Cardiac arrhythmias are a leading cause of morbidity and mortality in the Western world. Ventricular arrhythmias are reportedly responsible for the majority of sudden cardiac deaths and atrial fibrillation is responsible for 15% of all strokes in the USA. Recent evidence suggests a role for cholesterol in the development of these arrhythmias. In addition to its association with atherosclerotic plaques, high cholesterol has been shown to cause changes in membrane properties, including the function of hormone receptors, ion channels and pumps. These effects are mediated through direct interactions between cholesterol and the membrane proteins, through changes in membrane fluidity and/or an association with lipid rafts. Cholesterol-lowering therapy, therefore, may prove an effective method for the treatment of cardiac arrhythmias. Statins, a class of cholesterol-lowering drugs, have been frequently shown to protect against ventricular arrhythmias and atrial fibrillation. Some of this protection may stem from their cholesterol-lowering activities.