People diagnosed with depression are at increased risk of major cardiovascular events (MACEs), including coronary heart disease and stroke.
1-4 Arterial stiffness (AS), a hardening of the artery wall because of aging and diverse pathologic states, is a key mediator of MACE,
5 and growing evidence has found an association of depression with AS.
6 Components of metabolic syndrome (MetS), such as hypertension, dyslipidemia, obesity, and hyperglycemia, represent leading promoters of AS.
5 Consistent with the key role of AS in predicting MACE incidence, carotid pulse wave velocity represents the criterion-standard measure for central AS,
7,8 and several other noninvasive techniques (eg, photoplethysmography) are available as indicators of specific AS parameters (eg, wave reflections).
5,9 While the interchangeability of these measures needs further research,
10 they were found to be independently associated with incident MACE across different subgroups.
9,11,12 Therefore, a key unanswered question for public health is the extent to which the adverse effect of depression on MACE might be mitigated by targeting modifiable metabolic mediators. To address this concern, we need to better understand the role of MetS in mediating the association of depression with AS. The extent to which this mediation differs by sex is critical given that the prevalence of MACE, MetS, and depression is often greater among women compared with men.
13,14 Sex-specific mediating effects of MetS are generally underresearched but are a growing issue given the increasing prevalence of MetS in women.
15 The present study adopted a mediation analysis approach to quantify to what extent MetS and its individual components mediated the association of depression with AS. The study also aimed to investigate the extent to which the hypothesized mediation varied by sex.