Histopathological and epigenetic changes in myocardium associated with cancer therapy‐related cardiac dysfunction

Terada, Chiyoko-Ikeda; Onoue, Kenji; Fujii, Tomomi; Itami, Hiroe; Morita, Kohei; Uchiyama, Tomoko; Takeda, Maiko; Nakagawa, Hitoshi; Nakano, Tomoya; Baba, Youichirou; Amemiya, Kisaki; Saito, Yoshihiko; Hatakeyama, Kinta; Ohbayashi, Chiho

doi:10.1002/ehf2.14034

Cited by 9 publications

(6 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…To these ends, endomyocardial biopsies of autopsied cancer cases and of controls without cancer were compared. Their results indicated distinct morphological characteristics in myocardial histopathology for cancer therapies‐related cardiac dysfunctions, and they proposed the mechanistic involvement of epigenetic changes and identified sensitive markers for cardiotoxicity 59 …”

Section: Preclinical and Translational Investigationsmentioning

confidence: 99%

“…Their results indicated distinct morphological characteristics in myocardial histopathology for cancer therapies-related cardiac dysfunctions, and they proposed the mechanistic involvement of epigenetic changes and identified sensitive markers for cardiotoxicity. 59 Congenital heart disease-associated pulmonary hypertension is a severe condition with unknown mechanism. Relying on a number of complimentary preclinical approaches and animal models, Zhou tested whether synemin, an intermediate filament protein, is involved in the above clinical situation.…”

Section: Preclinical and Translational Investigationsmentioning

confidence: 99%

See 1 more Smart Citation

A year in heart failure: updates of clinical and preclinical findings

et al. 2023

View full text Add to dashboard Cite

We witnessed major advances in the management of heart failure (HF) in 2022. Results of recent clinical and preclinical investigations aid preventive strategies, diagnostic efforts, and therapeutic interventions, and collectively, they hold promises for a more effective HF care for the near future. Accordingly, currently available information extends the 2021 European Society of Cardiology guidelines and provides a solid background for the introduction of improved clinical approaches in the number of HF‐related cases. Elaboration on the relationships between epidemiological data and risk factors lead to better understanding of the pathophysiology of HF with reduced ejection fraction and HF with preserved ejection fraction. The clinical consequences of valvular dysfunctions are increasingly interpreted not only in their haemodynamic consequences but also in association with their pathogenetic factors and modern corrective treatment possibilities. The influence of coronavirus disease 2019 pandemic on the clinical care of HF appeared to be less intense in 2022 than before; hence, this period allowed to refine coronavirus disease 2019 management options for HF patients. Moreover, cardio‐oncology emerges as a new subdiscipline providing significant improvements in clinical outcomes for oncology patients. Furthermore, the introduction of state‐of‐the‐art molecular biologic methods, multi‐omic approaches forecast improved phenotyping and precision medicine for HF. All above aspects are addressed in this article that highlights a selection of papers published in ESC Heart Failure in 2022.

show abstract

Section: Preclinical and Translational Investigationsmentioning

confidence: 99%

Section: Preclinical and Translational Investigationsmentioning

confidence: 99%

A year in heart failure: updates of clinical and preclinical findings

et al. 2023

View full text Add to dashboard Cite

show abstract

“…Acute toxicity is the term used to describe the negative effects from a single or brief exposure. Heart toxicity ultimately results in a fibrotic response that needs to be confirmed histologically—a process that has not been conducted much up to this point [ 5 ]. The phrase “cardiac dysfunction related to cancer treatment” has been used interchangeably.…”

Section: Cardiac Toxicitymentioning

confidence: 99%

“…Approximately 30% of patients receiving taxanes have developed hypersensitivity reactions. Proposed mechanisms include IgE-mediated anaphylaxis with elevated tryptase levels, direct activation of mast cells and/or basophils, and complement activation [ 5 ]. Cross-reactivity in various types of taxanes increases to 50%.…”

Section: Hypersensitivity To Cytotoxic Agents and Kounis Syndromementioning

confidence: 99%

Cardio-Oncoimmunology: Cardiac Toxicity, Cardiovascular Hypersensitivity, and Kounis Syndrome

