Reviewed research

Authors Banks E, Joshy G, Abhayaratna WP, Kritharides L, Macdonald PS, Korda RJ, Chalmers JP

Review Date February 2013

Citation PLoS Med 2013; 10 (1): e1001372 (Online open access)



Erectile dysfunction (ED) is a common condition in Australian men with about 20% of Australian men aged 40 or over reporting moderate or severe ED (Holden et al, Lancet 2005). ED is an emerging risk marker for future cardiovascular disease (CVD) events; however, evidence on dose response and specific CVD outcomes is limited. This Australian study investigates the relationship between severity of ED and specific CVD outcomes.



The aim of the study was to investigate the relationship of severity of erectile dysfunction, as a marker of risk, to a range of CVD outcomes and all-cause mortality, among men with and without CVD at baseline.



The authors used a prospective population-based Australian study (the 45 and Up Study) to link questionnaire data from 2006–2009 with hospitalisation and death data to 30 June and 31 Dec 2010, respectively. Cox proportional hazards models were used to examine the relationship of reported severity of erectile dysfunction (measured using a single question based on that used in the Massachusetts Male Aging Study) to all-cause mortality and first CVD-related hospitalisation since baseline, in men with and without previous CVD. Models were adjusted for age, smoking, alcohol consumption, marital status, income, education, physical activity, body mass index, diabetes, and hypertension and/or hypercholesterolaemia treatment. 



95,038 men aged ≥ 45 y (mean age 62 y) were included in the analysis, from the 123,775 men in the 45 and Up study. Prevalence of severe ED was 2.2% in men aged 45-54 y, 6.8% at age 55-64, 20.2% at age 65-75, 50.0% at age 75-84 and 75.4% at age 85 or over. There were 7,855 incident admissions for CVD and 2,304 deaths during follow-up (mean time from recruitment, 2.2 y for CVD admission and 2.8 y for mortality). Risks of CVD and death increased steadily with severity of erectile dysfunction. Among men without previous CVD, those with severe versus no erectile dysfunction had significantly increased risks of ischaemic heart disease (adjusted relative risk [RR] = 1.60, 95% CI 1.31–1.95), heart failure (8.00, 2.64–24.2), peripheral vascular disease (1.92, 1.12–3.29), ‘‘other’’ CVD (1.26, 1.05–1.51), all CVD combined (1.35, 1.19–1.53), and all-cause mortality (1.93, 1.52–2.44). For men with previous CVD, corresponding RRs (95% CI) were 1.70 (1.46–1.98), 4.40 (2.64–7.33), 2.46 (1.63–3.70), 1.40 (1.21–1.63), 1.64 (1.48–1.81), and 2.37 (1.87–3.01), respectively. Among men without previous CVD, RRs of more specific CVDs increased significantly with severe versus no erectile dysfunction, including acute myocardial infarction (1.66, 1.22–2.26), atrioventricular and left bundle branch block (6.62, 1.86–23.56), and (peripheral) atherosclerosis (2.47, 1.18–5.15), with no significant difference in risk for conditions such as primary hypertension (0.61, 0.16–2.35) and intracerebral haemorrhage (0.78, 0.20–2.97).



The study findings give support for CVD risk assessment in men with erectile dysfunction who have not already been assessed. However, the utility of erectile dysfunction as a clinical risk prediction tool needs to be tested.


Points to Note
  1. This study has extended findings from previous studies by showing a dose-response association between ED and a variety of incident CVD events and all-cause mortality, and by stratifying by prior CVD diagnosis.
  2. Limitations of the study include: a single question measure of ED; mostly self-reported data; a large number of endpoints increases the probability of a type 1 error; duration of ED was not recorded; and use of PDE5 inhibitors was not known.
  3. Advantages of the study are: a large sample size; the consistency of the association over a number of types of CVD outcomes; and controlling for a variety of known CVD risk factors.
  4. As CVD treatments might lead to ED, the findings for the men with prior CVD need to be viewed with caution. However, the presence of ED might give a greater incentive for men to adhere to secondary prevention measures.
  5. The biological plausibility of the association is supported by the fact that endothelial dysfunction is a cause of ED and it is possible that the small blood vessels in the penis may be the first vessels affected by atherosclerosis.
  6. This findings of this study combined with previous publications suggest that a diagnosis of ED could be an indicator for a man to have a CVD risk assessment but the potential clinical utility of ED in predicting CVD quantitatively requires further exploration.


Website: www.plosmedicine.org/article/info%3Adoi%2F10.1371%2Fjournal.pmed.1001372

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