Abstract
The role of catestatin (CST) in acutely decompensated heart failure (ADHF) and myocardial infarction (MI) is poorly elucidated. Due to the implicated role of CST in the regulation of neurohumoral activity, the goals of the study were to determine CST serum levels among ninety consecutively enrolled ADHF patients, with respect to the MI history and left ventricular ejection fraction (LVEF) and to examine its association with clinical, echocardiographic, and laboratory parameters. CST levels were higher among ADHF patients with MI history, compared to those without (8.94 ± 6.39 vs. 4.90 ± 2.74 ng/mL, p = 0.001). CST serum levels did not differ among patients with reduced, midrange, and preserved LVEF (7.74 ± 5.64 vs. 5.75 ± 4.19 vs. 5.35 ± 2.77 ng/mL, p = 0.143, respectively). In the multivariable linear regression analysis, CST independently correlated with the NYHA class (β = 0.491, p < 0.001), waist-to-hip ratio (WHR) (β = −0.237, p = 0.026), HbA1c (β = −0.235, p = 0.027), LDL (β = −0.231, p = 0.029), non-HDL cholesterol (β = −0.237, p = 0.026), hs-cTnI (β = −0.221, p = 0.030), and the admission and resting heart rate (β = −0.201, p = 0.036 and β = −0.242, p = 0.030), and was in positive association with most echocardiographic parameters. In conclusion, CST levels were increased in ADHF patients with MI and were overall associated with a favorable cardiometabolic profile but at the same time reflected advanced symptomatic burden (CATSTAT-HF ClinicalTrials.gov number, NCT03389386).
Highlights
Acute decompensated heart failure (ADHF) is a complex clinical syndrome associated with high morbidity, mortality, and healthcare expenditures [1,2,3]
Out of 118 consecutive patients that presented with acute dyspnea, a total of 90 patients were included in the final analysis, after applying the study exclusion criteria (Figure 1)
Results of this study are novel for this population and suggest that the role of CST in HF is complex and multidimensional
Summary
Acute decompensated heart failure (ADHF) is a complex clinical syndrome associated with high morbidity, mortality, and healthcare expenditures [1,2,3]. Viquerat et al showed that levels of endogenous norepinephrine and dopamine are elevated in patients with congestive heart failure (HF), compared to the healthy controls, reflecting an increased sympathetic nervous system (SNS) activity [5]. Among patients with established HF, activation of the SNS, renin-angiotensin-aldosterone system (RAAS), and T-cell-mediated immune response is higher among those with ischemic etiology of the disease compared to non-ischemic idiopathic dilated cardiomyopathy [6]. Previous studies have demonstrated that high levels of CST might reflect increased sympathoadrenal activity [11,12,13], are associated with increased mortality in HF [14,15], and are a marker of poor ventricular remodeling after myocardial infarction (MI) [16]. CST levels were associated with disease severity in HF [17,18] and were similar between patients with preserved (HFpEF) and reduced (HFrEF) left ventricular ejection fraction (LVEF) phenotypes [17]
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