We also found that PSELT reduced myocardial production of GAL-3, a β-galactoside–binding lectin, whose plasma and myocardial levels can reflect the progression of LV fibrosis and cardiomyopathy, and which represents a diagnostic and prognostic marker in both acute and chronic HF, particularly when assessed together with N-terminal pro–BNP (NT-proBNP) [58, 59]. This evidence concerns the gene LGALS3 and cardiomyopathy.