Key result
Low LV apical cholinergic nerve density may explain unopposed adrenergic vasoconstriction in Takotsubo cardiomyopathy.
Why the study?
The pathophysiological explanation behind the selective involvement of the LV, predominantly the LV apex, in Takotsubo cardiomyopathy remains poorly understood.
This review proposes a pathophysiological explanation for the selective LV apical involvement in Takotsubo cardiomyopathy based on differential autonomic nerve distribution.
Answers are grounded in this paper and cite their sources.
Suggests autonomic mechanism for Takotsubo apical involvement; leaves open histologic and clinical validation before any practice implications.
Takotsubo cardiomyopathy (TCM) has gained global recognition as a unique cardiovascular disease that mimics acute myocardial infarction. Since its initial description, more than three decades ago, we have significantly advanced our understanding of diagnosing, treating, and prognosticating this reversible cardiovascular phenomenon. However, the pathophysiological explanation behind its selective involvement of the left ventricle (LV), predominantly the LV apex in poorly understood. In this brief review on differential distribution of the adrenergic nerve (AN) and cholinergic nerve (CN) in the normal human heart, we try to extrapolate an idea of poor CN distribution in the LV apex as an associated factor augmenting microcirculatory dysfunction due to an unopposed AN activity from the catecholamine surge, as a plausible explanation for this characteristic phenomenon.
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Pasupula et al. (2019) conducted a review in Takotsubo cardiomyopathy. The low density of cholinergic nerves in the left ventricular apex may lead to unopposed adrenergic vasoconstriction during a catecholamine surge, explaining the selective apical involvement in Takotsubo cardiomyopathy.
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