Mechanisms underlying coronary spasm are still poorly understood. The aim of the study was to assess the hypothesis that fluctuations in the development of coronary spasm might reflect inputs from the surroundings esophageal system. We enrolled patients admitted to the coronary care unit for episodes of nocturnal angina. Seven patients with variant angina and 5 with coronary artery disease (CAD) had concurrent ECG and esophageal manometric monitoring. ECG-monitoring documented 28 episodes of ST-elevation in variant angina and 16 episodes of ST-depression in CAD group. Manometric analysis showed that esophageal spasms resulted remarkably more frequent in variant angina (143; range 10-31) than in CAD (20; range 0-6; p<0.001). Time series analysis was used to assess fluctuations on the occurrence of abnormal esophageal waves and its relationship with spontaneous episodes of ST-shift. Episodes of esophageal spasm in CAD were sporadic (<1 in 30 min) and not related to ECG-ischemia. In variant angina, esophageal spasms were time related to ischemia (>1 into 5 min before ECG-ischemia) (p<0.05). A bi-directional analysis of casual effects showed that the influence processes between esophageal and coronary spasms were mutual and reciprocal (transfer function model, p<0.05) in variant angina. We concluded that in variant angina patients, episodes of esophageal spasms and myocardial ischemia influenced each other. Mechanisms that cause esophageal spasm can feed back to produce coronary spasm. Coronary spasm may feed forward to produce additional episodes of esophageal spasm.