Vascular risk factors for depression and apathy | Part 1 38 Our findings are in line with previous research of the relationship between depressive symptoms and the incidence of stroke in populations with a high cardiovascular risk, such as patients with hypertension or diabetes mellitus 30 31 32, and offer an explanation for negative results. They are also consistent with previous studies 12 33 34 reporting a poorer cardiac prognosis and an increased mortality among cardiac patients with depression. Our study shows that the cerebrovascular prognosis of cardiac patients with depressive symptoms is worse, as is the cardiac prognosis, and this may be a factor underlying the higher mortality seen in depressed cardiac patients. Nevertheless, these findings have some limitations. First, stroke was not confirmed by neuroimaging and, thus, no distinction was made between ischemic and hemorrhagic stroke. Pathophysiologically, depression would be expected to be primarily associated with ischemic stroke. Misclassification due to overreporting of stroke is probably not a major issue because self-reported stroke had to be confirmed by a GP or a specialist. Although there was selective dropout, with the more frail individuals being more likely to have missing data on depression during follow-up, this would tend to lead to a conservative estimate of the relationship between depressive symptoms and incident stroke. The relatively few participants with an MDD at baseline (n = 58) limited the power to find associations between MDD and stroke. However, the use of a broader category of CRDSs, which included MDD and SDD, is in line with research showing that subsyndromal depressive states form a continuum with major depression in elderly populations 35 36 37. Furthermore, the strongest results were found when depressive symptoms were used as a continuous measure (based on the CES-D), and the results for time-dependent analysis of an association between MDD and stroke in cardiac patients pointed in the same direction. Last, we did not fully control for the severity of cardiac disease because of the lack of electrocardiographic or ultrasonographic information 12. As strong points, we used a clinical diagnosis of depression in combination with a valid measurement of depressive symptoms and required confirmation of self-reported stroke by the patients’ GPs, a method that has been validated in LASA,20 or by information obtained from the death certificate. We also assessed depressive disorders and symptoms, functional limitations, and blood pressure during follow-up, which enabled us to use adjusted extended Cox proportional hazards models with time-dependent variables. These extended models are probably more realistic because depression has a fluctuating course, and these models incorporate all available information about depression and depressive symptoms. We also distinguished between participants with and without cardiac disease at baseline, which enabled us to establish that cardiac disease moderates the relationship between stroke and depressive symptoms. To understand how cardiac disease moderates the association between depression and stroke morbidity and mortality, we initially have to consider why depression is associated with incident stroke in cardiac patients. Depression could aggravate atherosclerosis and in this way worsen the prognosis of cardiac patients, which could explain the dose-response effect that we found. Suggested pathways by which depression could specifically affect the vascular system of cardiac patients are a diminished heart rate variability, altered platelet responses,8 more arrhythmia in depressed patients with premature ventricular
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