Summary We report on a three and a half year old child with episodic sinus bradycardia during habitual seizures and prolonged interictal discharges due to focal cortical dysplasia in the anterior 2/3 of the insula and the inferior frontal cortex. Seizureinduced bradycardia is rarely reported in children. Bradycardia is suspected to be related to sudden death, a rare complication of a chronic seizure disorder. Several well-documented cases in adult patients reveal a high incidence of temporal epilepsy, but MRI and PET studies in healthy subjects suggest a major role of the insular cortex, especially the right, in cardiac regulation. Our finding underlines the predominance of the right insula in cardiac control, which already seems to be present in children.
This report describes a patient with complex partial seizures arising from the right temporal lobe who developed symptomatic sinus arrest following the end of his seizure activity. A ventricular pacemaker was implanted and was documented to function appropriately, preventing development of bradycardia associated symptoms during subsequent seizures. Possibly relevant cerebral structures are briefly discussed.
With standard microelectrode techniques, electrical activity of cells in the epicardial border zones of infarcts in the canine heart were studied. Either automaticity or triggered activity (or both) occurred in each of the 12 preparations studied from 24-hour infarcts. One 24-hour preparation had continuous activity indistinguishable from low-potential (abnormal) automaticity. This automaticity was not effected by flecainide 1-5 mg/l. Two other 24-hour subepicardial muscle preparations also were automatic. However, nine preparations from the subepicardium were not automatic during superfusion with standard Tyrode's solution. Delayed afterdepolarizations (DADs) and triggered activity could be induced in all of these preparations by treatment with catecholamines. The amplitude of these DADs was directly related to the stimulus rate of the train of impulses used to elicit them, and their coupling interval was inversely related to this rate of stimulation. Triggered activity occurred from maximal diastolic potentials of -58 to -88 mV in the 24-hour infarct zone preparations. In seven preparations from 72-96-hour infarct zones, the epicardial muscle cells did not show triggered activity after treatment with catecholamines. In one preparation from a 72-hour infarct, however, 3-5-mV DADs occurred. No DADs or triggered impulses occurred in subepicardial muscle from normal, noninfarcted hearts. Thus, triggered impulses and lowpotential automaticity could contribute to arrhythmias occurring in the canine heart 24 hours after coronary ligation. (Circulation 1988;78:1020-1030 M ultiform ventricular tachycardias occur 24 hours after ligation of the left anterior descending coronary artery in the canine heart.1 These tachycardias are frequently used to model the arrhythmias that occur in humans hospitalized after myocardial infarction.2 Most investigators have concluded that the ectopic beats primarily originate in subendocardial Purkinje fibers that survive on the endocardial surface of the infarct.3-8 However, some ectopic activity may also begin in working myocardium on the lateral'l9 or epicardial borders5 of the infarct. It is known that a thin rim of surviving ventricular muscle cells on the epicardial
There is a relation between the peak heart rate attained during exercise and the subsequent HRR. A low peak heart rate increases the likelihood of a less than normal HRR. Assessment of the entire heart-rate response seems warranted for more thorough risk-stratification.
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