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The inflammation inherent in rejection is another possible cause of apparent left ventricular hypertrophy (LVH), disappearing with its treatment. Delayed post-transplant development of a true LVH is not uncommon. It is generally of mild degree and associated with the development of arterial hypertension, although it has also been described in relation to calcineurin inhibitors.<a class="elsevierStyleCrossRefs" href="#bib0030"><span class="elsevierStyleSup">1,2</span></a> The development of severe left ventricle hypertrophy is less common, as in the case presented below.</p><p id="par0010" class="elsevierStylePara elsevierViewall">It is a 77-year-old man with a heart transplant performed in 2009. Since the transplant, he had been receiving treatment with tacrolimus 2<span class="elsevierStyleHsp" style=""></span>mg/24<span class="elsevierStyleHsp" style=""></span>h and mycophenolate 500<span class="elsevierStyleHsp" style=""></span>mg/12<span class="elsevierStyleHsp" style=""></span>h. He was asymptomatic and in NYHA functional class I until its follow-up visit in May 2015, when he mentioned having symptoms of asthenia and dyspnoea, in functional class II. A normal ejection fraction with severe LVH and high levels of brain natriuretic peptides (500.37<span class="elsevierStyleHsp" style=""></span>ng/l) were observed in the follow-up echocardiogram. A coronary angiography was performed, showing no lesions, as well as a biopsy without significant rejection signs. MRI showed a severe concentric hypertrophy predominantly septal, with a maximum diastolic thickness of 23<span class="elsevierStyleHsp" style=""></span>mm, observing a 71% ventricular cavity obliteration, small in size and without hypertrabeculation.</p><p id="par0015" class="elsevierStylePara elsevierViewall">Due to these findings, treatment with tacrolimus was discontinued and everolimus was started (0.75<span class="elsevierStyleHsp" style=""></span>mg/12<span class="elsevierStyleHsp" style=""></span>h). The patient experienced a significant clinical improvement six months after the change of medication, reporting less dyspnoea and a better general condition. In the hypertrophy echocardiographic evaluation, a 3<span class="elsevierStyleHsp" style=""></span>mm thick septum was observed, inferior with respect to the echocardiogram reported 6 months earlier (5 points in the Naranjo algorithm: probable cause).<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">3</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall">Currently, the most widespread immunosuppressive regimen in these patients includes a calcineurin inhibitor (cyclosporine or, more commonly, tacrolimus), an antiproliferative agent (especially mycophenolate mofetil), and steroids. LVH has been described as an adverse effect secondary to treatment with calcineurin inhibitors after heart transplantation,<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">4</span></a> and also of other organs, although its precise incidence has not been estimated. This hypertrophy may be reversible after changing the immunosuppressive regimen.<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">5</span></a></p><p id="par0025" class="elsevierStylePara elsevierViewall">This case illustrates an uncommon complication derived from immunosuppressive treatment and limited representation in the literature, which must be included in the differential diagnosis of LVH after heart transplantation. In cases that require a change in immunosuppressive medication, the eventual rejection should be monitored before treatment discontinuation. Acute rejection (cellular or humoral) and graft vascular disease are also reasons that justify an increase in myocardial thickness after transplantation, therefore, their presence should be ruled out with specific examinations. Also, this case highlights the great importance of early diagnosis and treatment, since a therapeutic delay could determine the irreversibility of the condition.</p></span>" "pdfFichero" => "main.pdf" "tienePdf" => true "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as: González Saldivar H, Vicent Alaminos L, Fernández-Yáñez J. Hipertrofia ventricular izquierda grave por inmunodepresores tras trasplante cardíaco: una complicación rara. 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Journal Information
Vol. 150. Issue 7.
Pages 286 (April 2018)
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Vol. 150. Issue 7.
Pages 286 (April 2018)
Letter to the Editor
Severe left ventricular hypertrophy due to immunosuppressive treatment after heart transplantation: A rare complication
Hipertrofia ventricular izquierda grave por inmunodepresores tras trasplante cardíaco: una complicación rara
Hugo González Saldivar
, Lourdes Vicent Alaminos, Juan Fernández-Yáñez
Corresponding author
Servicio de Cardiología, Hospital Gregorio Marañón, Centro de Investigación Biomédica en Red de Enfermedades Cardiovasculares (CIBERCV), Instituto de Investigación Sanitaria Gregorio Marañón (IiSGM), Universidad Complutense de Madrid, Madrid, Spain
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