CCCardiol CroatCardiologia CroaticaCardiol. Croat.1848-543X1848-5448Croatian Cardiac SocietyCC_13(11-12)_35010.15836/ccar2018.350Extended AbstractCirculating levels of catestatin are significantly higher in heart failure patients with ischemic vs. non-ischemic cardiomyopathy: the role of catestatin as a compensatory marker of neurohumoral activationCirkulirajuće razine katestatina su značajno više u ishemijskoj u odnosu na neishemijsku etiologiju kardiomiopatije u bolesnika sa zatajivanjem srca: uloga katestatina kao kompenzatornog biljega neurohumoralne aktivacijehttps://orcid.org/0000-0002-4878-8146BorovacJosip Anđelo12*https://orcid.org/0000-0003-1634-0635BožićJoško1https://orcid.org/0000-0002-5584-3182Šupe DomićDaniela2https://orcid.org/0000-0001-9999-7557Sušilović GrabovacZora2http://orcid.org/0000-0003-2649-0936GlavašDuška12Medicinski fakultet Sveučilišta u Splitu, Split, HrvatskaKlinički bolnički centar Split, Split, HrvatskaUniversity of Split School of Medicine, Split, CroatiaUniversity Hospital of Split, Split, CroatiaADDRESS FOR CORRESPONDENCE: Josip Anđelo Borovac, Klinički bolnički centar Split, Spinčićeva 1, HR-210000 Split, Croatia. / Phone: +385-92-172-1314 / E-mail: jborovac@mefst.hr1120181311-1235035121092018051120182018Croatian Cardiac SocietyKLJUČNE RIJEČI: zatajivanje srcakatestatinneurohumoralna aktivacijaKEYWORDS: heart failurecatestatinneurohumoral activation
Introduction: Heart failure (HF) is a syndrome characterized by the activation of the complex cascade of neurohumoral mechanisms in order to maintain cardiac output. (1) Previous studies have shown that activation of a sympathetic nervous system (SNS) is more pronounced in patients with ischemic cardiomyopathy (IC) compared to those with non-ischemic cardiomyopathy (NIC). (2, 3) On the other hand, catestatin is a pleiotropic endogenous peptide that inhibits nicotinic receptor-mediated catecholamine release into the circulation and, therefore, exhibits inhibitory action on SNS activity. The main goal of the study was to determine and compare circulating catestatin levels among HF patients with IC and NIC.
Patients and Methods: This study included a total of 38 patients admitted to the University Hospital Centre Split during the March-June of 2018 with an acute decompensation of HF determined by the current diagnostic criteria for HF laid out in the European Society of Cardiology guidelines from 2016. Patients with the acute coronary syndrome and/or infectious disease were excluded. Serum levels of catestatin were determined by the enzyme-linked immunosorbent assay (ELISA).
Results: Twenty-one (55%) patient had IC while 17 (45%) had NIC. Both groups did not significantly differ in baseline anthropometric, clinical and echocardiographic parameters as well as medication intake (Table 1). Almost all patients were in NYHA III or IV class regarding the functional classification of HF (N=36, 95%). Patients with IC had significantly higher mean NYHA degree compared to NIC patients (3.4±0.6 vs. 3.1±0.4, p=0.039). Serum catestatin levels did not significantly differ between women and men (18.9 vs. 15.7 ng/mL, p=0.570). HF patients with IC had more than 2-fold higher catestatin serum levels compared to HF patients with NIC (22.8±20 vs. 10.6±8.5 ng/mL, p=0.025) (Figure 1). Catestatin showed positive significant correlation with NT-proBNP in a total sample of patients, independent of sex, age, body mass index and estimated glomerular filtration rate (r=0.516, p<0.001).
Baseline characteristics of heart failure patients with non-ischemic and ischemic etiology.
