Background: Inflammation is essential in cardiorenal syndrome, however
there is still a lack of evidence proving the interaction between cardiac injury,
renal dysfunction and the inflammatory response. This study aimed to illustrate
the association between renal dysfunction and cardiac injury with a specific
focus on the role of inflammation. Methods: A single-center,
retrospective study included patients with heart failure admitted to the
cardiovascular department from September 2019 to April 2022. Patients received
cardiovascular magnetic resonance (CMR) imaging (T1 mapping and late gadolinium
enhancement (LGE)). Demographic, creatinine and native T1 were analyzed using
pearson correlation, linear regression and adjusted for confounders. Interaction
and subgroup analysis were performed. Results: Finally, 50 validated
heart failure (HF) patients (age 58.5 14.8 years; 78.0% men) were
included. Cardiac global native T1 for the high estimated glomeruar filtration
rate (eGFR) group was 1117.0 56.6 ms, and for the low eGFR group was
1096.5 61.8 ms. Univariate analysis identified global native T1
( = 0.16, 95% confidence interval (CI): 0.04–0.28, p = 0.014)
and C-reactive protein (CRP) ( = 0.30, 95% CI: 0.15–0.45, p 0.001) as determinants of creatinine. Multivariable linear regression
analysis identified global native T1 ( = 0.12, 95% CI: 0.01–0.123,
p = 0.040) as a determinant of creatinine
while age and diabetes were adjusted. Significant interactions between CRP and
global native T1 in relation to creatinine level (p for interaction =
0.005) were identified. Conclusions: Kidney dysfunction was associated
with cardiac injury and inflammation, respectively. The interaction between
myocardial injury and kidney dysfunction is contingent on the severity of the
inflammatory response. Further studies were needed to identify the mechanisms of
the inflammatory response in cardiorenal syndrome.