Patients in subtype B demonstrated persistent elevation in levels of markers of inflammation (procalcitonin and interleukin-6), endothelial dysfunction (bio-adrenomedullin), myocardial injury and stress (high sensitivity cardiac troponin I, brain natriuretic peptide and galectin 3) and renal dysfunction (plasmatic cystatin C) compared to subtype A (Fig. 3). This evidence concerns the gene TNNI3 and Abnormal renal physiology.