Abstract 11684: Impaired Cortical Pain Processing in Patients With Silent Myocardial Ischemia

Purpose: In the present study, we investigated whether the function of brain areas specifically devoted to nociception presents any abnormalities in patients with silent myocardial ischemia (MI), as compared to those with symptomatic MI. Methods: We studied 3 groups of individuals: 1) 11 asymptomatic, non-diabetic patients with documented obstructive coronary artery disease (CAD) (67±10 years, 6 men; group 1); 2) 10 patients with obstructive CAD and a clinical pattern of chronic stable angina (66.5±10 years, 6 men; group 2); 3) 14 apparently healthy subjects matched for age and gender to patients (63.2±9 years, 8 men; group 3). Patients with any chronic pain syndrome other than anginal chest pain were excluded. Cortical nociception function was assessed by cortical laser evoked potentials (LEPs) recording in response to chest skin stimulation by cutaneous CO2 laser pulses. Specifically, the N2/P2 wave of LEPs, which reflects cortical pain processing, was measured. Three sequences of painful stimuli (at the intensity of 2.5 times the individual sensory threshold) were applied, separated by 5-minute intervals. Results: N2/P2 amplitude during the first sequence of chest skin stimuli was 9.3±4.0, 14.0±7.3 and 15.5±6.4 μV in group 1, group 2 and group 3, respectively (p=0.03). N2/P2 amplitude decreased across the three sequences of pain stimuli in group 2 (-37.5±14 %) and group 3 (-23.0±15 %), but not in group 1 (-0.14±37 %) (comparison among groups, p=0.015). Conclusion: CAD patients with silent MI show a reduced amplitude of N2/P2 LEP component and inadequate habituation to painful stimuli, compared to symptomatic angina CAD patients and healthy controls. This pattern is likely due to thalamic gate modulation of pain signals and can contribute to the lack of pain perception during MI in these patients.