if the defect is large and left uncorrected during the first year of life&#46; Thus&#44; shunts resulting in volume overload are more typically found in asymptomatic or practically asymptomatic patients with right cavity dilation and mild or moderately increased pulmonary pressure&#44; while systemic or suprasystemic pulmonary pressures with shunt reversal are found in shunts with both volume and pressure overload &#40;Eisenmenger&#39;s syndrome&#41;&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">Secondly&#44; in PAPVD patients with significant PAH&#44; other etiologies must be ruled out&#46; These include respiratory disease&#44; obstructive sleep apnea&#44; connective tissue disease&#44; chronic thromboembolism&#44; portal hypertension&#44; human immunodeficiency virus&#44; use of appetite suppressants or toxic substances&#44; and left heart disease&#46; In the latter&#44; patients with multiple cardiovascular risk factors&#44; as discussed in the article&#44; or coronary heart disease &#40;not specified by the authors&#41; may develop left ventricular diastolic dysfunction and secondary pulmonary arterial hypertension&#44; even in the absence of evidence of heart failure&#46;<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">4</span></a> Special precautions must be taken in these cases&#44; since PAPVD can add to left atrial decompression and total correction of the defect may lead to a sudden increase in pulmonary venous pressure and the development of pulmonary edema&#46;<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">5</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall">Finally&#44; before PAPVD or IAC correction is attempted&#44; pulmonary vascular and systemic resistances and pressures must be identified&#44; in order to prevent converting an Eisenmenger&#39;s syndrome into a disease with a similar course as that of primary PAH&#44; with its correspondingly poorer prognosis&#46;<a class="elsevierStyleCrossRefs" href="#bib0040"><span class="elsevierStyleSup">3&#44;5</span></a></p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Funding</span><p id="par0025" class="elsevierStylePara elsevierViewall">None of the authors received funding&#46;</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0010">Authorship</span><p id="par0030" class="elsevierStylePara elsevierViewall">All authors participated in the interpretation of the data&#44; writing of the article and final approval of the version for publication&#46;</p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0015">Conflict of Interest</span><p id="par0035" class="elsevierStylePara elsevierViewall">The authors declare that they had no conflict of interests&#46;</p></span></span>"
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Article information
ISSN: 15792129
Original language: English
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