In recent years, electrical remodeling has emerged as an important pathophysiologic mechanism in many types of cardiac pathology. Because clinical heart disease often involves both hypertrophic and failure phenotypes, identification of disease-specific mechanisms is essential. This review focuses on mechanisms of electrical remodeling in cardiac hypertrophy, emphasizing transmembrane Ca2+ fluxes and Ca(2+)-responsive signaling pathways. Where information is available, the remodeling of hypertrophy is contrasted with what is known about heart failure.