An acute ST-elevation myocardial infarction occurs due to occlusion of one or more coronary arteries, causing transmural myocardial ischemia which in turn results in myocardial injury or necrosis. Acute myocardial infarction (AMI) may lead to the development of heart failure (HF). Accessible diagnostic tools commonly used in HF such as natriuretic peptides and (NYHA) classification reflect already overt clinical HF. Troponin and creatine kinase reflect myocardial damage, but their usefulness in predicting long-term LVR is limited. Recent guidelines on HF management stressed that HF onset may be delayed or prevented through certain Interventions, such as pharmacotherapy ,post infarction rehabilitation, or modification of HF risk factors. Therefore, it is important to identify potential markers, which would be more informative of HF preclinical stages to recognize patients with an increased risk of HF onset, and to start treatment in advance (1) Gal-3 participates in inflammation and pro fibrotic pathways, while sST2 is a biomarker of inflammation, cardiac mechanical strain, and tissue fibrosis, both of which may predict LVR (2).

sST is a biomarker of inflammation, cardiac mechanical strain, and tissue fibrosis(3).

B_type natriuretic peptide (BNP) is elevated in acute myocardial infarction and is a quantitative biochemical marker related to the extent of infarction and left ventricular systolic dysfunction(4).

Inclusion Criteria:

1. Age ≥ 18 years.
2. Hospital admission due to first-time STEMI treated with pPCI.

Exclusion Criteria:

• History of previous acute coronary syndrome, Previously diagnosed HF or asymptomatic LV dysfunction with LVEF <50% or previously diagnosed significant valvular disease or any other previously diagnosed structural heart disease Severe renal dysfunction, Severe liver disease, Chronic inflammatory disease, Current neoplastic disease

Assuit University Hospital.