American journal of translational research · 2026
Application of 131I-MIBG imaging in assessing renal sympathetic overdrive in heart failure with preserved ejection fraction (HFpEF).
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Yang Zhiqiang, Li Yue, Yin Pei, Zhao Qingzhen, Zhen Yuzhi, Liu Ruisi, Li Lizhuo, Liu Chao
Аннотация
OBJECTIVE: To quantitatively assess cardiac and renal sympathetic nerve activity using 131I-metaiodobenzylguanidine (MIBG) imaging, in patients with heart failure with preserved ejection fraction (HFpEF) diagnosed via left heart catheterization, compared with matched controls.
METHODS: The study enrolled 18 HFpEF patients (diagnosed via left heart catheterization for exertional dyspnea as the test group) and 10 matched controls. All subjects underwent cardiac and renal 131I-MIBG imaging. We measured early (15 min, reflecting nerve density/uptake) and delayed (4 h, reflecting neurotransmitter storage/turnover) kidney-to-mediastinum (K/M) and heart-to-mediastinum (H/M) ratios, as well as washout rates (WR).
RESULTS: Invasive hemodynamic measurements showed elevated mean left ventricular end-diastolic pressure (mLVEDP) in the test group [21 (18, 24) mmHg vs. 7.5 (5, 8) mmHg, P < 0.05]. Notably, 131I-MIBG imaging indicated significantly higher renal sympathetic activation in the test group during both the early and delayed phases (K/M15min: 10.5 ± 2.5 vs. 3.7 ± 0.45 and K/M4h: 8.1 ± 3.3 vs. 4.6 ± 0.3, P < 0.05), the former being approximately two to three times greater than the latter. This hypersympathetic state significantly paralleled the elevation in LAD and mLVEDP (P < 0.05), indicating a direct link between renal neuro-overactivity and cardiac diastolic impairment.
CONCLUSIONS: 131I-MIBG imaging successfully quantifies renal-cardiac sympathetic crosstalk in HFpEF. The markedly elevated K/M ratios demonstrate that renal sympathetic overactivity is a core driver of hemodynamic congestion in these patients. Clinically, this technique may serve as a powerful non-invasive biomarker to identify candidates for sympatho-inhibitory therapies and provides a precise tool for monitoring therapeutic efficacy in HFpEF management.
METHODS: The study enrolled 18 HFpEF patients (diagnosed via left heart catheterization for exertional dyspnea as the test group) and 10 matched controls. All subjects underwent cardiac and renal 131I-MIBG imaging. We measured early (15 min, reflecting nerve density/uptake) and delayed (4 h, reflecting neurotransmitter storage/turnover) kidney-to-mediastinum (K/M) and heart-to-mediastinum (H/M) ratios, as well as washout rates (WR).
RESULTS: Invasive hemodynamic measurements showed elevated mean left ventricular end-diastolic pressure (mLVEDP) in the test group [21 (18, 24) mmHg vs. 7.5 (5, 8) mmHg, P < 0.05]. Notably, 131I-MIBG imaging indicated significantly higher renal sympathetic activation in the test group during both the early and delayed phases (K/M15min: 10.5 ± 2.5 vs. 3.7 ± 0.45 and K/M4h: 8.1 ± 3.3 vs. 4.6 ± 0.3, P < 0.05), the former being approximately two to three times greater than the latter. This hypersympathetic state significantly paralleled the elevation in LAD and mLVEDP (P < 0.05), indicating a direct link between renal neuro-overactivity and cardiac diastolic impairment.
CONCLUSIONS: 131I-MIBG imaging successfully quantifies renal-cardiac sympathetic crosstalk in HFpEF. The markedly elevated K/M ratios demonstrate that renal sympathetic overactivity is a core driver of hemodynamic congestion in these patients. Clinically, this technique may serve as a powerful non-invasive biomarker to identify candidates for sympatho-inhibitory therapies and provides a precise tool for monitoring therapeutic efficacy in HFpEF management.