Elsevier

The American Journal of Medicine

Volume 130, Issue 9, September 2017, Pages 1112.e9-1112.e15
The American Journal of Medicine

AJM online
Clinical research study
Prognostic Value of Soluble ST2 After Myocardial Infarction: A Community Perspective

https://doi.org/10.1016/j.amjmed.2017.02.034Get rights and content

Abstract

Background

Soluble ST2 (sST2) is a marker of cardiac mechanical strain hypothesized to adversely impact short-term prognosis after myocardial infarction. We examined the association of sST2 with longer-term outcomes after myocardial infarction in a geographically defined community.

Methods

Olmsted County, Minnesota residents who experienced an incident (first-ever) myocardial infarction between November 1, 2002 and December 31, 2012 were prospectively enrolled; sST2 levels were measured. Patients were followed for heart failure and death.

Results

We studied 1401 patients with incident myocardial infarction (mean age 67 years; 61% men; 79% non-ST-elevation myocardial infarction). Median sST2 (ng/mL) was 48.7 (25th-75th percentile 32.5-103.3). Soluble ST2 was elevated in 51% of patients. Higher values of sST2 were associated with increased age, female sex, and comorbidities. During 5 years of follow-up, 388 persons died and 360 developed heart failure. After adjustment for age, sex, comorbidities, Killip class, and troponin T, the hazard ratios for death were 1.73 (95% confidence interval [CI], 1.22-2.45) and 3.57 (95% CI, 2.57-4.96) for sST2 tertiles 2 and 3, respectively (Ptrend <.001). For heart failure, the hazard ratios were 1.67 (95% CI, 1.18-2.37) and 2.88 (95% CI, 2.05-4.05), respectively (Ptrend <.001). Results were similar among 30-day survivors.

Conclusions

In the community, sST2 elevation is present in half of myocardial infarctions. Higher values of sST2 are associated with a large excess risk of death and heart failure independently of other prognostic indicators. Measurement of sST2 should be considered for risk stratification after myocardial infarction.

Section snippets

Study Setting

This prospective community surveillance study was conducted in Olmsted County, Minnesota and utilized the resources of the Rochester Epidemiology Project. The Rochester Epidemiology Project is a medical records linkage system that links and archives the medical records of nearly all persons living in the county.6 All medical diagnoses are maintained through an electronic index, and patients can be identified through their in- and outpatient contacts across the local medical providers.7 This

Results

A total of 1401 patients with incident myocardial infarction between November 2002 and December 2012 and stored samples for sST2 measurement were included in the study. The mean (SD) age was 67.3 (14.9) years, 61% were male, and 79% presented with non-ST-elevation myocardial infarction. The median sST2 value (ng/mL) was 49 (25th-75th percentiles, 33-104); 720 patients (51%) were considered to have elevated sST2, compared with published normal values.23

Higher values of sST2 were associated with

Discussion

To the best of our knowledge, we report herein on the largest community study to date, which evaluated, among incident myocardial infarction, the frequency of sST2 elevation, its clinical correlates, and its prognostic value. Our findings that, in a nonselected geographically defined cohort, sST2 is elevated in more than half of the patients presenting with an incident myocardial infarction, were unexpected. The substantial increase in the risk of death and heart failure with increasing levels

Conclusion

In this community cohort, sST2 is elevated in more than half of patients with incident myocardial infarction. Higher values of sST2 confer a markedly adverse prognosis characterized by a large excess risk of death and heart failure over a long period of follow-up. Measurement of sST2 should be considered as part of contemporary approaches to risk stratification after myocardial infarction.

Acknowledgment

We thank Susan Stotz, RN, Ellen Koepsell, RN, and Deborah Strain for their study support.

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  • Funding: This work was supported by a grant from the National Heart, Lung, and Blood Institute (NHLBI; HL120957), Bethesda, MD and The Rochester Epidemiology Project (R01-AG034676). The funding sources played no role in the design, conduct, or reporting of this study.

    Conflict of Interest: VLR reports grants from NHLBI, grant number HL 120957 during the conduct of the study. ASJ reports consulting from Beckman, Coulter, Siemens, Abbott, Roche, Alere, NeurogenomeX, Sphingotec, Single, and Novartis, outside the submitted work. All other authors report no conflicts of interest.

    Authorship: All authors had access to the data and a role in writing the manuscript.

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