It’s often very expensive or time-consuming to measure the effect of a drug on an ultimate goal such as mortality. Drugs to reduce cholesterol, for example, are intended ultimately to reduce the number of heart attacks and thus to lengthen life expectancy. It could take twenty or more years to test this hypothesis adequately, however. A surrogate endpoint, such as a reduction in cholesterol counts, is a more easily measured endpoint. A drug may be approved based on clinical trials showing a positive surrogate endpoint if there is evidence from other studies that the surrogate endpoint accurately predicts an ultimate benefit (we know, for example, that men with high cholesterol are at greater risk of a heart attack, but this is not the same as knowing that a reduction in cholesterol will reduce heart attacks, although it is suggestive). Postmarketing studies can continue to tract the effectiveness of drugs that were approved using surrogate endpoint methodology. The use of surrogate endpoints is controversial because a positive surrogate endpoint does not necessarily predict a positive ultimate endpoint. Encainide and flecainide were widely prescribed because they prevented premature beats of the heart on the theory that such prevention would reduce heart attacks. The Cardiac Arrhythmia Suppression Trial later showed that not only was this claim false but that encainide and flecainide could actually increase the number of heart attacks.