افسردگی، اضطراب و خطر 6 سال ابتلا به بیماری های قلبی و عروقی
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|29813||2015||6 صفحه PDF||سفارش دهید||محاسبه نشده|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Journal of Psychosomatic Research, Volume 78, Issue 2, February 2015, Pages 123–129
Objective Depression and anxiety are considered etiological factors in cardiovascular disease (CVD), though their relative contribution and differentiation by clinical characteristics have not been studied intensively. We examined 6-year associations between depressive and anxiety disorders, clinical characteristics and newly-developed CVD. Methods DSM-IV diagnoses were established in 2510 CVD-free participants of the Netherlands Study of Depression and Anxiety. Data on subtype, severity, and psychoactive medication were collected. The 6-year incidence of CVD was assessed using Cox regression analyses adjusted for sociodemographic, health and lifestyle factors. Results One-hundred-six subjects (4.2%) developed CVD. Having both current depressive and anxiety disorders (HR = 2.86, 95%CI 1.49–5.49) or current depression only (HR = 2.30; 95%CI 1.10–4.80) was significantly associated with increased CVD incidence, whereas current anxiety only (HR = 1.48; 95%CI 0.74–2.96) and remitted disorders (HR = 1.48; 95%CI 0.80–2.75) were not associated. Symptom severity was associated with increased CVD onset (e.g., Inventory of Depressive Symptomatology per SD increase: HR = 1.51; 95%CI 1.25–1.83). Benzodiazepine use was associated with additional CVD risk (HR = 1.95; 95%CI 1.16–3.31). Conclusions Current depressive (but not anxiety) disorder independently contributed to CVD in our sample of initially CVD-free participants. CVD incidence over 6 years of follow-up was particularly increased in subjects with more symptoms, and in those using benzodiazepines.
According to the World Health Organisation, ischemic heart disease and cerebrovascular disease have been and will be leading causes of death for decades . Longitudinal research thus far has provided us with potential etiological factors of cardiovascular disease (CVD), including those concerning negative mental health. Meta-analytic studies have demonstrated that anxiety  and depression  increase the incidence of CVD in healthy populations by 26% to 81%. Despite the high co-morbidity between these psychiatric disorders  and , most previous studies examined the influence of either depression or anxiety on CVD, or examined both but showed the effect size for one condition. The relative contribution of depressive and anxiety disorders to the development of CVD therefore remains unclear. In addition, many studies have assessed depression or anxiety symptoms by using self-report measures, which are more likely to overdiagnose psychopathology and thereby artificially inflate the effect size of an association with CVD in the presence of underlying somatic health problems. Particular clinical characteristics may also elucidate the association between depression, anxiety and CVD. For clinical practice it is of great importance to know whether specific subgroups of depressed or anxious patients carry a higher CVD risk and should be closely monitored for cardiovascular dysfunction. Despite the heterogeneity in depression and anxiety, the potentially differentiating role of disorder subtype in the association with CVD has only sparsely received attention. With respect to symptom severity, some prospective studies support a dose–response association between severity of depressive or anxiety symptoms and CVD , ,  and . As to the use of psychoactive medication and subsequent CVD, some studies found a detrimental cardiovascular effect for tricyclic antidepressants (TCAs) , ,  and , serotonin reuptake inhibitors (SSRIs) or other antidepressants , and benzodiazepines , whereas others found no significant association (TCAs ; SSRIs/other antidepressants  and ; benzodiazepines  and ).
نتیجه گیری انگلیسی
The findings discussed in this paper suggest that depression, more than anxiety, carries an increased risk of subsequent CVD. A dose–response association was found for severity of symptoms. Treating depression adequately might decrease onset of CVD. Clinicians should be aware of the risk associated with (severe) depression, as this provides the opportunity to advise their patients regarding additional risk factors for CVD, such as physical activity and hypertension. Researchers would do well to distinguish between diagnostic subtypes, since these may moderate the relationship between depression or anxiety and cardiovascular risk. Future studies are needed to better look into the potential cardiovascular risk associated with the use of benzodiazepines.