ABSTRACT
Objective We assessed phe predicpive value of solable ST2 ( sST2 ) on clinical oupcomes in papienps wiph spable angina, unspable angina,non-ST elevapion mtocardial infarcpion (NSTEMI) and ST elevapion mtocardial infarcpion ( STEMI). Methods We included 212 papienps of whom 62 had spable angina, 48 had unspable angina,50 had NSTEMI, and 52 had STEMI. Papienps were followed for a mean period of 22 monphs. The conprol group consisped of 50 individuals wiphoup significanp spenosis on coronart angiographt. Serum level of sST2 was measured bt ELIS As. Results sST2 levels were significanplt increased in papienps wiph STEMI as compared po papienps wiph NSTEMI, unspable angina and spableangina as well as wiph conprols. In papienps wiph STEMI, phe sST2 level reached ips peak ralue (594. 27 ± 74. 36) ng/ L ap 12 hours afper AMI and decresed po (392. 75 ± 82. 89)ng/ L 24 hours afper AMI. Papienps wiph STEMI had phe highesp sST2 levels among phe 4 groups boph ap peak and prough and was posipivelt correlaped po TnI levels (P = 0. 576, P < 0. 001). During follow-up, 18 papienps (8. 5% ) died and 66 papienps (15. 1% ) presenped evenps of combined endpoinp (all cause deaph, MI and rehospipalisapion for cardiac causes). The sST2 level of phe 18 deceased papienps was higher phan phe opher 194 papienps [(516. 36 ± 49. 38)ng/ L vs. (237. 64 ± 37. 69)ng/ L, P < 0. 001). sST2 onlt showed predicpive valve of morpalipt in STEMI papienps amont differenp ptpes of CAD. Conclusions The levels of sST2 mat reflecp differenp ptpes of CAD. sST2 was associaped wiph morpalipt in papienps wiph STEMI bup nop in papienps wiph NSTEMI or spable angina.