Over the past two decades, cardio-oncology has emerged as a pivotal discipline at the intersection of cardiology and oncology. It focuses on strategies for the prevention, early detection and management of cardiovascular complications in patients undergoing anticancer treatments. Despite remarkable advances in oncological therapies, cardiovascular disease remains a major determinant of morbidity and mortality, often complicating clinical pathways and impacting long-term outcomes.1,2
The field initially arose to address cancer therapy-related cardiovascular toxicity, encompassing both short- and long-term sequelae induced by antineoplastic compounds. Both cardiology and oncology have made significant strides in understanding disease mechanisms, refining therapeutic strategies and optimising patient management.2,3 These parallel improvements have gradually aligned the disciplines, highlighting the necessity for integrated cardio-oncology expertise.1 With increasing evidence suggesting that cardiovascular conditions can also influence cancer progression, the concepts of forward and reverse cardio-oncology have emerged.4–6 Forward cardio-oncology focuses on the cardiotoxic effects of oncologic treatments, while reverse cardio-oncology examines how pre-existing heart disease, in particular heart failure, might promote tumour growth and spread.4–6
As a developing discipline, cardio-oncology still faces critical unanswered questions and knowledge gaps. Identifying high-risk patients using predictive biomarkers and implementing strategies to mitigate cardiotoxicity without affecting oncologic outcomes remains challenging. Structured clinical pathways, dedicated services and the systematic application of advanced cardiovascular imaging tools, particularly echocardiography or cardiac magnetic resonance, are becoming essential to guide patient management and detect subclinical cardiac dysfunction prior to clinical presentation.7
From an epidemiological perspective, the growing number of cancer survivors in Europe reinforces the importance of cardiovascular surveillance. According to recent EUROCARE-6 estimates, in 2020 approximately 23.7 million individuals, around 5% of the total population, survived after a cancer diagnosis.8 This expanding but vulnerable population underscores the urgent need for structured surveillance and preventive strategies throughout the cancer care continuum.
As the discipline has evolved, scientific societies have increasingly promoted research, education and clinical frameworks through dedicated position papers, guideline recommendations and formal training pathways aimed at improving cardiovascular outcomes in patients with cancer.2,9,10 These efforts have facilitated a more standardised approach to risk stratification, surveillance and cardiovascular management, reinforcing the maturation of cardio-oncology as a clinically integrated and research-oriented field.1
This special collection in the European Cardiology Review brings together contributions from global experts who address these challenges, analysing innovative research and clinical practice. It highlights the evolving landscape of cardio-oncology, including translational findings and novel themes, such as reverse cardio-oncology (Figure 1 ). The collection aims to stimulate reflection, discussion and new proposals among readers.
Camilli et al. provide a comprehensive overview of emerging concepts in cardio-oncology, focusing on cardiovascular sequelae of both conventional cytotoxic therapies and novel targeted or immune-based treatments.4 They illustrate how treatment-related cardiovascular toxicities encompass a broad clinical spectrum, extending beyond myocardial dysfunction to include arrhythmias, hypertension, inflammatory complications and ischaemic or vasospastic events.4,11,12 The authors detail the role of serum biomarkers, such as troponins and natriuretic peptides, and imaging techniques, including echocardiography and cardiac magnetic resonance, in identifying early signs of cardiotoxicity and enabling timely intervention.4,7,13 They illustrate the importance of translational research in elucidating the mechanisms of cardiotoxicity using preclinical models, such as human-induced pluripotent stem cell-derived cardiomyocytes and animal models, while acknowledging that a major challenge remains the development of models able to faithfully reproduce clinical scenarios influenced by cancer burden, comorbidities and previous or concurrent therapies.4 The review also sheds light on reverse cardio-oncology, examining the bidirectional interplay between cardiovascular disease and cancer through shared risk factors, inflammatory and neurohormonal mechanisms, genetic predisposition and clonal haematopoiesis. In particular, the authors describe how heart failure may promote a pro-neoplastic milieu through neurohormonal activation and secretion of oncogenic factors, while systemic inflammation may represent a shared substrate for both tumour development and heart failure, as also suggested by the Cantos study.14 Finally, the paper advocates a novel “cardio-oncology mindset,” similar to the one proposed for cardiomyopathies, as well as multidisciplinary, evidence-based strategies to support the early recognition, prevention and management of cardiotoxicity in oncology patients.3,4
Tamburrini et al. complement these insights by examining cardioprotective strategies in breast cancer, emphasising personalised approaches that combine pharmacologic therapy, lifestyle interventions and comprehensive monitoring.15 The authors stress the importance of cardiac biomarkers, ranging from troponins and natriuretic peptides to emerging molecular markers, such as microRNAs, for risk stratification and longitudinal surveillance of therapy-related cardiac dysfunction.15 While neurohormonal antagonists, including β-blockers and renin–angiotensin system inhibitors, have shown variable results, their use may benefit selected high-risk patients, particularly those with elevated troponin levels during treatment or high cumulative anthracycline exposure. Moreover, emerging pharmacologic options, such as sodium–glucose cotransporter 2 inhibitors, mineralocorticoid receptor antagonists and/or dexrazoxane, may offer additional avenues to mitigate cardiotoxicity.12 The authors integrate biomarker assessment with advanced cardiac imaging and pharmacogenomic insights to tailor cardioprotective strategies, aiming to preserve cardiac function without compromising cancer therapy.7,15 In this way, their approach reinforces the integrated, evidence-based framework outlined by Camilli et al., providing a cohesive synthesis of current knowledge, ongoing research and persisting gaps in both biomarker validation and pharmacological prevention.4,15
