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Chemotherapy-induced Cardiotoxicity and Mitigation / Atherosclerosis and Cardiovascular Diseases · Journal article
Frontiers in Immunology · August 12, 2026
Raises a question worth testing. It does not answer one.
This is a narrative review of mechanistic pathways potentially linking coronary artery disease and malignancy through shared inflammatory, metabolic, thrombotic, and immune mechanisms. The review acknowledges that epidemiological coincidence alone does not explain CAD–malignancy comorbidity, but does not present empirical data demonstrating causality or clinical outcomes. It raises hypotheses for future investigation and highlights cardio-oncology translation opportunities, particularly around immune checkpoint inhibitor toxicity and prevention strategies.
Narrative review. Aging populations with comorbid coronary artery disease and malignancy; cardio-oncology patients exposed to immune checkpoint inhibitors.
CAD and malignancy frequently coexist and share multiple risk factors (smoking, obesity, diabetes, dyslipidemia, chronic inflammation, metabolic dysfunction) Convergent mechanisms identified include chronic systemic inflammation, clonal hematopoiesis, inflammasome activation, immunometabolic remodeling, endothelial dysfunction, platelet activation, neutrophil extracellular trap formation, coagulation, and immune checkpoint disruption Clonal hematopoiesis is proposed as a molecular bridge between malignant predisposition and atherosclerosis
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
Clinicians should recognize that CAD and cancer comorbidity may reflect shared biological pathways beyond common risk factors. This framework may guide preventive strategies and inform cardiovascular monitoring in cancer patients, particularly those receiving immune checkpoint inhibitors, though clinical evidence for specific interventions is not presented here.
A narrative review synthesizing mechanistic evidence and existing literature on shared pathways between CAD and malignancy, raising hypotheses about causal mechanisms rather than testing them empirically.
As stated by the source record.
Clinicians should recognize that CAD and cancer comorbidity may reflect shared biological pathways beyond common risk factors. This framework may guide preventive strategies and inform cardiovascular monitoring in cancer patients, particularly those receiving immune checkpoint inhibitors, though clinical evidence for specific interventions is not presented here.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
What is missing. This record has no reported figures. That is a gap in the analysis, not a judgement about the study.
Coronary artery disease (CAD) and malignancy frequently coexist in aging populations and share multiple risk factors, including smoking, obesity, diabetes, dyslipidemia, chronic inflammation, and metabolic dysfunction. However, increasing evidence suggests that CAD–malignancy comorbidity cannot be fully explained by epidemiological coincidence alone, although its causal direction remains difficult to establish because of shared risk factors, surveillance bias, reverse causality, cancer stage, and treatment exposure. Instead, convergent inflammatory, metabolic, thrombotic, and immune mechanisms may contribute to the observed clinical overlap. This review summarizes recent evidence linking CAD and cancer through chronic systemic inflammation, clonal hematopoiesis, inflammasome activation, immunometabolic remodeling, endothelial dysfunction, platelet activation, neutrophil extracellular trap formation, coagulation, and immune checkpoint disruption. Particular attention is given to clonal hematopoiesis as a molecular bridge between malignant predisposition and atherosclerosis, macrophage and T-cell immunometabolism as shared immune programs, and thromboinflammation as a mechanism connecting cancer-associated thrombosis with coronary vascular events. We further discuss cardio-oncology translation, including immune checkpoint inhibitor-related cardiovascular toxicity, CHIP-guided anti-inflammatory prevention, antiplatelet and antithrombotic strategies, endothelial-targeted interventions, and immune checkpoint-aware cardiovascular monitoring. Understanding these shared pathways may help move cardio-oncology beyond the management of therapy-induced cardiotoxicity toward mechanism-guided prevention and treatment of inflammatory, thrombotic, and immune mechanisms that jointly promote CAD progression and cancer development.
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