In a model of HF with preserved ejection fraction by AngII infusion for 2 weeks in mice, the cardiomyocyte-specific and temporally inducible Orai1 knockout mouse line (Orai1CM-KO) show a slight decrease in systolic function with increased fibrosis compared to WT mice, suggesting a worsening of the pathology and a transition towards maladaptive hypertrophy. This evidence concerns the gene AGT and hydrops fetalis.