Testa-Fernández et al. Journal of Medical Case Reports 2011, 5:304 http://www.jmedicalcasereports.com/content/5/1/304 Page 2 of 6 Figure 1 Basal electrocardiogram. abnormalities. At minute one of the recovery phase, the ECG showed a giant R wave pattern in the inferolateral leads, including an increase of R wave voltage rising to 34 mm, loss of S wave, and merging of the QRS com- plex with the ST segment, causing a monophasic QRS- ST complex (Figure 2a). A nodal rhythm was also observed (Figure 2b). Clinically, the patient experienced chest pain and dizziness. His blood pressure was 183/98 mmHg, and we administered sublingual nitroglycerin, and the patient’s ECG gradually returned to normal sta- tus (Figure 3). In Figure 4, we show the evolution in lead III during the episode. The maximal level of tropo- nin I measured after the ETT was 0.1 ng/mL (normal 0.0 ng/mL to 0.2 ng/mL). Emergency coronary arterio- graphy showed single coronary vessel disease with severe stenosis in a mid-dominant circumflex coronary artery (Figure 5). The patient was successfully treated with coronary percutaneous revascularization (Figure 6), and, two days later, he was discharged without further symptoms. Discussion The giant R wave syndrome was first described by Prinzmetal et al. [4] in the context of variant angina. Since then, similar ECG changes have been recorded in percutaneous transluminal coronary angioplasty, experi- mental coronary ligation, and in patients who had an acute MI (in this latter case, infrequent documentation exists in association with inferior MI, probably because of the smaller size of ischemic injury as compared to the anterior MI, resulting in less impressive ECG changes) [6]. The electrophysiological mechanism of the giant R waves in the setting of myocardial ischemia has been attributed by most investigators to the aberrant propagation of ventricular activation from the normal myocardium toward the ischemic area, in which there is a marked slowing of conduction velocity [6]. In variant angina, ST-segment elevation can be provoked by exer- cise, hyperventilation, or cold stimulation in about 30% of patients [7]. In our patient, the giant R wave pattern was provoked by exercise during ETT, which also showed nodal rhythm, and resolved with sublingual nitroglycerin administration. Coronary catheterization showed severe stenosis in a mid-dominant circumflex coronary artery, with an extensive territory at risk. We hypothesize that, in our patient, the giant R wave pat- tern was related to severe hyperacute ischemia due to a coronary spasm superimposed on the atherosclerotic lesion, which probably caused a complete occlusion of the artery. This severe ischemic response could explain