CREM and Premature ventricular contraction: Our results show that heart-directed expression of CREM-IbΔC-X, a CREM repressor isoform isolated from failing human hearts [25], evokes arrhythmogenic alterations in non-hypertrophied ventricular mouse cardiomyocytes including an increased incidence of transient-like spontaneous Ca2+ releases and early afterdepolarizations associated with an increased occurrence of ventricular extrasystoles.