Key result
A review of 30 studies found that sustained, low-grade inflammation is an important component of post-AMI depression, with TNF-α, CRP, and IL-6 showing promise as reliable indicators.
Why the study?
Depression after acute myocardial infarction is prevalent and linked to poor outcomes, but the specific role of inflammation in the etiology of both conditions remains poorly understood.
Are inflammatory biomarkers associated with depression following acute myocardial infarction?
Are inflammatory biomarkers associated with depression following acute myocardial infarction?
Sustained, low-grade inflammation, particularly indicated by TNF-α, CRP, and IL-6, appears to be an important component in the pathogenesis of depression following acute myocardial infarction.
Heightened vigilance for post-AMI depression is warranted; leaves open optimal management strategies.
Among patients with recent acute myocardial infarction (AMI), there is an increased prevalence of depression which is associated with elevated morbidity, mortality, and rehospitalization. Yet, depression is frequently underdiagnosed and undertreated in patients following AMI. The paucity of data informing the management and treatment of depression in this population emphasizes the need for further investigation into the pathophysiological relationship between depression and AMI. Depressive symptoms following AMI may arise due to a range of factors, including the activation of the immune system. However, the specific role of inflammation in the etiology of both depression and AMI remains poorly understood. Therefore, the present review systematically identifies and critically evaluates the relevant inflammatory biomarkers of depression in the high-risk AMI population. Articles published between January 1st, 2000, and December 31st, 2020 in the PubMED, Cochrane, EMBASE, and Web of Science databases were assessed. A total of 30 documents were considered and found eligible for this review. The inflammatory biomarkers reviewed include tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6, IL-8, IL-10, IL-17a, IL-18, IL-12p70, interferon-λ (IFNλ), C-reactive protein (CRP), intracellular adhesion molecule-1 (ICAM-1), endothelin-1 (ET-1), platelet factor 4 (PF4), and beta-thromboglobulin (BTG). The studies reviewed suggest sustained, low-grade inflammation is an important component of depression following AMI. TNF- α, CRP, and IL-6 showed significant promise as reliable indicators for depression following AMI. Accordingly, it is postulated that inflammation is relevant in the pathogenesis of post-AMI depression. Further investigation of the inflammatory markers detected in patients with post-AMI depression will extend the pathophysiological understanding of this condition and potentially lead to the identification of novel therapeutic targets.
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Mensour et al. (2022) conducted a review in Acute myocardial infarction and depression (n=30). Inflammatory biomarkers was evaluated on Role of inflammatory biomarkers in post-AMI depression. A review of 30 studies found that sustained, low-grade inflammation is an important component of post-AMI depression, with TNF-α, CRP, and IL-6 showing promise as reliable indicators.
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