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Silent Ischemia as a Central Problem: Regional Brain Activation Compared in Silent and Painful Myocardial Ischemia
- Stuart D. Rosen, MA, MRCP;
- Eraldo Paulesu, MD;
- Petros Nihoyannopoulos, MD;
- Dimitris Tousoulis, MD;
- Richard S.J. Frackowiak, MD, FRCP;
- Christopher D. Frith, PhD;
- Terry Jones, DSc; and
- Paolo G. Camici, MD
- From Hammersmith Hospital and the Institute of Neurology, London, United Kingdom, and Istituto Scientifico H San Raffaele, Universita degli Studi, Milano, Italy. Acknowledgments: The authors thank Mr. Andrew Blythe, MSc, DCR, and Ms. Andreana Williams, DCR, for assistance with positron emission tomography; Dr. Ignathios Ikonomides for assistance with echocardiography; and Professor Alberto Malliani, Universita di Milano, for helpful advice. Grant Support: In part by British Heart Foundation project grant PG/94/039. Requests for Reprints: Dr. S.D. Rosen, Cyclotron Unit, MRC Clinical Sciences Centre, Hammersmith Hospital, Du Cane Road, London W12 0NN, United Kingdom. Current Author Addresses: Drs. Rosen, Jones, and Camici: Cyclotron Unit, MRC Clinical Sciences Centre and Royal Postgraduate Medical School, Hammersmith Hospital, Du Cane Road, London W12 0NN, United Kingdom.
Abstract
Objective: To test whether the silence of painless myocardial ischemia is caused by abnormal handling by the central nervous system of afferent messages from the heart.
Design: Nonrandomized study.
Setting: A tertiary referral center (postgraduate medical school).
Patients: 2 matched groups of nondiabetic patients with coronary artery disease. Group 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 µg/kg per minute) and high-dose (20 to 35 µg/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 and silent myocardial ischemia induced by intravenous dobutamine.
Results: Regional cerebral blood flow changes during myocardial ischemia were compared with those during baseline conditions and during placebo infusion. During myocardial ischemia, regional cerebral blood flow increased bilaterally in the thalami and prefrontal, basal frontal, and ventral cingulate cortices in patients in group A. Both thalami were activated in group B, but cortical activation was limited to the right frontal region. A formal comparison of groups A and B showed significant differences (P < 0.01) in activation of the basal frontal cortex, ventral cingulate cortex, and left temporal pole. In both groups, thalamic regional cerebral blood flow remained increased after the symptoms and signs of ischemia had ceased.
Conclusions: Bilateral activation of the thalamus can be shown in both angina and silent ischemia; thus, peripheral nerve dysfunction cannot completely explain silent ischemia. Frontal cortical activation appears to be necessary for the sensation of pain. Abnormal central processing of afferent pain messages from the heart may play a determining role in silent myocardial ischemia.
- Copyright ©2004 by the American College of Physicians
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