Early and late onset cardiotoxicity following anthracycline-based chemotherapy in breast cancer patients: Incidence and predictors.

INTRODUCTION: Cardiotoxicity represents a major limitation for the use of anthracyclines or trastuzumab in breast cancer patients. Data on longitudinal studies about early and late onset cardiotoxicity in this group of patients is scarce. The objective of the present study was to assess predictors of early and late onset cardiotoxicity in patients with breast cancer treated with A. METHODS: 100 consecutive patients receiving anthracycline-based chemotherapy (CHT) to treat breast cancer were included in this prospective study. All patients underwent evaluation at baseline, at the end of CHT, 3 months after the end of CHT and 1 and 4 years after the beginning of CHT. Clinical data, systolic and diastolic echo parameters and cardiac biomarkers including high sensitivity Troponin T (TnT), N-terminal pro-brain natriuretic peptide (NT-proBNP) and Heart-type fatty acid binding protein (H-FABP) were assessed. RESULTS: Mean doxorubicin dose was 243 mg/m2. Mean follow-up was 51.8 ± 8.2 months. At one-year incidence of anthracycline related-cardiotoxicity (AR-CT) was 4% and at the end of follow-up was 18% (15 patients asymptomatic left ventricular systolic dysfunction, 1 patients heart failure and 2 patients a sudden cardiac death). Forty-nine patients developed diastolic dysfunction (DD) during first year. In the univariate analysis DD during first year was the only parameter associated with AR-CT (Table 1). In the logistic regression model DD was independently related with the development of AR-CT, with an odds ratio value of 7.5 (95% CI 1.59-35.3). CONCLUSIONS: Incidence of late-onset cardiotoxicity is high but mostly subclinical. Diastolic dysfunction early after chemotherapy is a strong predictor of anthracycline cardiotoxicity.

Ectasia coronaria y lesiones trombóticas como causa de síndrome coronario agudo / Coronary ectasia and thrombotic injuries as a cause of acute coronary syndrome

Resumen Se presenta un caso de manejo complicado y decisiones difíciles. Un paciente con antecedente de disección aórtica tipo A y dilatación residual de la aorta descendente de hasta 60 mm es ingresado por un síndrome coronario agudo sin elevación del ST. La coronariografía pone de manifiesto una marcada ectasia coronaria y unos defectos de perfusión de dudoso origen. ¿Trombos o falsas imágenes por flujo muy lentificado? Asumiendo que pudiera tratarse de trombos, el paciente es tratado con anticoagulación repitiéndose la coronariografía al cabo de dos meses. En este segundo estudio se observa la completa desaparición de las imágenes, confirmándose el origen trombótico de las mismas. En este momento se plantea ¿cuál debe ser el tratamiento crónico del paciente? No hay evidencia científica disponible acerca del tratamiento de la ectasia coronaria y se trata de un paciente de alto riesgo por su antecedente de disección aórtica. Finalmente se decide, de forma empírica, mantener la anticoagulación de forma indefinida. Tras dos años y seis meses de seguimiento no ha habido incidencias clínicas.

Abstract A case with complicated management and difficult decision-making is presented. A patient with history of type A aortic dissection and residual dilatation of the descending aorta up to 60 mm is admitted for acute coronary syndrome without ST elevation. Coronary angiography reveals a marked coronary ectasia and perfusion defects of unclear origin. Thrombosis or fake images due to flow reduction? Assuming that it could be caused by thrombosis the patient is treated with anticoagulant therapy and the coronary angiography is repeated after two months. This second study shows complete clearing of imaging findings, confirming the thrombotic origin. At this stage considerations are taken so as to plan a chronic treatment for the patient? There is no scientific evidence regarding the treatment for coronary ectasia and this is a high-risk patient because of his aortic dissection history. Finally it is empirically decided to indefinitely keep anticoagulant therapy. After two years and six months of follow-up there has been no clinical incidents.