SILENT ISCHEMIA AS A CENTRAL PROBLEM - REGIONAL BRAIN ACTIVATION COMPARED IN SILENT AND PAINFUL MYOCARDIAL-ISCHEMIA

Objective: To test whether the silence of painless myocardial ischemia is caused by abnormal handling by the central nervous system of affer ent messages from the heart. Design: Nonrandomized study. Setting: A t ertiary referral center (postgraduate medical school). Patients: 2 mat ched groups of nondiabetic patients with coronary artery disease. Grou p A consisted of nine patients with reproducible stress-induced angina ; group B consisted of nine patients with reproducible stress-induced myocardial ischemia but no angina. Interventions: Intravenous placebo infusion and low-dose (5 and 10 mu g/kg per minute) and high-dose (20 to 35 mu g/kg per minute) dobutamine infusions. Measurements: Positron emission tomography was used to measure regional cerebral blood flow changes as an index of neuronal activation during painful arid silent myocardial ischemia induced by intravenous dobutamine. Results: Region al cerebral blood flow changes during myocardial ischemia were compare d with those during baseline conditions and during placebo infusion. D uring myocardial ischemia, regional cerebral blood flow increased bila terally in the thalami and prefrontal, basal frontal, and ventral cing ulate cortices in patients in group A. Both thalami were activated in group B, but cortical activation was limited to the right frontal regi on. A formal comparison of groups A and B showed significant differenc es (P < 0.01) in activation of the basal frontal cortex, ventral cingu late cortex, and left temporal pole. In both groups, thalamic regional cerebral blood flow remained increased after the symptoms and signs o f ischemia had ceased. Conclusions: Bilateral activation of the thalam us can be shown in both angina and silent ischemia; thus, peripheral n erve dysfunction cannot completely explain silent ischemia. Frontal co rtical activation appears to be necessary for the sensation of pain. A bnormal central processing of afferent pain messages from the heart ma y play a determining role in silent myocardial ischemia.