Mourning and Takotsubo cardiomyopathy: neuroendocrine implications and nutritional management

Abstract

SUMMARY This article aims to make reference to some recent mourning aspects considered risk factors for cardiovascular disease, specifically the Takotsubo cardiomyopathy. The objective was to describe the stress from the death of a loved one combining it to the possibility of occurrence of Takotsubo cardiomyopathy through the perception of a traumatic event by the cortex, which triggers the subcortical brain circuit affecting the endocrine response. Given the growing acknowledgement of this cardiomyopathy, it is possible to contextualize the nutritional behaviours and decisions surrounding it, whose benefits must exceed the condition of temporary cardiac dysfunction and extend to food choices that have some influence in the limbic system. It is a descriptive analysis that aims to problematize the theme into reflections based on this experience, considering the foundation with the science of nutrition.

Takotsubo Syndrome and Its Genetic Relationship: Case Report and Narrative Literature Review

“…There are several factors that can predispose the development of Takotsubo syndrome, including the death of a loved one or even some trauma suffered by the patient [29], [30]. In comparison with the literature, the patients presented in this study had several risk factors, among which we can mention: female gender, post-menopause period and emotional stressor [27]- [31].…”

“…The pathophysiology of this involvement is not well defined, but several mechanisms for its development [5] have been described before. It is known that when the patient suffers trauma or the loss of a loved one, there is a possibility of catecholamine release, causing excessive myocardial adrenergic stimulation and a marked increase in calcium in myocytes [6]. Otherwise, the experience of trauma stimulates the subcortical brain circuit, resulting in the release of norepinephrine in the hypothalamus.…”

“…Otherwise, the experience of trauma stimulates the subcortical brain circuit, resulting in the release of norepinephrine in the hypothalamus. This process causes stimulation of the adrenal gland function and, consequently, it causes an increase in cortisol release and an increase in the release of catecholamines [5], [6]. Thus, due to this entire process, the patient evolves to the expression of characteristic symptoms of acute myocardial syndrome, yet in a transitory way [5], [6].…”