Compelling Benefit of Soluble Suppression of Tumorigenicity‐2 in Post–Myocardial Infarction Estimation of Risk: The Time Is Right for Its Routine Use in the Clinic

I t is estimated that in the United States, each year, >780 000 people will experience an acute coronary syndrome. Approximately 70% of these people will have a non–ST-elevated myocardial infarction (NSTEMI), and the rest will have an ST-elevated myocardial infarction (STEMI). Patients with NSTEMI typically have more comorbidities, both cardiac and noncardiac, than patients with STEMI. In both STEMI and NSTEMI, risk estimation by current guidelines recommends the use of the TIMI (Thrombolysis in Myocardial Infarction) or GRACE (Global Registry of Acute Cardiac Events) risk scores. The TIMI risk score is composed of 7, 1-point risk indicators (≥65 years of age, ≥3 risk factors for coronary artery disease, prior coronary stenosis ≥50%, ST deviation on ECG, ≥2 anginal events in prior 24 hours, use of aspirin in prior 7 days, and elevated cardiac enzyme levels), and it has been validated internally within the TIMI 11B trial and in 2 separate cohorts of patients from the ESSENCE (Efficacy and Safety of Subcutaneous Enoxaparin in Non–QWave Coronary Events) trial, published 20 years ago. The TIMI risk score calculator is available at http://www.timi.org. The GRACE risk model predicts in-hospital and postdischarge mortality of MI. The GRACE tool was developed from 11 389 patients in GRACE and validated in subsequent GRACE and GUSTO (Global Utilization of Streptokinase and TPA [Tissue Plasminogen Activator] for Occluded Arteries) IIb cohorts, also reported a couple of decades ago. The GRACE clinical application tool is available at http://www.outcomesumassmed.org/grace. During the past 2 decades, since these scores were developed, several things have changed in the management of patients with STEMI and NSTEMI, as well as the phenotype of these patients, who are generally older and have more comorbidities. Remarkably, biomarkers have entered into the center stage in cardiovascular diseases. Among them, natriuretic peptides (NPs) have had a successful path from research studies to clinical guidelines and routine implementation, mainly to rule in and rule out heart failure (HF). Despite the versatility of NPs, other biomarkers have provided additional and complementary information. The soluble suppression of tumorigenicity-2 (sST2) protein is one such biomarker. It is regarded as a 3-in-1 biomarker because of its comprehensive added value in cardiovascular pathological features. In the setting of NSTEMI, higher sST2 levels are associated with an increased risk of adverse outcomes. In a study of 577 patients with NSTEMI, predischarge sST2 levels provided independent prediction of 18-month risk of death, HF admission, or reinfarction. Subsequently, a substudy from the larger MERLIN (Metabolic Efficiency with Ranolazine for Less Ischemia in Non-ST-Elevation Acute Coronary Syndromes)TIMI 36 study of 4426 high-risk patients with NSTEMI found that sST2 levels were independently associated with increased risk of cardiovascular death or new/worsened HF at 30 days and 1 year. In this study, sST2 levels remained predictive of risk, even after adjusting for NP and troponin levels. In patients with STEMI, several studies have found that sST2 levels are independently associated with an increased risk of death or HF. This risk appears to be additive to standard risk factors and NP levels. ST2 levels in patients with STEMI also improved on short-term risk prediction using the GRACE score and NP levels, with significant improvement in risk discrimination when all 3 were combined. Remarkably, in the setting of an acute MI with HF signs or symptoms, an sST2 level >35 ng/mL before discharge identified the The opinions expressed in this article are not necessarily those of the editors or of the American Heart Association. From the Program of Cardiovascular Diseases, Center for Applied Medical Research (J.D.), and Department of Cardiology and Cardiac Surgery, University Clinic (J.D.), University of Navarra, Pamplona, Spain; Centro de Investigaci on Biom edica en Red Enfermedades Cardiovasculares (CIBERCV), Instituto de Salud Carlos III, Madrid, Spain (J.D., A.B.-G.); Heart Institute, Hospital Universitari Germans Trias i Pujol, Badalona, Spain (A.B.-G.); and Department of Medicine, Autonomous University of Barcelona, Barcelona, Spain (A.B.-G.). Correspondence to Javier D ıez, MD, PhD, Program of Cardiovascular Diseases, Center for Applied Medical Research, University of Navarra, Pamplona, Spain. E-mail: [email protected] J Am Heart Assoc. 2017;6:e007665 DOI: 10.1161/JAHA.117.007665. a 2017 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley. This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.