Ischaemic heart disease and major depression are the two leading causes of disease burden as measured using disability-adjusted life years in OECD countries, contributing 9.0% and 6.8% of the total burden respectively. The associated conditions of stroke, diabetes and alcohol abuse are also among the top ten causes of disease burden [1
]. Dementia contributes a further 2.9% and is increasing in the ageing Australian population.
The World Mental Health study demonstrated that the individual health decrement (disability) arising from depression-physical disorder co-morbidity produces greater disability than would be expected from purely additive effects [2
]. Furthermore, treatments are typically targeted only at those with major depressive disorder although the public health impact of lesser symptom severity is highly significant [3
]. The large numbers with sub-clinical or 'subsyndromal' disease contribute a greater disease burden than the few with severe illness [5
]. Providing acceptable, non-toxic interventions on a large scale for those with less severe depressive symptoms in the community is therefore a key public health goal.
The relationships between depression and cardiovascular disease (CVD) are complex with bidirectional pathways [6
]. Depression has been shown to have a relatively strong association with the development of fatal coronary heart disease as well as myocardial infarction. This finding has been demonstrated by a number of longitudinal studies published over the last 40 years, is particularly true in men [7
] and is apparent across the range of depression symptom severity [7
Although depression is consistently associated in observational studies with poor outcome in people with both established CVD and with risk factors for CVD [7
], all major randomised controlled trials (RCTs) have evaluated the effect of treating depression only in those with an established event
such as myocardial infarction. These trials aiming to treat depression and thus reduce CVD have produced mixed results. Despite demonstrating reasonable evidence for an antidepressant response in a number of studies [8
], no benefits were found in prevention of recurrent events or cardiac death. This was also true of the most recently reported trial (CREATE; [11
]). There remains, however, the possibility that intervention in people with less severe disease (i.e., either less severe depressive symptoms or cardiovascular risk factors) might be of benefit [12
]. For example, people at high risk for CVD (e.g. raised cholesterol, smokers) but without established disease may have suboptimal medical management, in addition to psychosocial factors, which may play a greater role in factors such as adherence. We propose that new interventions need to target these 'at risk' individuals.
Poor adherence to medications is an issue that is often linked with depression in conceptual papers but rarely addressed in clinical studies. Adherence describes a person's implementation of a health related behavioural prescription, such as correctly taking a medication, or exercising according to an agreed plan. Depression is one the most consistent determinants of poor adherence to physical treatments [13
] and medication [14
]. Poor adherence is often postulated to mediate the effects of depression on cardiovascular outcomes. To date, however, there has been no RCT evaluating whether an intervention designed to improve depression in those with co-morbid CVD also improves adherence to preventative therapies.
In addition to the range of poor physical health outcomes, depression is also associated with impaired cognition. Typically, dysfunction is evident in those regions mediated by fronto-subcortical brain circuitry, with impairments being most pronounced in processing speed, executive functioning and memory [15
]. These impairments are predictive of disability and poor quality of life [16
] and often persist despite symptom resolution [17
]. While the precise mechanisms are unknown, cognitive impairment in older people with depressive symptoms may be due to a combination of underlying cerebrovascular disease, as well as the direct neurotoxic effects of depression itself. This research underscores the need to deliver targeted interventions for these modifiable risk factors as early as mid-life [18
]. To-date, no known trials have evaluated the effect of treating depressive symptoms upon the subtle early cognitive impairments observed in this 'at risk' group.
Taken together, the literature on depression and CVD would suggest that there exists a group of individuals with both higher cardiovascular risk and depressive symptoms whose coexistence can initiate a negative spiral towards worse CVD and mental health outcomes. Taken in turn, this is likely to have deleterious effects on cognitive functioning, and levels of disability. Given the rapidly, ageing population, there is a need to address these issues on a large-scale at primary and secondary levels of prevention. Internet or web-based interventions (e-health) may be ideally suited for this purpose since they have been shown to deliver efficacious psychological intervention programs for depression [19
] on a large scale in a cost effective manner. Moreover, there is evidence that internet interventions are preferentially sought for their anonymity, their capacity to be used privately at home and for their lack of face-to-face contact. As such they may increase participation among individuals who might not otherwise seek care [20
]. Middle-aged men, a key target group for early cognitive decline, are particularly hard to engage in standard health care. Internet interventions - if automated - are able to deliver interventions with fidelity, giving them an advantage over other types of programs. In younger samples, data suggests that internet interventions are effective for a range of mental health symptoms including depression, post traumatic stress disorder, and eating disorders [21
] and some studies have shown sustainable benefits [22
]. To-date, there have been no published evaluations of web-based treatments for mood and co-morbid physical disorders in older people, although trials in younger samples appear to be underway [23
The primary aim of the Cardiovascular Risk, E-couch Depression Outcome (CREDO) research trial is to determine the efficacy of an internet intervention program for depression (e-couch) on depressive symptoms in people being treated for, or at risk of developing CVD. The secondary aims are to determine the immediate, six and 12-month efficacy of the same intervention on cognitive function and adherence to treatment for CVD.