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We read with great interest the paper by Herrmann et al .1 describing the effects of inducible HCN4-positive cell deletion in the mouse. This novel study using Cre- lox P adds to their previous work using this system to knock down HCN4 expression in adult mice and is a valuable contribution to unravelling the complexities of sinoatrial node (SAN) function and disease.1 The authors claim that their DTA/KiT mouse represents an accurate analogue of human sick sinus syndrome (SSS). For example, in the DTA/KiT mouse, following HCN4-positive cell deletion, there is a marked cell loss and fibrosis in the SAN. Literature is cited that alleges age-related degenerative fibrosis is the primary pathological mechanism of SSS. However, careful analysis of the published literature casts doubt on …

Not so fast! Sick sinus syndrome is a complex and incompletely understood disease that might prove hard to model in animals