Ischaemic heart disease in patients with cancer

Graphical Abstract The occurrence of IHD in cancer patients is due to many factors. Three main drivers are CV risk factors, inflammation, and ageing, which promote both diseases. Risk factors and ageing act via specific pathways and induction of chronic, systemic inflammation. Microbiome and hormonal alterations are variably interconnected with risk factors and ageing, and also contribute to the development of IHD and cancer. Moreover, a role is played by the genetic background. CTR-CVT can cause or facilitate IHD, and experimental evidence indicates that IHD and cancer fuel one another. Social determinants of health represent non-biological factors further favouring the association between the two conditions. For the clinician, the coexistence of IHD and cancer is challenging, as outcomes are worse and evidence from RCTs is limited. The forest plot in the right panel shows the increased incidence rate ratio of all-cause mortality in patients undergoing percutaneous coronary intervention with vs. without cancer. CHIP, clonal haematopoiesis of indeterminate potential; CI, confidence interval; CTR-CVT, cancer treatment-related cardiovascular toxicity; CV, cardiovascular; ECM, extracellular matrix; IHD, ischaemic heart disease; IRR, incidence rate ratio; RCT, randomized controlled trial.Cardiologists are encountering a growing number of cancer patients with ischaemic heart disease (IHD). Several factors account for the interrelationship between these two conditions, in addition to improving survival rates in the cancer population. Established cardiovascular (CV) risk factors, such as hypercholesterolaemia and obesity, predispose to both IHD and cancer, through specific mechanisms and via low-grade, systemic inflammation. This latter is also fuelled by clonal haematopoiesis of indeterminate potential. Furthermore, experimental work indicates that IHD and cancer can promote one another, and the CV or metabolic toxicity of anticancer therapies can lead to IHD. The connections between IHD and cancer are reinforced by social determinants of health, non-medical factors that modify health outcomes and comprise individual and societal domains, including economic stability, educational and healthcare access and quality, neighbourhood and built environment, and social and community context. Management of IHD in cancer patients is often challenging, due to atypical presentation, increased bleeding and ischaemic risk, and worse outcomes as compared to patients without cancer. The decision to proceed with coronary revascularization and the choice of antithrombotic therapy can be difficult, particularly in patients with chronic coronary syndromes, necessitating multidisciplinary discussion that considers both general guidelines and specific features on a case by case basis. Randomized controlled trial evidence in cancer patients is very limited and there is urgent need for more data to inform clinical practice. Therefore, coexistence of IHD and cancer raises important scientific and practical questions that call for collaborative efforts from the cardio-oncology, cardiology, and oncology communities.