Table 1.

Studies relating well-known biomarkers for risk stratification in dilated cardiomyopathy.

Scheme	Population and Follow-Up	Characteristics	Clinical End Points	Results
High-sensitivity Cardiac Troponin-T (hs-cTnT)
Kawahara et al. [51]	-85 patients with NIDCM, prospective study, 4.1 years	-68.2% males, 59.1 ± 15 years; -LVEF 33.9% ± 7.6.	-23.53% cardiac deaths	-hs-cTnT was elevated (≥0.01 ng/mL) in 54% of the survivors and in 85% of the non-survivors, independent of LVEF or BNP.
Baba et al. [52]	-54 patients with DCM, prospective study, 5.1 ± 1.6 years	-79.6% males, 61.2 ± 13.5 years; -LVEF 37.9% ± 11.8.	-11.11% HF deaths; -3.70% SCD; -14.81% HF hospitalizations.	-elevated hs-cTnT values were associated with a greater risk of adverse cardiac events (p = 0.003), being useful for the prediction of LV remodeling or reverse remodeling.
N-terminal-pro Hormone BNP (NT-proBNP)
Tigen et al. [40]	-75 NIDCM patients, prospective study, 29 ± 16 months	-69.3% males, 40 ± 15 years; -LVEF 25.4% ± 7.4.	-38.66% HF deaths; -8% SCD; -6.66% heart transplantation.	-92.5% patients with clinical end points had right ventricular systolic dysfunction and/or plasma NT-proBNP > 1700 pg/mL; both of these parameters may help identify the very high-risk NIDCM patients.
Li et al. [19]	-622 DCM patients, retrospective cohort study, 2.6 ± 1.6 years	-73.5% males, 51.4 ± 14.6 years; -LVEF 31.1% ± 8.4.	-21.1% all-cause mortality.	-plasma NT pro-BNP and hs-CRP were strong predictors of all-cause mortality in DCM patients, independent of age, LV diameter, NYHA functional class and LVEF.
Soluble ST2 (sST2)
Binas et al. [30]	-262 DCM patients (44.7%-iDCM, 33.2%- ivDCM, 22.1%-fDCM) prospective cohort study, 3.9 years	-75.2% males, 50.2 ± 12.8 years; -LVEF 30% ± 8.4.	-all cause mortality: 14.5% in iDCM, 17.2% in ivDCM and 19% in fDCM; -cardiac mortality: 12% in iDCM, 11.5% in ivDCM and 15.5% in fDCM.	-sST2 predicts all-cause mortality and cardiac -mortality in patients with NIDCM and could be -useful especially in patients with inflammatory -myocardial disease and viral persistence.
Broch et al. [47]	-102 NIDCM patients, prospective study, 3.5 years	-73% males, 51 ± 14 years; -LVEF 26% ± 10.	-2.1% HF deaths; -2.1% SCD; -6.31% heart transplantation.	-sST2 was elevated in patients with severe symptoms, but did not vary with etiology, viral presence or the amount of myocardial fibrosis; thus, sST2 reflects hemodynamic stress rather than pathogenic processes in the myocardium.
Wojciechowska et al. [48]	-107 NIDCM patients, prospective study, 4.8± 0.4 years	-80.37% males, 50.3 ± 17.5 years; -LVEF 25% ± 10.	-25.2% deaths; -11.2% heart transplantation; -0.9% LVAD.	-increased sST2 levels are associated with death, heart transplantation and LVAD implantation, independent of NT-proBNP.
Galectin-3 (Gal-3)
Vergano et al. [25]	-150 NIDCM patients, prospective cohort study	-73% males, 58 ± 14 years; -LVEF 35% ± 13.	-not evaluated	-Gal-3 is involved in cardiac fibrosis and remodeling, contributing to the progression of the HF and in the selection of high-risk NIDCM patients.
Hu et al. [28]	-192 NIDCM patients (85 with DCM and 107 with HCM), prospective study, 7 years.	-75.5% males, -53.77 ± 15.07 years; -LVEF 42.6% ± 13.5 in DCM patients.	-in DCM patients: 4.7% deaths, 18.82% arrhythmic events and 7.05% aggravated HF.	-galectin-3 is involved in cardiac remodeling and progression of HF; Gal-3 with LGE status is capable of predicting clinical outcomes in patients with NIDCM

DCM—dilated cardiomyopathy; iDCM—idiopathic dilated cardiomyopathy; ivDCM—inflammatory and/or viral dilated cardiomyopathy; fDCM—familial dilated cardiomyopathy; HCM—hypertrophic cardiomyopathy; HF—heart failure; LV—left ventricle; LVAD—left ventricular assist device; LVEF—left ventricular ejection fraction; NIDCM—non-ischemic dilated cardiomyopathy; NT pro-BNP—N-terminal-pro hormone brain natriuretic peptide; NYHA—New York Heart Association; SCD—sudden cardiac death.