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Association of depressive symptoms and hypertension prevalence, awareness, treatment

医学 联想(心理学) 抑郁症状 内科学 精神科 认知 认识论 哲学
作者
Jana Brguljan Hitij
出处
期刊:Journal of Hypertension [Lippincott Williams & Wilkins]
卷期号:40 (9): 1655-1657 被引量:1
标识
DOI:10.1097/hjh.0000000000003225
摘要

The etiology of hypertension has several faces with two main categories: essential or primary, and secondary hypertension. The cause of primary hypertension is multifactorial in nature. It originates from a combination of genetic and environmental factors [1]. The heritability of BP is around 30–60% [2]. A lot of environmental and social determinants have the potential to contribute to its development. A better understanding of the interplay between these components has continued to unfold. There is strong evidence that mental distress is associated with cardiovascular disease and unhealthy lifestyle. Against this background, one would expect a clear relationship between mental distress and hypertension (HTN). However, cross-sectional and longitudinal studies have shown conflicting results: some studies reported close positive associations between HTN and mental distress, whereas others found no or even inverse association. A recent evaluation of the claim data of one million persons from a National Health Insurance found that persons with major depression had an increased prevalence of and risk for developing HTN as compared to persons without depression. In contrast, Hildrum et al.[3] reported from a large longitudinal community-based study, that the level of self-reported symptoms of depression predicted lower blood pressure at baseline and at 11- and 22-year follow-up. To better understand this issue, Fang and colleges from Atlanta, Georgia have gone through the National Health and Nutrition Examination Survey (NHANES) data from 2007 to 2018 (n = 28 532), categorizing depressive symptoms as 'none or minimum', 'mild', 'moderate', and 'moderately severe or severe' by the Patient Health Questionnaire, and linked them with prevalence, awareness and treatment of hypertension. Hypertension was defined by history, blood pressure measures, and antihypertensive medication use. The conclusion of the study could be important for clinicians to unveil this connection and lead to treat hypertensive patients with depression better and also look for possible symptoms of depression in hypertensive patients. The study has some limitations; first, assessment of hypertension awareness and treatment was based on self-report and subject to recall biases. Secondly, some chronic conditions, such as cirrhosis and heart failure, which may relate to both depression and hypertension were not captured in NHANES. Despite these limitations, the conclusions of the study are relevant for our daily practice. Dose–response association was observed for hypertension awareness and treatment – the percentage increased more among those with greater depressive symptom and were highest among those with moderate severe or severe depressive symptoms. Greater depressive symptoms were associated with great hypertension awareness and treatment but not with control [4]. DEPRESSION DEFINITION Depression symptoms are unspecific and may overlap with individual behavioural attitudes. Depressive disorders (DD) are usually characterized by anhedonia, the inability to experience pleasure, even in circumstances and usually enjoyable activities such as sleeping, feeding, sexual experiences and social contact. DD may also be accompanied by somatic symptoms (psychological disturbance, fatigue and weight fluctuations) and cognitive symptoms (poor concentration and negative cognitions). DD are sub-categorized into major depressive disorder (MDD) and dysthymia, the latter with similar symptoms but longer duration and less intensity than MDD [5]. THE ROLE OF DEPRESSION IN PATHOPHYSIOLOGY OF HYPERTENSION Maintenance of a normal BP is dependent on the balance between cardiac output and peripheral vascular resistance. It follows that patients with arterial hypertension may have an increase in cardiac output, an increase in systemic vascular resistance, or both. Although this conceptual framework is used to understand the final physiological alterations leading to elevated BP, it is now well established that multiple renal, neural, endocrine, and cardiovascular (CV) control systems can affect cardiac and vascular homeostasis, making the pathophysiology of hypertension extremely complex. The contribution of each of these factors to elevated BP values is defined by gene–environment interactions and varies among different individuals [6]. DEPRESSION, HYPERTENSION AND CARDIOVASCULAR DISEASES Prospective Urban Rural Epidemiological (PURE) study was a large, population-based prospective cohort study in 51 centres of 21 high-, middle-, and low-income countries. Of 145 862 participants, 61 235 (58%) were male and mean (SD) age was 50.05 (9.7) years. Of those, 15 983 (11%) reported four or more depressive symptoms at baseline. Adults with depressive symptoms were associated with having increased risk of incident cardiovascular diseases (CVD) and mortality in economically diverse settings, especially in urban areas [7,8]. Data drawn from the Whitehall II Study, established in 1985 as a longitudinal study to examine the socioeconomic gradient in health and disease among 10 308 civil servants (6895 men and 3413 women) examined longitudinal trajectories of depressive episodes and the probability of hypertension associated with these trajectories over time. Participants were 6889 men and 3413 women, London-based civil servants aged 35–55 years at baseline, followed for 24 years between 1985 and 2009. Depressive episode (defined as scoring 4 on the General Health Questionnaire-Depression subscale or using prescribed antidepressant medication) and hypertension (systolic/diastolic blood pressure 140/90 mmHg or use of antihypertensive medication) were assessed concurrently at five medical examinations. In the fully adjusted longitudinal logistic regression analyses based on generalized estimating equations using age as the time scale, participants in the 'increasing depression' group had a 24% (P < 0.05) lower risk of hypertension at ages 35–39 years compared with those in the 'low/transient depression' group. However, there was a faster age-related increase in hypertension in the increasing depression group, corresponding with a 7% (P < 0.01) greater increase in the odds of hypertension for each 5-year increase in age. A higher risk of hypertension in the first group of participants was not evident before 55 years of age. A similar pattern of association was observed in men and women, although it was stronger in men. This study suggests that the risk of hypertension increases with repeated experience of depressive episodes over time and becomes evident in later adulthood [9]. Bucciarelli et al.[5] nicely summarized the current knowledge about depression and CVD relationship in women, highlighting the sex differences in physiopathology, clinical presentation and treatments. Sex chromosomes are responsible for sex differences, as they influence gene expression, leading to specific sexual hormones secretion, which in turn act explicitly on biological factors, including neurotransmitters. DD are more prevalent in women than men, with a doubled chance of suffering from depression across a variety of nations, cultures and ethnicities. Another important study was reported from Spain. Connection between cardio-vascular risk factors (CVR) and depressive status in a population (55–75 years) with metabolic syndrome from the PREDIMED-Plus trial was investigated. The association between CVR and depressive status at baseline (n = 6545), and their changes after 2 years (n = 4566) were evaluated. Among women and participants with low levels of base-line total cholesterol (<160 mg/ml), CVR was directly associated with depression. On the contrary, among participants with elevated levels of total cholesterol CVR at baseline showed an inverse association with the presence of depressive symptomatology [10]. CONCLUSION FOR CLINICIANS Current literature clearly shows that there is a connection between hypertension and depression [11–13]. It might be that they share either common pathophysiological mechanisms or risk factors, or both. Mechanisms explaining the link between hypertension and depression are complex and remain unclear. Inflammation involving the immune system might be an important common mechanism and even more potential connections described by Bucciarelli et al.[5] combination of behavioural habits and physiological mechanisms are the explanation for its connection. The conclusion of the National Health and Nutrition Examination Survey data were important for clinicians treating hypertensive patient. We should pay attention to development of depressive syndromes; even more importantly, patient treated for depression should be closely followed for possible hypertension development and treated on time to prevent the cardiovascular consequence of untreated hypertension. Improving understanding and awareness of these physical health risks should be prioritized as part of a comprehensive strategy to reduce the burden of non-communicable diseases worldwide as it is hypertension and depression [14]. ACKNOWLEDGEMENTS Conflicts of interest There are no conflicts of interest.

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