The extent of insular damage following stroke is a strong predictor of pathological sympathetic activation, including cardiac arrhythmias and QTc prolongation.
The relationship between size of brain infarction, extent of insular damage, and stroke-associated pathological sympathetic activation was investigated in 52 patients. Evaluation of plasma norepinephrine levels, frequency of cardiac arrhythmias and QT prolongation and analysis of circadian blood pressure patterns were used to determine the extent of sympathetic activity. Whereas only a moderate correlation exists between size of infarction and norepinephrine levels (r = 0.69; p < 0.05), a highly significant relationship between percentage insular infarction and norepinephrine was found (r = 0.93; p < 0.001). Circadian blood pressure patterns were only moderately related to infarct size (p < 0.05) but were correlated substantially with the extent of insular infarction (p < 0.001). Patients with cardiac arrhythmias showed a significantly larger averaged infarct size (p < 0.01) and a larger extent of insular damage (p < 0.01) than patients without arrhythmia. In contrast, QTc prolongation was only associated with a larger extent of insular infarction (p < 0.01), whereas averaged infarct size was not notably different. These findings suggest that analysis of insular infarction may be a useful parameter to appraise the extent of pathological sympathetic activity following stroke.
Sander et al. (Wed,) studied this question.
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