Shared Risk Factors in Cardiovascular Disease and Cancer

Abstract

Cardiovascular disease (CVD) and cancer are the 2 leading causes of death worldwide. Although commonly thought of as 2 separate disease entities, CVD and cancer possess various similarities and possible interactions, including a number of similar risk factors (eg, obesity, diabetes mellitus), suggesting a shared biology for which there is emerging evidence. Although chronic inflammation is an indispensable feature of the pathogenesis and progression of both CVD and cancer, additional mechanisms can be found at their intersection. Therapeutic advances, despite improving longevity, have increased the overlap between these diseases, with millions of cancer survivors now at risk of developing CVD. Cardiac risk factors have a major impact on subsequent treatment-related cardiotoxicity. In this review, we explore the risk factors common to both CVD and cancer, highlighting the major epidemiological studies and potential biological mechanisms that account for them.

Keywords: cardiology; cardiovascular diseases; clinical oncology; risk factors.

Figure 1

Modifiable cardiac risk factors with their estimated cancer risk. Figure limited to only the positive and/or negative associations using the most recently published meta-analysis or prospective cohort study investigating the associations between a cardiac risk factor and various cancer sites; hyperlipidemia was excluded from the figure due to inconclusive evidence that it is associated with cancer risk. All cancer estimates were reported as a relative risk except where noted below. † Risk for BMI >30 kg/m² ‡ Note, there were several additional positive (bladder, esophageal, extrahepatic cholangiocarcinoma, gallbladder, gastric, hepatocellular carcinoma, kidney, leukemia, multiple myeloma, Non-Hodgkin’s lymphoma, ovarian cancer, pancreatic cancer) and negative (lung, prostate) associations by fixed effects models, but the authors did not deem these to be positive associations since their 95% prediction intervals included the null value. § Prospective observational cohort; Cox regression was used to calculate hazard ratios of cancer per 10 mmHg increments of midblood pressure. ¶ Only cancer sites with sufficient evidence of carcinogenicity related to tobacco exposure in humans were considered in the meta-analysis.