Heart failure [HF] has high morbidity and mortality. Once it sets in, it shortens the survival hence its treatment should be aimed at delaying the cardiac mortality. The pharmacotherapy should target the basic pathology of HF which consists of myocardial stretch, remodeling and fibrosis. Hormones of Renin Angiotensin Aldosterone system and Catecholamines are responsible for cardiac remodeling and fibrosis. The release of cardiac biomarkers natriuretic peptides [NPs] neutralize the myocardial stretch and reduce the volume overload but do not regress the process of remodeling and fibrosis. Hence they carry better diagnostic than prognostic specificity. Specific biomarkers of remodeling and fibrosis are soluble circulating form of suppression of tumerogenicity-2[sST2] and galectin-3. Like NPs, sST2is not affected by age, body mass index and renal insufficiency. In serial estimation, sST2 stands as a specific biomarker than Glalectin-3 for prognosis and risk stratification. High sST2 levels prompt the clinician to initiate the therapies like high dose of beta blockers, ACE inhibitors and Angiotensin receptor blockers, directed against the cardiac remodeling and fibrosis which result in to better cardiac outcome. Though the levels of sST2 get affected by certain inflammatory and immune diseases, still sST2 stands as a specific prognostic cardiac biomarker at present.