Understanding cardiovascular toxicities from cancer therapies also requires rigorous interpretation of data from onco-haematologic clinical trials. Minotti et al. provide guidance on the adjudication of cardiovascular adverse events in patients with chronic lymphocytic leukaemia receiving Bruton’s tyrosine kinase inhibitors, another critical issue in the cardio-oncology arena.16,17 They point out that events, such as AF, hypertension, heart failure, ventricular arrhythmias and sudden death, often reflect a complex interplay of patient-specific risk factors, including age-related vulnerability, comorbidities and polypharmacy, rather than direct drug toxicity alone.16 A critical appraisal of the GLOW trial demonstrates that several cardiac and sudden deaths initially attributed to therapy were largely unrelated when patient characteristics and the timing of events were considered.17,18 The authors delineate the importance of independent adjudication committees, structured baseline cardiac evaluation and ongoing monitoring to accurately distinguish drug-related cardiotoxicity from underlying patient risk. They further advocate for mechanism-oriented studies and patient-centred assessment to identify high-risk individuals and optimise protective strategies, reinforcing the need for careful cardiovascular assessment and management in patients receiving targeted therapies.16
Menezes et al. address the challenging and under-investigated topic of management of coronary artery disease, in particular revascularisation, in patients with cancer.19 As advances in anticancer therapies continue to extend survival, the role of interventional cardiovascular care in this population has become increasingly relevant.20 Although invasive strategies were historically withheld because of perceived poor prognosis and complication risk (i.e., high bleeding risk), this approach is considered no longer appropriate. In acute coronary syndromes, patients with cancer are frequently undertreated, despite evidence supporting an invasive approach, including coronary revascularisation when clinically indicated.21 Revascularisation should be considered in all patients and carefully weighted against life expectations and oncologic prognosis, with coronary artery bypass graft surgery remaining a viable option that should not be routinely disregarded.
In contrast, chronic coronary syndromes are more often managed conservatively, with revascularisation reserved for selected scenarios, such as refractory symptoms or planned major oncologic interventions.22 Patients with cancer face a consistently higher bleeding risk, supporting individualised antithrombotic strategies that favour shorter durations of dual antiplatelet therapy, preferential use of clopidogrel and contemporary procedural approaches including radial access, intracoronary imaging and drug-eluting stents. Clinical outcomes are strongly influenced by cancer-specific factors, particularly active versus past disease, metastatic burden and prior chest radiotherapy, reinforcing the need for tailored, multidisciplinary decision-making.19
Lastly, Szmit et al. address the management of venous thromboembolism (VTE) in patients with cancer, a population at markedly increased thrombotic risk, particularly at the time of diagnosis.23 The review frames this issue within the broader context of primary prophylaxis and secondary prevention, in which anticoagulation is generally continued as long as the cancer remains active, but is complicated by the need to balance high thrombotic and bleeding risk, making treatment personalisation essential.23 In line with the 2022 European Society of Cardiology cardio-oncology guidelines, which identify non-vitamin K antagonist oral anticoagulants and low-molecular-weight heparin as two equivalent therapeutic options for cancer-associated VTE, the authors review trials, including the Hokusai and Caravaggio studies, and meta-analyses to define settings in which one strategy may be more effective or safer.10,24,25 In particular, non-vitamin K antagonist oral anticoagulants may be preferred in patients with active cancer, especially those with solid tumours who require long-term treatment, as oral administration favours adherence and quality of life. By contrast, low-molecular-weight heparin remains relevant in higher-bleeding-risk settings, including gastrointestinal or genitourinary cancers, significant renal impairment, concomitant antiangiogenic therapy or thrombocytopenia.23–25 The duration of anticoagulation is a major determinant of management, since treatment in active cancer often extends beyond 6 months and may become indefinite, although dose reduction can reduce bleeding in selected patients. Supporting this strategy, the API-CAT trial showed that reduced-dose apixaban after the initial 6 months was noninferior to full-dose therapy in preventing recurrent VTE in patients with active cancer, with a lower incidence of clinically relevant bleeding.26
The presented reviews offer both practical and conceptual insights, encouraging readers to critically appraise current practice and consider future directions. Collectively, these contributions underscore the multidisciplinary nature of cardio-oncology and the transition from reactive to preventive and integrated care. By highlighting unresolved questions, emerging data and translational opportunities, this Special Focus collection actively challenges the reader to rethink conventional paradigms, develop new hypotheses and drive innovation. Looking ahead, the field of cardio-oncology will benefit from prospective, multicentre trials, integration of precision medicine approaches, genomic and biomarker-driven risk stratification, and real-world evidence derived from international registries, all of which will help refine the next generation of clinical strategies and research priorities.