Variable
Non-ischemic, N=17
Ischemic, N=21
p-value
Male sex
8 (47.1%)
14 (66.7%)
0.145
Age (years)
67.1 ± 9.3
70.7 ± 12.2
0.310
BMI (kg/m2)
31.1 ± 5.6
28.9 ± 3.9
0.178
BSA (Mosteller, m2)
2.1 ± 0.19
2.1 ± 0.18
0.904
Systolic BP (mmHg)
135 ± 24
138.1 ± 26
0.705
Diastolic BP (mmHg)
83.5 ± 10
83.1 ± 12
0.909
Mean NYHA class
3.1 ± 0.4
3.4 ± 0.6
0.039
Urea (mmol/L)
11.6 ± 7.1
13.3 ± 7.4
0.499
eGFR CKD-EPI (mL/min/1.73 m2)
60.7 ± 26.1
48.4 ± 25
0.145
NT-proBNP (pg/mL)
8205 ± 6638
9858 ± 7783
0.746
CRP (mg/L)
23.4 ± 17.6
18.6 ± 20.4
0.628
Glucose, fasting (mmol/L)
8.4 ± 3.1
10.3 ± 4.4
0.134
LVEF (biplane Simpson, %)
35 ± 15
37 ± 14
0.697
LVEDd (mm)
61.4 ± 8.9
61.1 ± 8.8
0.894
LVESd (mm)
48 ± 11.2
47.1 ± 12.8
0.843
LA diameter (mm)
50.9 ± 8.8
51.3 ± 8.1
0.884
Comorbidities (%)
Arterial hypertension
15 (88.2%)
21 (100%)
0.106
Diabetes mellitus
4 (23.5%)
10 (47.6%)
0.126
Atrial fibrillation
9 (52.9%)
12 (57.1%)
0.796
Dyslipidemia
12 (70.6%)
13 (61.9%)
0.575
History of stroke or TIA
2 (11.8%)
3 (14.3%)
0.819
Peripheral artery disease
5 (29.4%)
3 (14.3%)
0.255
COPD
4 (23.5%)
2 (9.5%)
0.239
Medication use (%)
Aspirin
5 (41.2%)
13 (61.9%)
0.393
ACE-I or ARB
14 (82.4%)
15 (71.4%)
0.431
Beta-blocker
15 (88.2%)
19 (90.5%)
0.823
Diuretics
17 (100%)
20 (95.2%)
0.362
Calcium channel blocker
3 (17.6%)
3 (14.3%)
0.778
Statins
6 (35.3%)
10 (47.6%)
0.444
Abbreviations: ACE-I-angiotensin-converting-enzyme inhibitor; ARB-angiotensin II receptor blocker; BMI-body mass index; BP-blood pressure; BSA-body surface area; COPD-chronic obstructive pulmonary disease; CRP-C-reactive protein; LA-left atrium; LVEDd-left ventricular end-diastolic diameter; LVEF-left ventricular ejection fraction; LVESd-left ventricular end-systolic diameter; eGFR-estimated glomerular filtration rate; NT-proBNP-N-terminal prohormone of brain natriuretic peptide; NYHA-New York Heart Association functional classification of heart failure; TIA-transient ischemic attack.
Difference in mean catestatin serum level (ng/mL) between heart failure patients with ischemic and non-ischemic cardiomyopathy.
Conclusion: Significantly increased circulating catestatin levels in HF patients with ischemic etiology of the disease might indirectly reflect an increased neurohumoral activation in this population, as well as ventricular pressure overload.
LITERATURELymperopoulosARengoGKochWJ. Adrenergic nervous system in heart failure: pathophysiology and therapy. . 2013 Aug 30;113(6):739–53. 10.1161/CIRCRESAHA.113.30030823989716DengMCBrisseBErrenMKhuranaCBreithardtGScheldHH. Ischemic versus idiopathic cardiomyopathy: differing neurohumoral profiles despite comparable peak oxygen uptake. . 1997 Oct 10;61(3):261–8. 10.1016/S0167-5273(97)00163-09363742NotariusCFSpaakJMorrisBLFlorasJS. Comparison of muscle sympathetic activity in ischemic and nonischemic heart failure. . 2007 Aug;13(6):470–5. 10.1016/j.cardfail.2007.03.01417675061