Silent myocardial ischaemia results from an imbalance between myocardial oxygen supply and demand. There is evidence in favour of both increased coronary vasomotor tone and increased oxygen demand as major independent causes of silent ischaemia. An ongoing study is assessing the efficacy of a slow release formulation of the calcium antagonist gallopamil in patients with stable angina pectoris. In a nonblind comparison with placebo in 13 patients, slow release gallopamil 100mg twice daily produced a marked reduction in exercise-induced myocardial ischaemia, and a moderate reduction in spontaneous ischaemia. The significance of these preliminary findings will emerge in the double-blind, placebo-controlled phase of the study. Studies using long term ECG monitoring to compare the anti-ischaemic efficacy of various calcium antagonists indicate that agents with negative inotropic actions suppress silent myocardial ischaemia to a greater extent than calcium antagonists such as nifedipine, which tend to increase heart rate. Also, beta-adrenoceptor blockers have produced excellent results in the treatment of myocardial ischaemia, despite their theoretical disadvantage of not reducing coronary vasomotor tone. The role of pharmacological therapy in the suppression of silent myocardial ischaemia will only be established when the drugs concerned have been adequately characterised with regard to their effect on prognosis, adverse effects and risk:benefit ratio.