LAUSR

As the intersection between cardiology and oncology continues to expand, much has been said about the shared risk factors of these conditions, in particular, tobacco use, a suboptimal diet and physical inactivity. In addition, the reported cardiovascular toxicity of cancer therapy in all its forms has been extensively documented and appropriately has raised our collective awareness. 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. The fantastic progress in the treatment and even cure of malignancies has undoubtedly highlighted the need for postcancer care like never before. We are now perhaps entering the next level of that care, where we can find direction related to what postcancer care needs to be, what are the specific warning signs and enhance the clinician’s focus, tailoring attention to specific issues related to the particular malignancy or treatment. Caregivers need to know what diagnostic tests to focus on and how aggressive the followup should be. Another critical level of work needed is to help understand associations of a genetic basis for shared risk. Studies from information contained in large databases have reported on human genes associated with cancer and cardiovascular comorbidities’ interconnection, predominantly genes related to pathways associated with DNA damage repair. In the case of heart failure (HF), the twist of a link between HF syndromes and subsequent cancer has also been revealed in recent studies. In this case, the link has been hypothesised due to the chronic activation of several systemic pathways well known to clinicians. As a result of chronic myocardial dysfunction and the consequent dysfunction of our downstream peripheral organs, the potential link to increased cancer risk is due to increased oxidative stress, inflammation/immune system upregulation and neurohormonal activation. For example, reported procancer molecules that increase HF syndromes are tumour necrosis factor-α, interleukin (IL) 6, IL1 and vascular endothelial growth factor. Basic research has supported and fuelled these concepts; animal model studies have clearly shown that the severity of left ventricular dysfunction and fibrotic scar in HF models strongly correlated with tumour growth. In the same study, several molecules that were elevated in humans with chronic HF were shown to cause marked proliferation effects in colon cancer cells. Making this intertwined relationship between cancer and cardiovascular disease (CVD) more dangerous, it is also possible that elevated cardiac and inflammation biomarkers in apparently healthy humans predict newonset cancer independent of the risk factors for cancer (age, smoking status, body mass index). In other studies, we have seen the promotion of tumour growth and metastasis, again possibly via secreted neurohormonal factors related to the cardiac remodelling process, such as increased afterload stress. Large population studies have contributed to explaining the complex relationship between cancer and CVD. They have helped point us in a general direction of focus (see table 1—summary of related studies). The study by RaisiEstabragh et al is significant in helping advance our knowledge and improve the clinician’s focus, providing us with well over a decade of prospective followup time. Only a few significant studies have reported associations of previous cancer with incident cardiovascular outcomes in large populationbased cohorts, but none have included cardiovascular imaging. The group defined incident CVD in the categories of ischaemic heart disease (IHD), stroke, atrial fibrillation/ flutter, HF, nonischaemic cardiomyopathies (NICMs), venous thromboembolism (deep vein thrombosis, pulmonary embolus and pericarditis) and mortality outcomes (IHD, stroke, hypertensive diseases, HF or NICMs) using hospital episode statistics and death registration records. Not far from similar reports, they found that almost onethird of participants with cancer developed one of the incident CVDs, with the highest rates for those with lung, haematological and prostate cancers. Not surprisingly, smoking was most common in those with lung, colorectal and prostate cancers. Also, not surprisingly, based on previous work, breast cancer history was associated with a significantly greater risk of death from HF. Interestingly in this group, they also noticed a significant risk of death from hypertensive diseases, despite noticing that the measured baseline blood pressure of the patients with breast cancer was reported lower than the controls and the amount of reported with a preexisting history of hypertension. Another interesting finding was that uterine cancer survivors had the highest average body mass index of all cancers, high rates of hypertension and diabetes and increased risk of stroke death, yet no particular statistically significant relationship to a specific cardiovascular event incidence. This group is the first to provide some insight with the help of advanced precision imaging. There is no denying that cardiac MR (CMR) is our current goldstandard quality for cardiac structure and function. The authors here show a strong association of cancer history with adverse cardiac remodelling, particularly more prominently in the case of haematological cancers. It is impressive to see the CMR findings in patients with haematological cancer and realise that these, in particular, had a significantly greater risk of all incident CVDs. These types of cancers have already demonstrated a severe relationship with cardiac disease in similar studies. 7 The investigators here had a significant number of their patients (well over a thousand) with troublesome imaging findings that generally have a solid association with poorer prognoses, such as increased cavity volumes and lower ejection fractions. They found that decreased mechanical function (using left ventricular strain measures) was notably worse in breast malignancy and blood cancer survivors. In this significant study, again, we see an evidence that cancer confers an increased risk to a wide range of cardiovascular events. We also get confirmation that this risk is independent of traditional cardiovascular risk factors and that this issue extends for a prolonged time after a cancer diagnosis. However, we start to take a peek into a window of cancerspecific cardiovascular issues in the followup Division of Cardiology, University of Colorado School of Medicine, Aurora, Colorado, USA Pharmacy, Beth Israel Lahey Health, Westwood, Massachusetts, USA