Associations between b-type natriuretic peptide and multiorgan native T1 mapping in heart failure with preserved ejection fraction
M Kobayashi, A Tezuka, R Ikeda, H Kosuge, K SatomiAbstract
Background
Heart failure (HF) and preserved ejection fraction (HFpEF) is proposed as a syndrome where systemic inflammation and fibrosis are disseminated to the kidney, liver and heart, while congestion is likely a key driver of inflammation and fibrosis in their tissues. Native T1 mapping allows non-invasive assessment of tissue abnormalities related to inflammation and fibrosis across organs.
Aims
To assess the association between B-type natriuretic peptide (BNP), as key biomarker of hemodynamic congestion, and native T1 values of the kidney, liver, and heart in patients at risk of or with HFpEF.
Methods
We studied patients at risk of or with HF and a left ventricular ejection fraction (LVEF) >40% who underwent cardiovascular magnetic resonance with native T1 mapping of the renal cortex and medulla, liver, and myocardium. Associations between BNP levels and organ-specific T1 values were assessed.
Results
Among 192 included patients (mean age 64±15 years and 66% male), the mean body mass index (BMI) was 24±5 kg/m2, and median BNP was 115 (47-271) pg/ml. Mean native T1 values were 1357±154 ms for the renal cortex, 1739±172 ms for the renal medulla, 798±138 ms for the liver, and 1246±71 ms for the myocardium. After adjustment for potential confounders (i.e., age, BMI, kidney function and FIB-4 index, laboratory-based fibrotic index), higher BNP levels were significantly associated with higher renal cortical, renal medulla, hepatic, and myocardial native T1 values (all-P values <0.05). During median follow-up period of 562 days (242-890), higher BNP levels were associated with higher risk of all-cause mortality or HF hospitalization, regardless of the severity of their T1 vales (all P for interaction>0.10).
Conclusion
In patients at risk of or with HFpEF, higher BNP levels were independently associated with increased native T1 values in the kidney, liver, and heart, as well as with worse clinical outcomes, irrespective of organ-specific T1 severity. These findings support a close link between hemodynamic congestion and multi-organ inflammation and fibrosis, and underscore the importance of targeting congestion even at subclinical stages of HFpEF.