August 17, 2018PLoS ONEOpen Access

Predictive value of soluble ST2 in adolescent and adult patients with complex congenital heart disease

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Why the study?

Do soluble ST2 levels predict major adverse cardiac events and all-cause mortality in adolescent and adult patients with complex congenital heart disease?

Structured PICO

Do soluble ST2 levels predict major adverse cardiac events and all-cause mortality in adolescent and adult patients with complex congenital heart disease?

Population

169 consecutive adolescent and adult patients with complex congenital heart disease (mean age 28.2 ± 12.0 years) and 32 healthy controls.

Intervention

Measurement of soluble ST2 (sST2) levels

Comparator

Healthy controls (for baseline comparison) and lower sST2 levels (for prognostic comparison)

Outcome

Occurrence of major adverse cardiac events (MACE), acute heart/Fontan failure, and all-cause mortalityhard clinical

In patients with complex congenital heart disease, sST2 levels provide additive prognostic value to natriuretic peptides for predicting all-cause mortality.

Implication

sST2 may refine mortality risk stratification in complex CHD; hypothesis-generating and requires prospective validation before practice change.

Abstract

BACKGROUND: Soluble suppression of tumorogenicity 2 (sST2) has been shown to be of prognostic value in patients with chronic and acute left heart failure. The present study aims to assess the predictive value of sST2 levels in adult patients with complex congenital heart disease (CHD). METHODS: In 169 consecutive patients with complex CHD and a mean age of 28.2 ± 12.0 years, sST2 levels were compared to 32 healthy controls and associated with clinical status as well as the occurrence of major adverse cardiac events (MACE). Mean follow-up time was 35.6 ± 24.9 months. RESULTS: In CHD patients, median sST2 levels were 29.7 ng/ml compared to 26.4 ng/ml in healthy controls (p = 0.007) and increased with different types of CHD and the severity of MACE. According to ROC analysis, the most important predictors of acute heart/Fontan failure were NYHA class III/IV (AUC 0.804, p<0.001, CI 0.668-0.941), NT-proBNP levels (AUC 0.794, p<0.001, CI 0.640-0.948), γGT levels (AUC 0.793, p<0.001, CI 0.678-0.909) and sST2 levels (AUC 0.742, p = 0.004, CI 0.626-0.858), with NYHA class III/IV as the strongest independent predictor (p<0.001). All-cause mortality was best predicted by sST2 levels (AUC 0.890, p<0.001, CI 0.741-1.000), NT-proBNP levels (AUC 0.875, p = 0.001, CI 0.766-0.984) and NYHA class III/IV (AUC 0.837, p = 0.003, CI 0.655-1.000) with sST2 as the strongest independent predictor (p<0.001). Moreover, AUC increased to 0.918 combining both biomarkers and net reclassification improved with the addition of sST2. CONCLUSION: In patients with complex CHD, sST2 may have additive value to natriuretic peptides for the prediction of all-cause mortality.