Objective: Background: The association between depression and cardiovascular disease (CVD) is well documented. However, depression has also been proposed to be involved in the pathological pathways linking the main risk factors of CVDs. Several studies including one meta-analysis have suggested that depression may be an independent risk factor for hypertension. Objective:To evaluate the relationship between depression and incident hypertension Design and method: Bibliographic databases Medline, EMBASE, Web of Science and PsycINFO without language restrictions were searched from 2005 up to 2019. We included prospective cohort studies, involving normotensive subjects at baseline with diagnosis of depression measured using clinical evaluation or a standardised psychometric tool and recorded as a dichotomous variable. Outcome was new-onset hypertension. We excluded studies that enrolled participants with a history of antihypertensive medication at the time of study initiation. Methodological quality was assessed using the Newcastle-Ottawa Scale. Pooled hazard ratios (HR) were calculated using inverse variance method in random effects models. Results: We identified five studies with a total of 201,886 participants and an average follow-up of 7.52 years. Out of the five studies, only two reported a positive association between depression and incident hypertension. The pooled effect of three studies included in the meta-analysis showed that depression was associated with 20% increased risk of hypertension (HR = 1.20, 95%CI 1.01–1.43) but with a substantial heterogeneity (I2 = 70%). One study reported a null result for a dose-response relationship between depressive symptoms and incident hypertension. Quality analysis showed increased risk of bias notably in the ascertainment of the outcome as most studies relied on self-report and/or prescription of antihypertensive medication as a proxy for hypertension. Conclusions: Our findings indicate a possible increased risk of hypertension with depressive symptoms, but this result is limited by heterogeneity and ascertainment bias in the studies included.

Objective: There is growing evidence indicating a bidirectional relationship between depression and cardiovascular diseases (CVDs). Among the limitations of previous studies include the use of a single baseline measure of depressive symptoms. Objective: To establish whether an independent association with CVD exists for depression either measured at baseline or at multiple instances in a population free of CVD and cerebrovascular diseases. Design and method: Bibliographic databases were searched from 2005 up to 2019 using Medline, EMBASE, Web of Science and PsycINFO without language restrictions. Prospective cohort studies which reported the association between depression and incidence of three CVD outcomes (stroke, coronary heart disease (CHD), myocardial infarction (MI) and heart failure (HF)) were included. Pooled hazard ratios (HR) were calculated using inverse variance method in random effect models. Results: Twenty-two prospective cohorts with 43 independent reports were identified, of which twenty were suitable for meta-analysis with a total of 3,642,913 participants and an average follow-up of 10 years. Participants with depressive symptoms at baseline had a 25% higher risk of stroke (HR = 1.25 95%CI 1.11–1.40, I2 = 67%), a 20% higher risk of CHD (HR = 1.20 95%CI 1.08–1.32, I2 = 82%) and a 24% higher risk of MI (HR 1.24 95%CI 1.20–1.28, I2 = 0%) comparing to participants without depressive symptoms at study entry. Similar associations were observed after restricting analysis to studies that measured depression as a time-varying exposure - stroke (HR = 1.32 95%CI 1.10–1.59, I2 = 0%) and CHD (HR = 1.21 95%CI 1.02–1.43, I2 = 34%). Two studies reported HF outcomes and this showed a similar association (HR = 1.18 95%CI 1.08–1.29, I2 = 0%). In subgroup-analysis by type of depression assessment, clinical depression appeared to be a stronger predictor than depressive symptoms for stroke and CHD. Conclusions: Depression is associated with increased risk for the development of CVDs.