Introduction

Cardiovascular disease (CVD) and prostate cancer represent major public health problems. In 2009, over 180 000 people died from CVD in the UK (http://www.bhf.org.uk). Over the past 30 years, the incidence of prostate cancer has almost tripled, with much of this increase attributable to increased early detection due to widespread prostate specific antigen (PSA) testing. Although many of these cases are related to localised disease, around one-third of the 37 000 men diagnosed in the UK annually (http://info.cancerresearchuk.org) will have advanced prostate cancer. The mainstay of treatment for such men is androgen suppression therapy (AST). Immediate initiation of AST is well supported by proven clinical benefits for men with symptomatic skeletal metastases,1 established lymphatic metastases2 and when combined with radiotherapy in locally advanced disease.3 4 However, as a result of PSA testing, men outside these groups are now started on AST much earlier, and remain on therapy for many years. AST is associated with a number of adverse effects, such as reduced bone mineral density, increased fracture risk, decreased skeletal muscle function and fatigue.5 However, more recently attention has turned to the risk of CVD in association with AST. Although AST clearly improves prostate cancer specific mortality (RR reduction of 17%) it does so at the expense of a 15% increase in the RR of non-disease specific mortality.1 Although CVD is of course highly prevalent in the population on AST (ie, older men), evidence accruing from observational data now suggests AST may significantly increase CVD morbidity and mortality.