A case report of myocardial inflammation in takotsubo syndrome. A chicken-or-the-egg phenomenon

Rroku, Andi; Grahl, Simon; Landmesser, Ulf; Heidecker, Bettina

doi:10.1016/j.ijcha.2022.100958

Cited by 1 publication

(2 citation statements)

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“…Canonically, viral infections are considered the most common trigger and cause of inflammatory cardiomyopathy thus leading to immune mechanisms which potentially damage the myocardial function [56][57][58][59][60][61][62][63] . However, an alternative model consistent with our findings could position chronic low-grade inflammation as a shared risk factor for depression, CAD, and cardiomyopathy.…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, genetic results of our study raised the hypothesis that a predisposition to both depression and CAD (clinically observed as (m)dCAD) may further predispose individuals to cardiomyopathy. Canonically, viral infections are considered the most common trigger and cause of inflammatory cardiomyopathy thus leading to immune mechanisms which potentially damage the myocardial function 56–63 . However, an alternative model consistent with our findings could position chronic low-grade inflammation as a shared risk factor for depression, CAD, and cardiomyopathy.…”

Section: Discussionmentioning

confidence: 99%

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Genes associated with depression and coronary artery disease are enriched for inflammation and cardiomyopathy-associated pathways

Singh

Lee

Sealock

et al. 2022

Preprint

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Background: Depression and Coronary Artery Disease (CAD) are highly comorbid conditions. Approximately 40% of individuals who have one diagnosis will also develop the other within their lifetime. Prior research indicates that polygenic risk for depression increases the odds of developing CAD even in the absence of clinical depression. However, the specific genes and pathways involved in comorbid depression-CAD remain unknown. Results: We identified genes that are significantly associated with both depression and CAD, finding that this gene set is enriched for pathways involved in inflammation and previously implicated in cardiomyopathy. We observed increased rate of prevalent, but not incident, cardiomyopathy cases in individuals with comorbid depression-CAD compared to those with CAD alone in three electronic large health record (EHR) datasets. Conclusions: The results of our study implicate genetically regulated inflammatory mechanisms in depression-CAD. Our results also raise the hypothesis that depression-associated CAD may be enriched for cardiomyopathy.

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