Kounis,

Hung,

de Gregorio

et al. 2024

Life

View full text Add to dashboard Cite

Cancer therapy can result in acute cardiac events, such as coronary artery spasm, acute myocardial infarction, thromboembolism, myocarditis, bradycardia, tachyarrhythmias, atrio-ventricular blocks, QT prolongation, torsades de pointes, pericardial effusion, and hypotension, as well as chronic conditions, such as hypertension, and systolic and diastolic left ventricular dysfunction presenting clinically as heart failure or cardiomyopathy. In cardio-oncology, when referring to cardiac toxicity and cardiovascular hypersensitivity, there is a great deal of misunderstanding. When a dose-related cardiovascular side effect continues even after the causative medication is stopped, it is referred to as a cardiotoxicity. A fibrotic response is the ultimate outcome of cardiac toxicity, which is defined as a dose-related cardiovascular adverse impact that lasts even after the causative treatment is stopped. Cardiotoxicity can occur after a single or brief exposure. On the other hand, the term cardiac or cardiovascular hypersensitivity describes an inflammatory reaction that is not dose-dependent, can occur at any point during therapy, even at very low medication dosages, and can present as Kounis syndrome. It may also be accompanied by anti-drug antibodies and tryptase levels. In this comprehensive review, we present the current views on cardiac toxicity and cardiovascular hypersensitivity, together with the reviewed cardiac literature on the chemotherapeutic agents inducing hypersensitivity reactions. Cardiac hypersensitivity seems to be the pathophysiologic basis of coronary artery spasm, acute coronary syndromes such as Kounis syndrome, and myocarditis caused by cancer therapy.

show abstract

“…Acute toxicity is the term used to describe negative effects from a single or brief exposure. Heart toxicity ultimately results in a fibrotic response that needs to be confirmed histologically-a process that hasn't been carried out much up to this point [5]. The phrase "cardiac dysfunction related to cancer treatment" has been used interchangeably.…”

Section: Cardiac Toxicitymentioning

confidence: 99%

Cardio-Oncology: Cardiac Toxicity, Cardiovascular Hypersensitivity and Kounis Syndrome

Kounis,

Hung,

De Gregorio

et al. 2024

Preprint

View full text Add to dashboard Cite

The most frequent cause of cardiac failure globally is ischemic heart disease, with chemothera-py-related cardiovascular side effects emerging as the second most frequent cause. Cancer therapy can result in acute cardiac events, such as coronary artery spasm, acute myocardial infarction, thromboembolism, myocarditis, bradycardia, tachyarrhythmias, atrio-ventricular blocks, QT pro-longation, torsades de pointes, pericardial effusion and hypotension, as well as chronic conditions, such as hypertension, systolic and diastolic left ventricular dysfunction presenting clinically as heart failure or cardiomyopathy. In cardio-oncology, when referring to cardiac toxicity and cardiovas-cular hypersensitivity, there is a great deal of misunderstanding. When a dose-related cardiovas-cular side effect continues even after the causative medication is stopped, it is referred to as cardi-otoxicity. A fibrotic response is the ultimate outcome of cardiac toxicity, which is defined as a dose-related cardiovascular adverse impact that lasts even after the causative treatment is stopped. Cardiotoxicity can occur after a single or brief exposure. On the other hand, the term cardiac or cardiovascular hypersensitivity describes an inflammatory reaction that is not dose-dependent, can occur at any point during therapy, even with very low medication dosages, and can show up as Kounis syndrome. It may also be accompanied by anti-drug antibodies and tryptase levels. In this comprehensive review, we present the current views on cardiac toxicity and cardiovascular hypersensitivity, together with the reviewed cardiac literature on the chemotherapeutic agents inducing hypersensitivity reactions. Cardiac hypersensitivity seems to be the pathophysiologic basis of coronary artery spasm, acute coronary syndromes such as Kounis syndrome and myocardi-tis caused by cancer therapy.

show abstract

Histopathological and epigenetic changes in myocardium associated with cancer therapy‐related cardiac dysfunction

Cited by 9 publications

References 39 publications

A year in heart failure: updates of clinical and preclinical findings

A year in heart failure: updates of clinical and preclinical findings

Cardio-Oncoimmunology: Cardiac Toxicity, Cardiovascular Hypersensitivity, and Kounis Syndrome

Cardio-Oncology: Cardiac Toxicity, Cardiovascular Hypersensitivity and Kounis Syndrome

Contact Info

Product

Resources

About