To the best of our knowledge, this is the first prospective study to clarify the combined effects of CHD and sarcopenia on new-onset depressive symptoms. In addition, after adjusting for potential confounders, CHD and sarcopenia were found to be independent risk factors of new-onset depressive symptoms. Co-occurring CHD and sarcopenia presented the highest risk of incidence of depressive symptoms in the study population.
Our results showed the prevalence of depressive symptoms was 7.7%, and the onset of depressive symptoms was 11.5% in the elderly aged 60 years and older. The findings are in line with a previous study which reported that the prevalence of depressive symptoms was 7.9% and the incidence of depressive symptoms was 8.5% in the older adults over the age of 60 years. In addition, other research also found the incidence is 14.2%, which is similar to the new onset of depressive symptoms in our study. The small difference is mostly due to difference in evaluation of depressive symptoms and study populations.
Our results are in agreement with previous studies[11, 22–24],which reported that sarcopenia was associated with a higher risk of depressive symptoms in the elderly. However, conflicting results have also been reported. Byeon et al did not find a correlation between the two clinical conditions. The inconsistency in the results are likely due to limitations relating to the assessment of sarcopenia. In their study, sarcopenia was diagnosed only by decreased skeletal muscle mass, while muscle strength or function was ignored. Additionally, use of a subjective questionnaire, rather than a depression assessment tool to identify the depressed condition, could have resulted in underestimation of depression. Several possible mechanisms might be helpful for the explanation of the longitudinal association between sarcopenia and onset depressive symptoms. First, lifestyle factors such as physical inactivity act as common risk factors for sarcopenia and depression. Additionally, chronic low-grade inflammation and oxidative stress are both associated with sarcopenia and depression. Metabolic and endocrine mechanisms are other possible pathways between the two clinical conditions[27, 28].
An association between CHD and depressive symptoms has been consistently reported in the literatures[6, 7], which showed that depression is a risk factor for CHD. Although the causal direction and the underlying mechanisms are not completely understood, our data suggest that people with CHD (OR = 1.81, 95%CI = 1.07–3.07) had a nearly 2-fold risk of developing depressive symptoms. A recent review by Dickens et al showed that the onset of a depressive episode, with regards to the index cardiac event, may be important in predicting worse outcomes among people with CHD. Besides, a systematic review found that, compared to people who reported never experiencing depression, risks of poor outcomes (all-cause mortality, cardiac mortality or cardiac morbidity) were increased significantly in individuals whose first episode of depression started after CHD (OR = 2.11). These studies indicated that risk of poor outcomes is increased among CHD patients with new-onset depressive symptoms. Thus, findings from the present study may provide new insights into the adaption of treatment programs for CHD in older adults. As a major part of this, attention should be paid to the mental health and wellbeing of participants undergoing cardiac rehabilitation. However, Lawson et al. showed inconsistent findings, showing that depressive symptoms were not significantly associated with CHD. The discrepancy may result from differences in different tools to evaluate depression and differences in the composition of the study samples. That study focused on community samples initially free of heart disease.
A considerable amount of literature has developed around potential mechanisms that could explain the association between CHD and depression. Behavioural, genetic and inflammatory mechanisms, as well as endothelial dysfunction and platelet activation, may all explain the relationship between CHD and depression. On the other hand, polyunsaturated omega-3 free fatty acid deficiency, hypothalamic-pituitary-adrenal axis and autonomic mechanisms are also possible link pathways. Further studies involving larger populations and with longer follow-up durations are warranted to confirm our results.
Furthermore, the most compelling finding of our study was that CHD combined with sarcopenia had a further additive predictive value (adjusted OR = 7.12, 95%CI = 2.73–18.61) in discriminating elderly people at high risk of new-onset depressive symptoms. One possible mechanism to explain our results is that sarcopenia and CHD form a vicious cycle. Previous studies suggested that low muscle mass and muscle strength are associated with risk of atherosclerosis and endothelial dysfunction in the elderly[12, 32], which may worsen the progression of CHD. Our additional results demonstrated that low physical performance (walking speed ༜0.8 m/s was associated with new onset of CHD (adjusted OR = 2.08, 95%CI = 1.08-4.00). At the same time, CHD can lead to a decrease in walking speed, reducing people’s willingness to attempt tasks that they are otherwise capable of performing. Subsequently, this decrease in physical performance and increase in restriction might lead to decline of muscle mass or strength, eventually leading to sarcopenia. Based on these previously discussed studies and our current findings, sarcopenia and CHD in older adults appears to have an interactive effect on new-onset depressive symptoms.
This study suggests that older adults with CHD and sarcopenia should be identified early and targeted, so that further mental deterioration and other adverse health outcomes can be prevented. In particular, the American Heart Association (AHA) showed that depression was a risk factor for adverse medical outcomes in patients with CHD. Therefore, much greater attention must be paid to mental health during cardiac rehabilitation. Through our research we have also found the need to focus on physical function. The strength of this study is that it is the first study to report that CHD with sarcopenia is a stronger risk factor for incidence of depressive symptoms. Moreover, findings may provide new insights for cardiac rehabilitation in older adults. Despite extensive efforts to curb study limitations, some limitations did still exist. First, the present study didn’t describe the severity of CHD or its treatment in sarcopenia patients with CHD. In addition, our participants were relatively healthy. Thus, the population studied may not be comprehensive enough. As a result, we may have underestimated the prevalence of depression and its related health effects. Thirdly, this study sample was enrolled from a free physical examination program, rather than a representative sample. Thus, the potential selection bias would influence the study results. Lastly, the follow-up period was short. In future research, we plan to enlarge sample sizes and extend the time for follow-up, to increase the ability to evaluate relationships.