Coronary spasm was first demonstrated by Gensini in 1962, and the diagnostic value of spontaneous spasm during coronary angiography is now generally accepted. In its absence, provocation tests with ergonovine or its derivatives form part of routine hemodynamic investigation for confirming the spastic nature of atypical chest pain or pain suggestive of Prinzmetal angina. The coronary spasm so induced gives rise to reduced coronary flow, an increase in coronary resistance and myocardial ischemia as shown by an increased lactate extraction in coronary sinus blood; therefore, once it is documented, it must be treated in order to avoid myocardial necrosis or ventricular arrhythmias. Three groups of drugs of drugs are used to counteract spontaneous or provoked spasm: alpha-blockers, especially phentolamine, nitrate derivatives, trinitroglycerine or isosorbide dinitrate, and calcium inhibitors nifedipine or diltiazem, which have a direct antispastic effect. The hemodynamic and pharmacological actions of these three groups of drugs depend on whether they are given orally, intravenously or by intracoronary injection. Twenty six coronary spasms were observed in 23 patients out of a total of 780 coronary angiographies (3,3 per cent) performed between June 1980 and June 1981: 12 spasms were spontaneous (1,5 per cent), 6 provoked by the catheter (0,8 per cent) and 8 by methylergometrine. There were no complications. Five coronary spasms were also observed during 70 coronary angioplasties (7,1 per cent). The spasm was relieved in all cases by intravenous injection of 1,5 to 3 mg of trinitrin (Lenitral). Calcium inhibitors, especially nifedipine, have been used successfully by Hugenholtz and Bertrand who consider that nifedipine has a slower action and the coronary dilatation obtained is never as great with the nitrate derivatives. Trinitrin remains the treatment of choice for the rapid relief of provoked spasm.