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See article by Dong et al. [7] (pages 320–332) in this issue. The pathogenesis of cardiac ventricular hypertrophy (CVH), both compensated and that associated with cardiac dysfunction, has attracted a lot of attention and this field still continues to expand. This huge clinical and scientific interest is related to the fact that CVH has been identified as a powerful risk factor for total and cardiovascular mortality. Interestingly, the Framingham study also demonstrated that CVH significantly increases the risk of sudden cardiac death, both in men and in women [1]. Subsequent studies provided evidence that cardiac arrhythmias are an important mechanism contributing to the high mortality and sudden death in patients with CVH [2–4]. Not surprisingly, a lot of effort has been expended to characterize the electrophysiological phenotype and to elucidate the mechanisms of arrhythmias in CVH.New research tools have been provided with the advent of modern molecular biology techniques. Thus it is now possible to up- or down-regulate cardiac expression of various elements of intracellular signaling pathways in order to investigate their specific role in the process of myocardial normal growth as well as pathological remodeling. One such signaling pathway (although not the only one) is calcineurin-dependent activation of intracellular transcription factors.Calcineurin is an intracellular protein phosphatase regulated by Ca2+/calmodulin and activated by micromolar calcium concentrations [5]. Calcineurin and its downstream transcriptional effector NFAT (nuclear factor of activated T-cell) mediate cardiac hypertrophic responses initiated by increases in cytoplasmic calcium. Overexpression of calcineurin in mice has been previously shown to lead to extensive CVH, heart failure, and sudden death [6]. In the present issue of the Journal, Dong et al. [7] present new experimental data that shed some new light on the mechanisms of sudden death and cardiac electrophysiological remodeling in mice with … * Present address: Mayo Foundation, St. Mary's Hospital, DO-4-350, 1216 Second St. SW, Rochester, MN 55902, USA. Tel.: +1-507-255-1144; fax: +1-507-255-7070. wolk.robert{at}mayo.edu

Calcineurin, myocardial hypertrophy, and electrical remodeling