Advancing Cardio-Oncology: Mechanisms of Cardiotoxicity and Therapeutic Options for Old and New Anticancer Drugs

A special issue of Pharmaceuticals (ISSN 1424-8247). This special issue belongs to the section "Pharmacology".

Deadline for manuscript submissions: closed (31 July 2025) | Viewed by 547

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UCIBIO, Laboratory of Toxicology, Faculty of Pharmacy, University of Porto, Rua de Jorge Viterbo Ferreira, 228, 4050-313 Porto, Portugal
Interests: cardiotoxicity; cardio-oncology; chemobrain; clinical toxicology
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Special Issue Information

Dear Colleagues,

The incidence of cancer is growing worldwide and is projected to rise even further in the coming decades. Nonetheless, the life expectancy of cancer patients continues to improve due to advancements in early diagnosis and the development of both established and novel therapies. However, the cardiotoxicity associated with anticancer treatments, including traditional chemotherapy agents, targeted therapies, and emerging immunotherapies, remains a leading cause of death and morbidity in cancer patients. Drugs such as anthracyclines, HER2-targeted therapies, immune checkpoint inhibitors, and chimeric antigen receptor (CAR) T-cell therapies, while effective against cancer, are known to induce a range of cardiovascular toxicities, from arrhythmias and myocarditis to heart failure and vascular complications.

This growing burden underscores the critical importance of cardio-oncology as a focal clinical and scientific field. A major future challenge in cardiovascular medicine lies in elucidating the molecular and immunological mechanisms of cardiotoxicity associated with these therapies, enabling the development of more precise diagnostic tools, effective therapeutic strategies, and personalized approaches to mitigate risks.

It is for this reason that this Special Issue aims to bring together the latest findings in cardio-oncology, encompassing cell-based studies, preclinical and clinical investigations, case reports, and reviews. These contributions will highlight novel mechanisms underlying cardiac remodeling and dysfunction caused by anticancer therapies and explore innovative pharmacological and non-pharmacological solutions to address these challenges.

Dr. Vera Marisa Costa
Guest Editor

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Keywords

  • cardio-oncology
  • anticancer therapies
  • cardiac dysfunction
  • hypertension
  • heart failure
  • intercellular communication
  • treatment
  • prevention
  • diagnosis
  • cardiac remodeling

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Published Papers (1 paper)

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Research

16 pages, 1248 KiB  
Article
Coronary Artery Calcium Score as a Predictor of Anthracycline-Induced Cardiotoxicity: The ANTEC Study
by Anna Borowiec, Patrycja Ozdowska, Magdalena Rosinska, Agnieszka Maria Zebrowska, Sławomir Jasek, Beata Kotowicz, Joanna Waniewska, Hanna Kosela-Paterczyk, Elzbieta Lampka, Katarzyna Pogoda, Zbigniew Nowecki and Jan Walewski
Pharmaceuticals 2025, 18(8), 1102; https://doi.org/10.3390/ph18081102 - 25 Jul 2025
Viewed by 311
Abstract
Background: Many risk factors for cancer therapy-related cardiovascular toxicity overlap with risk factors for atherosclerosis. According to the ESC 2022 Cardio-Oncology Guidelines, coronary computed tomography angiography and coronary artery calcium score are not recommended as part of routine risk assessment prior to oncological [...] Read more.
Background: Many risk factors for cancer therapy-related cardiovascular toxicity overlap with risk factors for atherosclerosis. According to the ESC 2022 Cardio-Oncology Guidelines, coronary computed tomography angiography and coronary artery calcium score are not recommended as part of routine risk assessment prior to oncological treatment. The aim of this study was to prospectively assess the influence of coronary artery calcium score (CAC score) on cancer therapy-related cardiac dysfunction in patients with moderate and high risk of cardiovascular toxicity, qualified for anthracycline treatment. Methods: In all patients, risk factors were collected, laboratory tests, echocardiography with global longitudinal strain (GLS) assessment and coronary artery tomography with coronary artery calcium score were performed. A total of 80 patients were included in the study, of which 77 (96.25%) were followed for an average of 11.5 months. The mean age at baseline was 60.5 years and 72 (93.51%) were women. Results: During observation, five patients (6.49%) died, including two due to heart failure and three due to cancer progression. The majority of patients (59, 76.6%) had breast cancer, 11 (14.3%) were diagnosed with sarcoma and seven (9.1%) with lymphoma. According to the HFA-ICOS risk score, 40 patients (51.9%) were classified as moderate risk (MR), and 37 patients (48.1%) as high risk (HR) for cancer therapy-related cardiovascular toxicity. A CAC score greater than 100 was calculated in 17 (22.1%) patients and greater than 400 in three (3.9%) patients. The CAC score above zero was more common in older patients and in patients classified as high risk (p < 0.001). There was also a significant association between CAC score and hypertension, hyperlipidemia, chronic kidney disease, and the level of NT-proBNP. During 12-month follow-up, mild CTRCD occurred in 38 (49.4%) patients, moderate CTRCD was diagnosed in seven (9.1%), and severe in three (3.9%) patients. In the univariable analysis, CTRCD was more common in the high-risk group (p = 0.005) and in patients with a CAC score greater than zero (p = 0.036). In multivariable analysis, the incidence of CTRCD remains higher in the CAC score > 0 group, even after adjusting for age, hypertension, and hyperlipidemia. In this study group, the CTRCD rates increased with the HFA-ICOS risk score. Conclusions: In moderate and high-risk patients, a coronary artery calcium score greater than zero was identified as a significant risk factor for the development of cancer therapy-related cardiac dysfunction during anthracycline-based treatment. Furthermore, the HFA-ICOS risk score demonstrated good correlation with the incidence of CTRCD in this study, supporting its validity as a predictive tool in patients receiving anthracycline therapy. Full article
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