Cardiotoxicity of Anti-cancer Therapies: From Bench to Bedside

A special issue of Journal of Personalized Medicine (ISSN 2075-4426). This special issue belongs to the section "Mechanisms of Diseases".

Deadline for manuscript submissions: closed (1 April 2024) | Viewed by 746

Special Issue Editors


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Guest Editor
Department of Translational Medical Sciences, Federico II University, 80131 Naples, Italy
Interests: cardio-oncology; cardiotoxicity; heart failure; pulmonary hypertension

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Guest Editor
Pole of Cardiovascular Research, Institute of Experimental and Clinical Research (IREC), Université catholique de Louvain, 1200 Brussels, Belgium
Interests: characterization of molecular targets involved in tumour survival, resistance, progression, and immune escape; characterization of molecular mechanisms involved in cancer therapy-induced cardiotoxicity and evaluation of a clinical approach to prevent heart failure

Special Issue Information

Dear Colleagues,

As the world’s population grows older, the coexistence of cancer and cardiovascular diseases is becoming more common. In particular, cardiotoxicity induced by chemotherapy and targeted therapies is becoming a significant health problem for oncological patients. These antineoplastic treatments may induce adverse cardiovascular effects such as the impairment of cardiac contractility, which can be either transient or irreversible. Furthermore, cancer treatment is associated with life-threatening arrhythmia, ischemia, infarction, and damage to cardiac valves, the conduction system, and the pericardium. In addition, the presence of overt cardiovascular diseases might limit therapeutic options in cancer patients.

The onset of cardiotoxicity may depend on the class, dose, route, and duration of the administration of antineoplastic drugs, as well as on individual risk factors. There is an urgent need for early diagnostic tools and cardioprotective therapies to reduce the clinical and subclinical cardiotoxicity onset and progression and to limit the acute or chronic manifestation of cardiac damages.

This Special Issue welcomes contributions regarding the cellular and molecular mechanisms of cancer therapies, as well as the prevention, diagnosis, and treatment of the cardiotoxic effects of cancer therapies. Original research and review articles are particularly welcomed.

Dr. Alessandra Cuomo
Dr. Michele Russo
Guest Editors

Manuscript Submission Information

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Keywords

  • cardiotoxicity
  • cardio-oncology
  • anticancer therapy
  • chemotherapy
  • cardioprotection
  • oncological treatment
  • cardio-prevention

Published Papers (1 paper)

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Research

11 pages, 1095 KiB  
Article
T1 Mapping in Cardiovascular Magnetic Resonance—A Marker of Diffuse Myocardial Fibrosis in Patients Undergoing Hematopoietic Stem Cell Transplantation
by Audrone Vaitiekiene, Migle Kulboke, Monika Bieseviciene, Antanas Jankauskas, Agne Bartnykaite, Diana Rinkuniene, Igne Strazdiene, Emilija Lidziute, Darija Jankauskaite, Ignas Gaidamavicius, Paulius Bucius, Tomas Lapinskas, Rolandas Gerbutavicius, Elona Juozaityte, Jolanta Justina Vaskelyte, Domas Vaitiekus and Gintare Sakalyte
J. Pers. Med. 2024, 14(4), 412; https://doi.org/10.3390/jpm14040412 - 13 Apr 2024
Viewed by 564
Abstract
Introduction: Hematopoietic stem cell transplantation (HSCT) recipients are at increased risk of cardiovascular diseases. In our study, we aimed to find subclinical changes in myocardial tissue after HSCT with the help of cardiovascular magnetic resonance (CMR) tissue imaging techniques. Methods: The data of [...] Read more.
Introduction: Hematopoietic stem cell transplantation (HSCT) recipients are at increased risk of cardiovascular diseases. In our study, we aimed to find subclinical changes in myocardial tissue after HSCT with the help of cardiovascular magnetic resonance (CMR) tissue imaging techniques. Methods: The data of 44 patients undergoing autologous and allogeneic HSCT in the Hospital of Lithuanian University of Health Sciences Kaunas Clinics from October 2021 to February 2023 were analyzed. Bioethics approval for the prospective study was obtained (No BE-2-96). CMR was performed two times: before enrolling for the HSCT procedure (before starting mobilization chemotherapy for autologous HSCT and before starting the conditioning regimen for allogeneic HSCT) and 12 ± 1 months after HSCT. LV end-diastolic volume, LV end-systolic volume, LV mass and values indexed to body surface area (BSA), and LV ejection fraction were calculated. T1 and T2 mapping values were measured. Results: There was a statistically significant change in T1 mapping values. Before HSCT, mean T1 mapping was 1226.13 ± 39.74 ms, and after HSCT, it was 1248.70 ± 41.07 ms (p = 0.01). The other parameters did not differ significantly. Conclusions: Increases in T1 mapping values following HSCT can show the progress of diffuse myocardial fibrosis and may reflect subclinical injury. T2 mapping values remain the same and do not show edema and active inflammation processes at 12 months after HSCT. Full article
(This article belongs to the Special Issue Cardiotoxicity of Anti-cancer Therapies: From Bench to Bedside)
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