Takotsubo Cardiomyopathy and Experimental Analysis using an Animal Model

  • Ueyama Takashi
    Department of Anatomy and Cell Biology, Wakayama Medical University School of Medicine
  • Ishikura Fuminobu
    School of Allied Health Sciences, Osaka University Graduate School of Medicine

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  • たこつぼ心筋症と,そのモデル動物を用いた実験的解析
  • タコツボシンキンショウ ト ソノ モデル ドウブツ オ モチイタ ジッケンテキ カイセキ

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Abstract

The term, takotsubo cardiomyopathy, refers to a relatively recently described form of acute, reversible cardiomyopathy, in which apical akinesia gives the heart the shape of a takotsubo, a Japanese fishing pot for trapping octopus. Takotsubo cardiomyopathy seems to occur mainly in elderly women soon after exposure to severe emotional distress. Symptoms mimic acute myocardial infarction; however, coronary angiography fails to demonstrate coronary occlusion. The condition can trigger sudden cardiac failure or death, yet in survivors cardiac function typically normalizes within a few weeks. Takotsubo cardiomyopathy features remarkably elevated plasma catecholamine levels and depressed cardiac contractile function. Immobilization stress (IMO) of rats can reproduce the ECG and LVG changes that occur in takotsubo cardiomyopathy, both of which are prevented by combined blockade of α- and β-adrenoceptors. Increase of serum estrogen partially attenuates these cardiac changes. Estrogen receptors are expressed in the brain, where estrogen modulates central nervous function and autonomic nervous function. Estrogen attenuated the IMO stress-induced c-Fos expression in the lateral septum, medial amygdaloid nucleus, paraventricular hypothalamic nucleus, dorsomedial hypothalamic nucleus, laterodorsal tegmental nucleus and locus coeruleus; these same regions contain central sympathetic neurons and neurons with immunoreactive estrogen receptors. It also down-regulated c-fos mRNA expression in the adrenal gland and the heart, suggesting an increase of estrogen attenuated the stress-induced hypothalamo-sympathoadrenal outflow from the central nervous system to the target organs. Estrogen treatment also up-regulated the levels of cardio-protective substances such as ANP and HSP70 in the heart. These data suggest that reduction of estrogen levels following menopause might be involved in the primary cause of takotsubo cardiomyopathy both by indirect action on the nervous system and by direct action on the heart.

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