Current opinion in cardiology · 2026
Cardiometabolic vulnerability in cardio-oncology: mechanistic links, clinical implications, and emerging preventive strategies.
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Kim Jean, Muquith Maishara, Huang Le, Chandra Alvin
Аннотация
PURPOSE OF REVIEW: Cardiovascular disease is a leading cause of morbidity and mortality among patients with cancer, yet individual risk is highly heterogeneous. This review examines cardiometabolic vulnerability as a unifying framework linking baseline cardiometabolic risk factors with cancer therapy-related cardiovascular injury and discusses emerging pharmacologic and lifestyle interventions for cardiovascular risk mitigation.
RECENT FINDINGS: Epidemiologic and mechanistic studies demonstrate that obesity, insulin resistance, dyslipidemia, and hypertension, often exacerbated by cancer therapies, amplify systemic inflammation, neurohormonal activation, endothelial dysfunction, and metabolic inflexibility. These disturbances interact with specific anticancer treatments, including anthracyclines, HER2-targeted agents, VEGF pathway inhibitors, endocrine therapies, and immune checkpoint inhibitors, increasing susceptibility to diverse cardiovascular toxicities. Emerging evidence supports multimodal preventive strategies integrating pharmacologic interventions targeting neurohormonal, metabolic, and inflammatory pathways with lifestyle modifications, though optimal approaches require further validation in cancer populations.
SUMMARY: Cardiometabolic vulnerability provides a framework to understand heterogeneous cardiovascular risk in cancer patients. Integrating cardiometabolic profiling with therapy-specific risk assessment may improve prevention strategies in cardio-oncology. Continued research is needed to refine risk stratification and inform personalized approaches for this growing population.
RECENT FINDINGS: Epidemiologic and mechanistic studies demonstrate that obesity, insulin resistance, dyslipidemia, and hypertension, often exacerbated by cancer therapies, amplify systemic inflammation, neurohormonal activation, endothelial dysfunction, and metabolic inflexibility. These disturbances interact with specific anticancer treatments, including anthracyclines, HER2-targeted agents, VEGF pathway inhibitors, endocrine therapies, and immune checkpoint inhibitors, increasing susceptibility to diverse cardiovascular toxicities. Emerging evidence supports multimodal preventive strategies integrating pharmacologic interventions targeting neurohormonal, metabolic, and inflammatory pathways with lifestyle modifications, though optimal approaches require further validation in cancer populations.
SUMMARY: Cardiometabolic vulnerability provides a framework to understand heterogeneous cardiovascular risk in cancer patients. Integrating cardiometabolic profiling with therapy-specific risk assessment may improve prevention strategies in cardio-oncology. Continued research is needed to refine risk stratification and inform personalized approaches for this growing population.