Catestatin in Acutely Decompensated Heart Failure Patients: Insights from the CATSTAT-HF Study

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).

Serum Catestatin Levels and Arterial Stiffness Parameters Are Increased in Patients with Inflammatory Bowel Disease

“…Furthermore, it has been reported to be a key regulator of cardiovascular function, with cardioprotective effects including exhibiting the trough suppression of atherosclerosis [21], negative inotropic and lusitropic cardiac effects [22], inhibition of coronary vasoconstriction [21], a reduction in oxidative stress in ischemic-reperfused myocardium [22], a decrease in endothelial inflammation and regulation of blood pressure [10,[23][24][25]. CST is believed to have an important role in the pathophysiology of hypertension, heart failure, reperfusion injury and coronary heart disease [25][26][27]. Intestinal inflammation has been associated with dysfunctional ChgA production [28].…”

Plasma catestatin level predicts sPESI score and mortality in acute pulmonary embolism

“…These activities may give rise to the blood pressure-and heart rate-lowering functions of this endogenous peptide. Because CST is accepted as a part of the complex neurohumoral compensatory feedback system, higher levels of this peptide in peripheral blood might indirectly reflect increased neurohumoral burden [16]. However, it may be insufficiently compensatory when the level of CST increases in patients with APE.…”

“…In another study, it was suggested that catestatin might be a novel marker reflecting LV remodelling in the myocardium following AMI [19]. Boravac et al found that among patients with acutely decompensated heart failure, serum catestatin levels were higher [16]. They explained that higher CST levels are associated with beneficial metabolic and cardioprotective effects, but high CST levels reflect higher disease severity and probably parallel increased neurohumoral activity that might translate to adverse outcomes during the natural course of the disease.…”

“…CHGA is a protein located mainly in the secretory particles of chromaffin cells, postganglionic sympathetic neurons, and heart cells, where it is co-stacked and co-discharged with catecholamines [13][14][15]. CST is accepted as a part of the complex neurohumoral compensatory feedback system; higher levels of this peptide in peripheral blood might indirectly reflect increased neurohumoral burden [16]. For a long time it has been shown that CST can play a role in cardiovascular diseases such as hypertension, acute coronary syndrome, and cardiac remodelling [17][18][19], but there has been no study to investigate the role of CST in APE.…”

The chromogranin A-derived peptides catestatin and vasostatin in dogs with myxomatous mitral valve disease

“…Several studies have shown increased catestatin concentrations in people with acute myocardial infarction [15][16][17][18]. In contrast to the acute course in human myocardial infarction, the common canine cardiac disease MMVD is characterized by a slow but progressive disease development, usually over several years, eventually leading to development of CHF in some dogs [20,23].…”