ADRB1 and Ventricular arrhythmia: While changes in ion channel sialylation may contribute to the pathogenesis of the ventricular arrhythmias in these disorders, our studies provide a rationale to consider whether defective β1AR O-glycosylation and the accumulation of an N-terminally truncated β1AR species that displays enhanced signaling to proarrhythmic cAMP/PKA responses also might contribute to this pathologic cardiac phenotype.