Acute ischemic chest pain is not associated with increased calcitonin gene-related peptide (CGRP) levels in peripheral plasma nor in the coronary circulation

Calcitonin gene-related peptide (CGRP) and substance P co-exist in capsaici n-sensitive primary sensory neurons and are released from the myocardium af ter activation of sensory nerve fibres as well as by ischemia in animals. T his study was undertaken to try to clarify the potential involvement of imm unoreactive (ir) CORP in anginal pain and myocardial ischemia in humans. On e clinical group (n = 87) and one experimental group (n = 14) were studied. The clinical group was admitted to a coronary care unit with suspected or definite acute myocardial infarction (AMI). The experimental group consiste d of patients with severe angina pectoris (NYHA III-IV). This group was sub jected to atrial pacing up to the appearance of angina pectoris. Mean irCGR P levels at admission for the clinical group with and without AMI showed no significant difference. Neither were any significant differences found in irCGRP concentrations between patients with pain as compared to those witho ut pain or in the group who had had chest pain >30 min before hospital admi ssion as compared to those with chest pain <30 min. Extraction ratios for l actate and irCGRP was calculated in the experimental group. No statisticall y significant covariance was found between irCGRP extraction ratio and lact ate extraction ratio (r(xy) = -0.006) at the time of appearance of angina d uring atrial pacing. Despite the facts that CGRP may be liberated by a vari ety of physiological stimuli and may act as a potent vasodilator in the hum an vasculature, no evidence has been found in this study that CGRP release is increased as a consequence of ischemia or ischemic pain.