, Wenjia Wang 51 Department of Neurology, The First Affiliated Hospital of Anhui Medical University, 230022 Hefei, Anhui, China
2 Department of Psychology and Sleep Medicine, The Second Affiliated Hospital of Anhui Medical University, 230601 Hefei, Anhui, China
3 Anhui Province Key Laboratory of Cognition and Neuropsychiatric Disorders, 230032 Hefei, Anhui, China
4 Collaborative Innovation Center of Neuropsychiatric Disorders and Mental Health, 230032 Hefei, Anhui, China
5 Department of Neurology, The Second Affiliated Hospital of Anhui Medical University, 230601 Hefei, Anhui, China
We reviewed Dr. Y-Hassan’s [1] recently published paper that elucidates coronary artery changes in Takotsubo syndrome (TTS), which showed interesting findings regarding the constriction of microcirculation due to the effect of mechanical forces [1]. It is worth mentioning that TTS, for the first time, was also discussed with the occurrence of a coronary artery–left ventricular micro-fistulae (CALVMF). Some have undergone temporary compression in the early stages, then return after recovery of heart function. The findings reveal an association between cardiac structural dynamics and coronary blood flow. However, the review focuses primarily on explaining these changes as potential results of mechanical compression. While acknowledging the crucial role of sympathetic overactivity in TTS pathogenesis, its specific scope does not extensively detail the neurobiological pathways. Therefore, we have taken this opportunity to provide a supplementary perspective based on neurobiology for further consideration regarding the origin of the ischemia that causes TTS.
Current research shows that the heart–brain axis is significant for TTS [2]. This aligns with the vascular findings of the Y-Hassan study on TTS [1]. The gray matter volumes decrease in distinct areas of the brain in those suffering from TTS, as reported in magnetic resonance imaging (MRI) studies [3, 4]: in the amygdala, hippocampus, and cingulate gyrus. These reductions occur across multiple structural MRIs. In addition, researchers have reported reduced functional connectivity among the limbic and autonomic regulatory systems—most notably, the decreased connection between the sympathetic and parasympathetic systems [5].
Neurochemical modulation facilitates coronary microvascular dysfunction and also
represents an additional mechanism that amplifies the mechanical impairment
described by Y-Hassan [1]. Classic data demonstrate marked increases in plasma
catecholamines above baseline during TTS and which surpass those seen during
myocardial infarction (MI) [6]. Supraphysiological catecholamines cause
intracellular calcium overload, oxidative stress, and, ultimately, myocardial
damage via a direct pro-inflammatory effect [7, 8]. In vivo, this may
result in a switch of
These recent findings point to coronary anomalies of TTS originating from aberrant central nervous system signaling, neurochemical vasoconstriction, and mechanical compression working in concert. Bridging our current understanding of the psychoneurobiology and mechanics of the disease state is needed for a full picture of this syndrome [12] and underscores the overlap with neurogenic stunned myocardium [13].
LQ conceptualized the work and contributed to editorial revisions of the manuscript. WW conducted the investigation and drafted the manuscript. Both authors read and approved the final manuscript. Both authors have participated sufficiently in the work and agreed to be accountable for all aspects of the work.
Not applicable.
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This study was supported by the National Natural Science Foundation of China (grant numbers 82001429 and 82090034), National Key Research and Development Program (grant numbers 2021YFC3300500 and 2021YFC3300504), Anhui Province Clinical Medical Research Transformation Special Project (grant numbers 202204295107020006 and 202204295107020028), and Anhui Province Translational Medicine Research Institute Project (grant number 2023zhyx-C76).
The authors declare no conflicts of interest.
References
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