Close linkage between blood total ketone body levels and B-type natriuretic peptide levels in patients with cardiovascular disorders.

Close linkage between blood total ketone body levels and B-type natriuretic peptide levels in patients with cardiovascular disorders.
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DOI:
10.1038/s41598-021-86126-0
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发表时间:
2021-03-22
期刊:
影响因子:
4.6
通讯作者:
Yoshimura M
Yoshimura M
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Kashiwagi Y;Nagoshi T;Inoue Y;Tanaka Y;Takahashi H;Oi Y;Kimura H;Minai K;Yoshimura M

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在患有心血管疾病的患者中,血液总酮体(TKB)水平随着心力衰竭的恶化而增加,并作为脂肪酸和葡萄糖的替代燃料而被消耗。我们研究了导致心血管疾病患者血液 TKB 水平升高的因素。研究人群由 1030 名连续接受心导管插入术的患者组成。进行协方差结构分析,通过排除其他混杂因素,阐明血流动力学参数,包括左心室舒张末期压力(LVEDP)、左心室收缩末期容积指数(LVESVI)、左心室舒张末期容积指数(LVEDVI)和B型利钠肽(BNP)水平对TKB的直接贡献。这些分析表明,TKB 水平与 BNP 水平显着相关(P = 0.003),但与 LVEDP、LVESVI 或 LVEDVI 水平无关。贝叶斯结构方程模型在二维轮廓线上清楚地证明了这一点。 TKB 水平与 BNP 水平呈正相关,但 LVEDP、LVESVI 或 LVEDVI 不呈正相关。这些发现表明,BNP 增加比血流动力学恶化更能强烈刺激血液 TKB 水平升高。 BNP 可能会引起 TKB 水平升高,作为衰竭心脏的重要替代燃料。
In patients with cardiovascular disorders, blood total ketone body (TKB) levels increase with worsening heart failure and are consumed as an alternative fuel to fatty acid and glucose. We investigated factors contributing to the increase in the blood TKB levels in patients with cardiovascular disorders. The study population consisted of 1030 consecutive patients who underwent cardiac catheterization. Covariance structure analyses were performed to clarify the direct contribution of hemodynamic parameters, including the left ventricular end-diastolic pressure (LVEDP), left ventricular end-systolic volume index (LVESVI), left ventricular end-diastolic volume index (LVEDVI), and B-type natriuretic peptide (BNP) levels, to TKB by excluding other confounding factors. These analyses showed that the TKB levels were significantly associated with the BNP level (P = 0.003) but not the LVEDP, LVESVI, or LVEDVI levels. This was clearly demonstrated on a two-dimensional contour line by Bayesian structure equation modeling. The TKB level was positively correlated with the BNP level, but not LVEDP, LVESVI or LVEDVI. These findings suggested that elevated blood TKB levels were more strongly stimulated by the increase in BNP than by hemodynamic deterioration. BNP might induce the elevation of TKB levels for use as an important alternative fuel in the failing heart.
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