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CLINICAL RESEARCH: BIOMARKERS

Serum Soluble ST2

A Potential Novel Mediator in Left Ventricular and Infarct Remodeling After Acute Myocardial Infarction

Robin A.P. Weir, MBChB (Hons), BSc (Hons), MD^_*,_*, Ashley M. Miller, PhD, Grace E.J. Murphy, MBChB, BMedSci (Hons), Suzanne Clements, RGN^_*, Tracey Steedman, BSc^_*, John M.C. Connell, PhD, Iain B. McInnes, PhD, Henry J. Dargie, MD^_* and John J.V. McMurray, MD^_*

^_* Cardiology Department, Western Infirmary, Glasgow, Scotland, United Kingdom
Division of Immunology, Infection, and Inflammation, Glasgow Biomedical Research Centre, University of Glasgow, Glasgow, Scotland, United Kingdom
MRC Blood Pressure Group, Glasgow Cardiovascular Research Centre, University of Glasgow, Glasgow, Scotland, United Kingdom

Manuscript received March 21, 2009; revised manuscript received July 13, 2009, accepted August 3, 2009.

^_* Reprint requests and correspondence: Dr. Robin A. P. Weir, Cardiology Department, Western Infirmary, Dumbarton Road, Glasgow G11 6NT, Scotland, United Kingdom (Email: robinweir75{at}hotmail.com).

Objectives: This study sought to assess, for the first time, the relationship between serum concentrations of the soluble interleukin-1 receptor family member ST2 (sST2) and serial change in left ventricular (LV) function after acute myocardial infarction (AMI).

Background: Serum sST2 levels are elevated early after AMI and are associated with lower pre-discharge LV ejection fraction and adverse cardiovascular outcomes.

Methods: The sST2 levels were measured in 100 patients (mean age 58.9 ± 12.0 years; 77% male), admitted with AMI with resultant LV systolic dysfunction, at baseline and at 12 and 24 weeks. Patients underwent cardiac magnetic resonance imaging and measurement of N-terminal pro-brain natriuretic peptide, norepinephrine, and aldosterone at each time point.

Results: Median sST2 decreased from 263.3 pg/ml at baseline to 140.0 pg/ml at 24 weeks (p < 0.001). Serum sST2 correlated significantly with LV ejection fraction at baseline (r = –0.30, p = 0.002) and 24 weeks (r = –0.23, p = 0.026); change in sST2 correlated with change in LV end-diastolic volume index (r = –0.24, p = 0.023). Level of sST2 was positively associated with infarct volume index at baseline (r = 0.26, p = 0.005) and 24 weeks (r = 0.22, p = 0.037), and with change in infarct volume index (r = –0.28, p = 0.001). Level of sST2 was significantly higher in patients with greater infarct transmurality and endocardial extent, and in the presence of microvascular obstruction. Level of sST2 correlated significantly with norepinephrine and aldosterone, but not with N-terminal pro-brain natriuretic peptide.

Conclusions: Measurement of sST2 early after AMI assists in the prediction of medium-term LV functional recovery. Novel relationships were observed between sST2, infarct magnitude/evolution, and aldosterone. Serum sST2 may be of pathophysiological importance in ventricular and infarct remodeling after AMI. (Effects of Eplerenone on Left Ventricular Remodelling Following Heart Attack; NCT00132093)

Key Words: ST2 • cardiac magnetic resonance • myocardial infarction • remodeling • aldosterone

Abbreviations and Acronyms   AMI = acute myocardial infarction   ceCMR = contrast-enhanced cardiac magnetic resonance   CMR = cardiac magnetic resonance   IL = interleukin   LV = left ventricle/ventricular   LVEDVI = left ventricular end-diastolic volume index   LVEF = left ventricular ejection fraction   LVESVI = left ventricular end-systolic volume index   LVMI = left ventricular mass index   LVSD = left ventricular systolic dysfunction   MBL = Medical and Biological Laboratories   MVO = microvascular obstruction   NT-proBNP = N-terminal pro-brain natriuretic peptide   sST2 = soluble ST2   STEMI = ST-segment elevation myocardial infarction

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