Activation of the renin-angiotensin system during the process of heart failure may predispose the heart to reentrant malignant arrhythmias by reducing the cell coupling and conduction velocity. Here I discuss the possible role of the renin-angiotensin system on the modulation of cell coupling and impulse propagation with consequent generation of reentrant rhythms. Particular emphasis is given to the effects of angiotensin II on the electrical properties of the failing heart and the beneficial effects of angiotensin-converting enzyme inhibitors and angiotensin II AT1 receptor blockade.