Heartbeat: cancer history and risk of cardiovascular disease

The number of patients with a history of cancer is increasing due to improved cancer diagnosis and treatment over the past few decades. Although the issue of immediate cancer therapy related cardiotoxicity is well recognised, less attention has been directed towards the longterm risk of cardiovascular disease (CVD) in patients with prior cancer. In this issue of Heart, RaisiEstabragh and colleagues used a propensity matched design with competing risk regression to study the associations between cancer and CVD in 18 714 UK Biobank participants with a cancer history. Participants with cancer had a high burden of prevalent CVD and vascular risk factors. Interestingly, the associations with incident CVD were related to the specific type of cancer—breast cancer was associated with a higher risk of heart failure (HF), pericarditis and venous thromboembolism (VTE); lung cancer with pericarditis, HF and CVD death; prostate cancer with VTE; and haematological cancer with all types of CVD (figure 1). In a subset of participants with cardiovascular MRI data, adverse cardiac remodelling also was seen in those with prior cancer. Banchs and Lech comment that the biological basis for the association of CVD and cancer requires further study. Clearly, there are shared genetic and lifestyle risk factors for CVD and cancer, such as smoking, diet and physical activity. In addition, some types of CVD may be related to other biological pathways. For example, in HF patients ‘the potential link to increased cancer risk is due to increased oxidative stress, inflammation/immune system upregulation and neurohormonal activation.’ Banchs and Lech conclude that ‘the importance of heart disease in patients undergoing cancer care cannot be understated, but also how critical it becomes to prioritise a care continuum after cancer is survived.’ Restriction of physical activity (PA) in patients with CVD often in motivated by the concern that PA may increase the risk of adverse events, particularly arrhythmias. Yet, PA restrictions negatively impact quality of life. RamosMaqueda and colleagues report a observational study of 72 patients with arrhythmogenic cardiomyopathy (AC), showing that lifestyle PA, measured by accelerometer, was not associated with an increased risk of rapidrate nonsustained ventricular tachycardias (RRNSVTs) (figure 2). The authors conclude ‘The findings of this study suggest that lifestyle physical activity is not associated with the occurrence of RRNSVTs in patients with AC. This provides preliminary evidence for the active promotion of lifestyle physical activity among patients with AC to ensure they obtain the multiple benefits and risk reductions associated with physical activity.’ In the accompanying editorial, Bevan and Nazer argue that ‘Our understanding of the genetics underlying AC lends credibility to the hypothesis that exercise precipitates arrhythmia and structural remodelling in predisposed individuals.’ However, this association is best established for desmosomal AC variants with less data on the risk of exercise for nondesmosomal AC. The study group in the current publication is ‘roughly twothirds nondesmosomal or gene elusive, and 50% LV predominant AC.’ Bevan and Nazer conclude that ‘we remain reassured that shortduration (<30 min), moderateintensity Division of Cardiology, University of Washington, Seattle, Washington, USA