Effect of Inflammation on Amino Acid Profile in Heart Failure Patients

Inflammation and Amino Acid Profile in Heart Failure

Abstract

Background: Heart failure (HF) is a clinical syndrome which caused by a structural and/or functional cardiac abnormality, resulting in a decreased cardiac output. The pathophysiology of HF is quite complex, and inflammation play a critical role in the development and progression of HF. Heart can use many substrates including fatty acids, glucose, ketone bodies and amino acids (AAs) to meet its high energy demand. However, the metabolism of the substrates that heart use for energy demand change dramatically in HF. Studies demonstrated that the heart's dependence on AAs increased during HF and plasma AAs profile could have significant impact on the risk-stratifying in patients with HF. However, the underlying mechanism of impaired AAs metabolism in HF has not been clearly elucidated yet. The aim of our study is to evaluate the AAs profile in HF patients and to demonstrate the effect of inflammation on the AA profile.

Methods: Seventy-two patients with compensated HF and 64 age- and sex-matched healthy individuals were included in our study as the control group. A new marker, CRP/albumin ratio (CAR), was used to assess inflammation. High performance liquid chromatography technique was used to evaluate the AA profile.

Results: When compared to the control group, valine (P = 0.040), leucine (P <0.001) and methionine values ​​(P = 0.001) were significantly lower, whereas phenylalanine (P <0.001), tyrosine (P = 0.027), asparagine ( P <0.001), arginine (P <0.001), glycine (P = 0.006) and ornithine (P = 0.035) values ​​were higher in patients with HF. Also, CAR level (P < 0.001) was significantly higher in HF patients than in the control group. The best cut-off value of CAR for predicting HF was determined as 0.91 according to the ROC curve analysis. Our patient group with HF was divided into 2 groups according to this cut-off value. HF patients with CAR ≥0.91 were defined as the high inflammation group, and HF patients with CAR <0.91 were defined as the low inflammation group. When compared to low inflammation group, HF patients with high inflammation had significantly lower valine (P < 0.001) and leucine (P < 0.001), whereas higher phenylalanine (P < 0.001), tyrosine (P < 0.001), asparagine (P < 0.001) 0.001) and ornithine (P = 0.006). In correlation analysis, CAR level was negatively correlated with valin, leucine and methionine, whereas positively correlated with phenylalanine, tyrosine and asparagine. Leucine (odds ratio [OR]: 0.955, 95% Confidence interval [CI]: 0.929-0.981, P = 0.001) phenylalanine (OR: 1.142, 95% CI: 1.070-1.218, P <0.001) and asparagine (OR: 1.053, 95% CI: 1.025-1.082, P <0.001) were detected as the independent predictors of HF in multivariate logistic regression analysis showed that.

Conclusions: Significant changes occur in the AA profile in HF. In our study; we found that the impairment in AA metabolism was more pronounced in patients with higher inflammation compared to patients with lower inflammation. Therefore, it can be suggested that the main mechanism underlying the impaired AA profile in HF is increased inflammation.