The development of the chronic MH phenotype in HF patients is difficult to track, whereas the morphological features of chronic MH are well-established and characterized by PAS-positive cardiomyocytes, loss of cardiomyocytes by apoptosis, patchy reduction in Cx-43 content (contributing to impaired myocardial excitation-contraction coupling), hypertrophic and hypo-/atrophic cardiomyocytes, interstitial fibrosis, increased fibronectin and fibroblasts (vimentin-positive cells) [2]. The gene discussed is VIM; the disease is hydrops fetalis.