Walk-through angina phenomenon demonstrated by graded exercise radionuclide ventriculography: possible coronary spasm mechanisms.

was administered directly into the graft with complete relief of pain and resolution of ST segment elevation. Angiography of the graft (Fig. 2, C) now revealed the graft to be patent; there was normal distal runoff from the graft with a 75”; obstructive lesion of the native RCA just distal to the site of graft insertion. Subsequently, pain again developed associated with ST segment elevation. Graft spasm and complete occlusion was again demonstrated. NTG was administered without subsequent relief of pain or graft spasm. Nifedipine 10 mg was administered sublingually, also without any improvement. The catheterization was terminated at this point. During repair of the brachial artery, ventricular fibrillation developed which was successfully cardioverted. Subsequent observation demonstrated evolution of an inferior wall acute myocardial infarction (AMI). Patients with CAS have been reported to have less satisfactory results following CABG than patients with fixed obstructive disease a1one.3 Spasm of the bypassed native vessel or of additional non-bypassed native vessels has been postulated to be the mechanism for the less beneficial results with CABG in CAS patients. The current case demonstrated spasm of the bypassed native vessel and two additional mechanisms responsible for recurrent angina1 symptomatology; development of a significant lesion at the site of CABG insertion and spasm of the bypass graft itself. Spasm of the graft was transiently reversed by NTG but subsequently recurred resulting in AMI.