Intriguingly, this assumption is in agreement with the work of Heringlake et al. (2009), who reported that patients suffering from ischemic heart disease and with severe myocardial dysfunction present lower levels of relaxin-2 in plasma than patients with preserved myocardial function (Table 4) and that plasmatic relaxin-2 concentration is inversely associated with the severity of heart disorders in these patients; these findings suggest that systemic relaxin-2 could act as a compensatory vasodilatory reaction hormone during ischemic heart disease [102]. The gene discussed is RLN2; the disease is coronary artery disorder.