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. 2020 Mar 16;6:e02. doi: 10.15420/cfr.2019.10

Table 2: Studies Investigating the Association Between sST2 and a Variety of Clinical Features in HFpEF.

Study n Type of Analysis LVEF Clinical Features
Significant Correlation No Significant Correlation
Shah et al. 2011[47] 200 Post hoc ≥50% Association between increased baseline sST2 levels and:

  • ↑ age (p=0.001)

  • ↓ eGFR (p=0.002)

  • ↑ CRP (p<0.001)

  • ↑ MPO (p=0.004)

  • ↑ NT-proBNP (p<0.001)

  • ADHF diagnosis (p=0.001)

  • ↑ E/E’ (p=0.01)

 No association between increased baseline sST2 levels and:

  • male sex (p=0.8)

  • BMI (p=0.9)

  • SBP and DBP (p=0.7 and p=0.6)

  • African-American (p=0.5)

  • cTnI (p<0.1)

  • other echocardiographic indices
Manzano-Fernández et al. 2011[48] 197 Retrospective ≥50% Association between increased baseline sST2 levels and:

  • ↑ leukocytes (p=0.01)

  • ↑ creatinine (p=0.015)

  • ↓ eGFR (p=0.01)

  • ↑ CRP (p<0.001)

  • ↑ NT-proBNP (p<0.001)

  • ↑ cTnT (p=0.001)

 No association between increased baseline sST2 levels and:

  • age (p=0.65)

  • BMI (p=0.94)

  • SBP and DBP (p=0.47 and p=0.13)

  • HR (p=0.19)

  • Hb (p=0.09)

  • BUN (p=0.08)

  • LV end-systolic and end-diastolic diameter (p=0.16 and p=0.49)

  • RV systolic pressure (p=0.08)
Zile et al. 2016[54] 301 Post hoc (PARAMOUNT) ≥45% Association between increased baseline sST2 levels and:

  • ↑ NT-proBNP (p=0.002)

  • ↓ eGFR (p=0.005)

  • ↑ galectin-3 (p<0.001)

  • ↑ LA volume (p<0.001; p=0.02*)

  • female sex (p<0.001*)

  • ↑ NYHA class (p=0.002*)

 No association between increased baseline sST2 levels and:

  • SBP (p=0.64)

  • E/A (p=0.11)

  • E´ (p=0.31)

  • E/E´ (p=0.09)
AbouEzzedine et al. 2017[55] 174 Post hoc (RELAX) ≥50% Association between increased baseline sST2 levels and:

  • diabetes (p=0.005†), hypertension (p=0.023†), AF/flutter (p=0.049†), renal dysfunction (p<0.0001†)

  • treatment with diuretics (p=0.013†)

  • ↑ NT-proBNP (p<0.0001†)

  • higher prevalence of jugular venous pressure elevation (p=0.003†)

  • increased peripheral oedema (p=0.0006†)

  • ↑ NYHA class (p=0.029†)

  • higher RV systolic pressure (p=0.016†) and worse RV function (p=0.015†)

  • ↑ endothelin-1 (p<0.0001†)

  • ↑ CRP (p=0.002†)

  • ↑ C-telopeptide for type 1 collagen (p=0.0004†)

  • ↑ cTnI (p<0.0001†)

 No association between increased baseline sST2 levels and:

  • LV diastolic or systolic function

  • aldosterone

  • pro-collagen III N-terminal peptide
Nagy et al. 2018[59] 86 Retrospective ≥45% Association between increased sST2 levels 4–8 weeks (stable condition) after enrolment and:

  • ↓ LA-GS

  • ↓ RV function

  • ↑ NYHA class

 No association between increased sST2 levels 4–8 weeks (stable condition) after enrolment and:

  • degree of LA enlargement

  • indices of LV geometrical diameters

  • LV systolic functional parameters

  • measures of LV relaxation and end-diastolic function

  • indices of AV coupling and systemic vascular function

  • creatinine

  • eGFR
Najjar et al. 2019[50] 86 Retrospective ≥45% Association between increased sST2 levels 4–8 weeks (stable condition) after enrolment and:

  • ↑ NT-proBNP (p<0.001)

  • ↑ NYHA class (p=0.005)

  • ↑ LAVI (p=0.019)

 No association between increased sST2 levels 4–8 weeks (stable condition) after enrolment and:

  • age (p=0.295)

  • eGFR (p=0.513)

  • mean arterial pressure (p=0.668)

  • BMI (p=0.301)

  • E/E´ (p=0.248)

  • LVMI (p=0.795)

  • LVEF (p=0.634)
Sugano et al. 2019[51] 191 Post hoc (ICAS-HF) ≥50% Association between increased baseline sST2 levels and:

  • male sex (p=0.02)

  • ↓ BMI (p=0.02)

  • ↓ albumin (p<0.001)

  • ↓ Hb (p=0.02)

  • ↓ potassium (p=0.04)

  • ↑ CRP (p=0.02)

  • ↑ pentraxin3 (p<0.001)

  • ↑ noradrenaline (p=0.005)

  • ↑ BNP (p<0.001)

  • ↑ tricuspid regurgitation pressure gradient (p=0.01)

 No association between increased baseline sST2 levels and:

  • age (p=0.20)

  • body weight (p=0.11)

  • HR (p=0.35)

  • comorbidities: AF (p=0.28), coronary artery disease (p=0.19), hypertension (p=0.22), COPD (p=0.51), diabetes (p=0.32)

  • medications: beta-blocker (p=0.84), ACE inhibitor or ARB (p=0.73), diuretics (p=0.69), aldosterone antagonist (p=0.09), statin (p=0.15)

  • eGFR (p=0.35)

  • sodium (p=0.56)

  • total cholesterol (p=0.63)

  • HbA1c (p=0.13)

  • plasma aldosterone (p=0.12)

  • plasma renin activity (p=0.054)

  • other echocardiographic indices

*Multivariable analysis adjusted for age, sex, NYHA class, history of AF, diastolic blood pressure, eGFR, log NT-proBNP, E/E’ and LA volume. †Adjusted for sex. ADHF = acute decompensated heart failure; BNP = brain natriuretic peptide; BUN = blood urea nitrogen; COPD = chronic obstructive pulmonary disease; CRP = C-reactive protein; cTnI = cardiac troponin I; cTnT = cardiac troponin T; DBP = diastolic blood pressure; E’ = mean value of the lateral and septal mitral annular early diastolic velocity; E/A = ratio between early diastolic inflow velocity (E)/inflow velocity due to atrial contraction (A); E/E’ = early diastolic tissue velocity; eGFR = estimated glomerular filtration rate; Hb = haemoglobin; HFpEF = heart failure with preserved ejection fraction; HR = heart rate; LA = left atrium; LA-GS = left atrial global strain; LAVI = left atrial volume index; LV = left ventricle; LVEF = left ventricular ejection fraction; LVMI = left ventricular mass index; MPO = myeloperoxidase; NT-proBNP = N-terminal prohormone of brain natriuretic peptide; NYHA = New York Heart Association; RV = right ventricle; SBP = systolic blood pressure; sST2 = soluble suppression of tumourigenicity 2.