Kasama Shu, Toyama Takuji, Iwasaki Toshiya, Sumino Hiroyuki, Kumakura Hisao, Minami Kazutomo, Ichikawa Shuichi, Matsumoto Naoya, Nakata Tomoaki, Kurabayashi Masahiko
Eur J Nucl Med Mol Imaging. 2014 Sep;41(9):1683-91. doi: 10.1007/s00259-014-2754-2.
Aldosterone prevents the uptake of norepinephrine in the myocardium. Atrial natriuretic peptide (ANP), a circulating hormone of cardiac origin, inhibits aldosterone synthase gene expression in cultured cardiocytes. We evaluated the effects of intravenous ANP on cardiac sympathetic nerve activity (CSNA) and aldosterone suppression in patients with acute decompensated heart failure (ADHF).
We studied 182 patients with moderate nonischemic ADHF requiring hospitalization and treated with standard therapy containing intravenous ANP and 10 age-matched normal control subjects. ANP was continuously infused for >96 h. In all subjects, delayed total defect score (TDS), heart to mediastinum ratio, and washout rate were determined by 123I-metaiodobenzylguanidine (MIBG) scintigraphy. Left ventricular (LV) end-diastolic volume, end-systolic volume, and ejection fraction were determined by echocardiography. All patients with acute heart failure (AHF) were examined once within 3 days and then 4 weeks after admission, while the control subjects were examined only once (when their hemodynamics were normal). Moreover, for 62 AHF patients, plasma aldosterone concentrations were measured at admission and 1 h before stopping ANP infusion.
123I-MIBG scintigraphic and echocardiographic parameters in normal subjects were more favorable than those in patients with AHF (all p < 0.001). After treatment, all these parameters improved significantly in AHF patients (all p < 0.001). We also found significant correlation between percent changes of TDS and aldosterone concentrations (r = 0.539, p < 0.001) in 62 AHF patients.
The CSNA and LV performance were all improved in AHF patients. Furthermore, norepinephrine uptake of myocardium may be ameliorated by suppressing aldosterone production after standard treatment containing intravenous ANP.
醛固酮可阻止去甲肾上腺素在心肌中的摄取。心房利钠肽（ANP）是一种源自心脏的循环激素，可抑制培养心肌细胞中醛固酮合酶基因的表达。我们评估了静脉注射ANP对急性失代偿性心力衰竭（ADHF）患者心脏交感神经活动（CSNA）和醛固酮抑制的影响。
我们研究了182例需要住院治疗且接受含静脉注射ANP的标准治疗的中度非缺血性ADHF患者以及10名年龄匹配的正常对照者。持续输注ANP超过96小时。在所有受试者中，通过123I-间碘苄胍（MIBG）闪烁显像测定延迟总缺陷评分（TDS）、心纵隔比和洗脱率。通过超声心动图测定左心室（LV）舒张末期容积、收缩末期容积和射血分数。所有急性心力衰竭（AHF）患者在入院后3天内及入院后4周各检查一次，而对照者仅检查一次（当其血流动力学正常时）。此外，对62例AHF患者在入院时及停止ANP输注前1小时测量血浆醛固酮浓度。
正常受试者的123I-MIBG闪烁显像和超声心动图参数优于AHF患者（所有p < 0.001）。治疗后，AHF患者的所有这些参数均显著改善（所有p < 0.001）。我们还发现62例AHF患者中TDS百分比变化与醛固酮浓度之间存在显著相关性（r = 0.539，p < 0.001）。
AHF患者的CSNA和左心室功能均得到改善。此外，在接受含静脉注射ANP的标准治疗后，通过抑制醛固酮生成可能改善心肌对去甲肾上腺素的摄取。
