Abstract 19811: Circulating Soluble ST2 Levels are Independent of Cardiac Production after Acute Myocardial Injury

• Published in: Circulation (New York, N.Y.) Vol. 130; no. suppl_2
• Main Authors: See, Vincent Y, Fugate, Jessica, Gurm, Gagandeep, Ament, Dawn, Dickfeld, Timm-Michael, Shorofsky, Stephen R, Saliaris, Anastasios P, Klein, Thomas, Remo, Benjamin, Christenson, Robert, deFilippi, Christopher R
• Format: Journal Article
• Language: English
• Published: 25-11-2014
• ISSN: 0009-7322; 1524-4539
• DOI: 10.1161/circ.130.suppl_2.19811

Abstract only
Background:
Soluble ST2 (sST2) is a decoy receptor that modulates the anti-hypertrophic and anti-fibrotic IL-33/ST2 pathway. sST2 is associated with adverse prognosis in HF and ACS; both states are associated with cardiac injury. However, sST2 levels are also increased in non-cardiac disease. To determine the extent of cardiac production of sST2 both chronically and after acute myocardial injury, we measured fractional cardiac production of sST2 compared to the cardiac specific injury marker high sensitive (hs) cTnT before and after elective cardiac ablation.
Methods:
Twenty-three patients undergoing ablation of atrial fibrillation were enrolled [Caucasian 22 (96%); Male 17 (74%); Age 57.7±10.4 years; eGFR 58.7 ± 0.6 mL/min/1.73m2). Of the 23, 15 (65%) had paroxysmal atrial fibrillation. At baseline, 14 (61%) were in sinus rhythm. Samples were obtained from the radial artery and coronary sinus (CS) pre- and post-ablation. sST2 was measured by the Presage assay. Post ablation samples were measured 201±44 minutes after the first ablation.
Results:
At baseline, in contrast to cTnT, there was no cardiac production of sST2. Both arterial and CS levels of sST2 increased after ablation but not nearly to the extent of cTnT. No net cardiac production of sST2 was noted (Table).
Conclusion:
Cardiac production of sST2 is not observed at baseline. Systemic sST2 levels modestly increase following acute myocardial injury. Despite direct myocardial injury, no cardiac production of sST2 is observed. The source of sST2 is extra-cardiac both chronically and after acute injury.