IKEDA et al.：Ampulla cardiomyopathy and β-blocker南予医誌 Vol.14 No. １ 2013－67－spective study of patients with ampulla car-diomyopathy. On the other hand, poor clini-cal outcomes have also been documented. Matsuoka et al.5 reported a patient with fatal ampulla cardiomyopathy who failed to recover from shock despite the administra-tion of a catecholamine. In our case, an in-travenous inotropic agent was administered for shock. However, a remarkable hemo-dynamic feature in this patient was the left ventricular outflow obstruction mimicking hypertrophic obstructive cardiomyopathy; thus, we ceased the catecholamine admin-istration. The cessation of the inotropic agent and subsequent administration of aβ-blocker resulted in hemodynamic im-provement. Benecial effect of β-blockers on dy-namic left ventricular outow obstruc-tion associated with ampulla cardiomy-opathy β-adrenergic receptor blocking drugs are commonly used in the treatment of patients with idiopathic hypertro-phic subaortic stenosis. β-blockers are considered to attenuate the pres-sure gradient through their negative inotropic effect. The most remarkable hemodynamic feature in the present patient was the left ventricular outow obstruction. In fact, β-blockade result-ed in amelioration of the left ventricular pressure gradient and subsequent he-modynamic improvement. Therefore, it is suggested that β-blockers have ben-eficial effects in the treatment of am-pulla cardiomyopathy, especially that associated with left ventricular outow dynamic obstruction. However, further investigation is required to conrm the therapeutic usefulness of β-blockade in the treatment of ampulla cardiomy-opathy. Recent studies have revealed that cat-echolamines may play a pivotal role as causative factors in transient apical balloon-ing.6,7 Kono et al.6 reported that the cause of neurogenic stunned myocardium was in-creased local norepinephrine release in the heart. Based on the serial changes of the I-123-MIBG scintigraphic findings, Moriya et al.7 speculated that sympathetic nerve dysfunction in the apical region is a cause of the characteristic apical asynergy observed in patients with ampulla cadiomyopathy. In our case, I-123-MIBG demonstrated that cardiac sympathetic dysfunction continued even 6 months after the first episode. The MIBG findings in the present patient may confirm the contribution of adrenergic nerve dysfunction to the pathogenesis of ampulla cardiomyopathy. Several reports have shown that patients in the menopausal state are vulnerable to adrenergic stimulation. An experimental report by Ueyama et al.8 stated that ovari-ectomized rats frequently developed tran-sient apical akinesis through activation of β-adrenergic receptors. Furthermore, a recent report by Thawornkaiwong et al.9 demonstrated thatβ1-adrenergic receptors are upregulated in overiectomized rats and that ovarian sex hormones exert a direct in-
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