Letter to the Editor
Late anthracycline cardiotoxicity and genetic alteration of iron metabolism
Cardiotoxicidad tardía por antraciclinas y alteración genética del metabolismo del hierro
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Cardiotoxicity secondary to these drugs, especially in the long term, has been gaining importance in recent years, due to the increase in the number of cases detected as a consequence of improved prognosis and the development of some prevention strategies<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a>.</p><p id="par0010" class="elsevierStylePara elsevierViewall">We report the case of a 42-year-old female smoker with no other cardiovascular risk factors or drug treatment. She was diagnosed with acute T-lymphoblastic leukaemia with a poor prognosis at 2 years of age, treated with a chemotherapy regimen that included daunorubicin at a cumulative dose of 440 mg/m<span class="elsevierStyleSup">2</span>, achieving complete remission. Ventricular function determined by ultrasound one year after completion of treatment was normal. The patient presented with a 3-month history of progressive exertional dyspnoea, which progressed to minimal exertion with orthopnoea, paroxysmal nocturnal dyspnoea and oedema up to the knee. Without chest pain. The examination revealed tachycardia with third heart sound, jugular vein congestion and hepatomegaly. The laboratory tests revealed NT-ProBNP 17,161 pg/mL in addition to high levels of ferritin (848 ng/mL) of years of progression. The electrocardiogram showed sinus rhythm with narrow QRS, and the echocardiogram showed a non-dilated left ventricle with global hypokinesia and ejection fraction of 20%. A heart nuclear magnetic resonance confirmed severe left ventricular dysfunction without late gadolinium enhancement, and coronary computed tomography ruled out ischemic heart disease.</p><p id="par0015" class="elsevierStylePara elsevierViewall">The patient experienced progressive improvement after starting treatment with diuretics, angiotensin-converting enzyme inhibitors, beta-blockers, and antialdosterone therapy, recovering ventricular function several months later, although maintaining some limitation on exertion. A <span class="elsevierStyleItalic">HFE</span> gene study identified a heterozygous H63D mutation, and the patient was diagnosed with hypokinetic non-dilated cardiomyopathy possibly related to late anthracycline toxicity.</p><p id="par0020" class="elsevierStylePara elsevierViewall">The most accepted mechanism of toxicity is the generation of free oxygen radicals during the intracellular metabolism of the drug. It causes deoxyribonucleic acid damage and mitochondrial dysfunction<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a>, leading to apoptosis and fibrosis, with the myocardium being a particularly sensitive tissue. This leads to heart failure that can manifest from the time of treatment (acute toxicity) to several decades later (late toxicity). The most important risk factor is the total accumulated dose, with patients receiving more than 300 mg/m<span class="elsevierStyleSup">2</span> being especially susceptible. Other factors are: age younger than 5 years, concomitant chest irradiation, high cardiovascular risk, as well as the time elapsed since treatment, with an incidence of 7.5% at 30 years<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a>. Myocyte injury is believed to occur at the time of exposure, followed by progressive functional impairment that makes it dependent on compensatory mechanisms leading to clinical heart failure.</p><p id="par0025" class="elsevierStylePara elsevierViewall">Iron is known to be involved as a cofactor in anthracycline-mediated free radical production<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a>. In this context, the existence of a genetic alteration of iron metabolism has been shown to increase the risk of long-term cardiotoxicity and has been associated with both C282Y and H63D mutation carriers, even in heterozygous cases<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a>. Considering the high prevalence of these polymorphisms in our population, it might be advisable to carry out a screening to identify high-risk patients who may benefit from a closer follow-up or preventive treatment with iron chelators (dexrazoxane).</p><p id="par0030" class="elsevierStylePara elsevierViewall">In general, symptomatic cardiotoxicity has a poor prognosis. The approach focuses on prevention strategies, such as dose control or use of dexrazoxane, clinical and echocardiographic monitoring, in order to initiate early treatment to improve prognosis. In addition, a healthy lifestyle and control of cardiovascular risk factors should be recommended.</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: Peña Irun A, Bengochea Botín E, Pariente Rodrigo E. Cardiotoxicidad tardía por antraciclinas y alteración genética del metabolismo del hierro. Med Clin (Barc). 2022;158:499–500.</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:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Cardiotoxicidad tardía inducida por antraciclinas" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:3 [ 0 => "C. Pérez" 1 => "M.A. Agustí" 2 => "P. 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Insodaite" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1007/s12012-020-09595-1" "Revista" => array:6 [ "tituloSerie" => "Cardiovasc Toxicol" "fecha" => "2021" "volumen" => "21" "paginaInicial" => "59" "paginaFinal" => "66" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/32748118" "web" => "Medline" ] ] ] ] ] ] ] ] ] ] ] ] ] "idiomaDefecto" => "en" "url" => "/23870206/0000015800000010/v1_202206100851/S2387020622001978/v1_202206100851/en/main.assets" "Apartado" => array:4 [ "identificador" => "43309" "tipo" => "SECCION" "en" => array:2 [ "titulo" => "Letters to the Editor" "idiomaDefecto" => true ] "idiomaDefecto" => "en" ] "PDF" => "https://static.elsevier.es/multimedia/23870206/0000015800000010/v1_202206100851/S2387020622001978/v1_202206100851/en/main.pdf?idApp=UINPBA00004N&text.app=https://www.elsevier.es/" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S2387020622001978?idApp=UINPBA00004N" ]
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