WASHINGTON —The flood of catecholamines released during status epilepticus appears to damage myocardium, and may be the root cause of death during status, Dr. Edward Manno reported in a poster presented at the joint annual meeting of the American Epilepsy Society and the American Clinical Neurophysiology Society.
When he examined cardiac pathology slides obtained at autopsy, Dr. Manno found a high occurrence of cardiac contraction band necrosis among patients who died during status. These necrotic areas form when myocardium dies in a hypercontracted state. “These findings provide presumptive evidence that excessive catecholamine released during status epilepticus is the mechanism for cardiac decompensation and death during status,” wrote Dr. Manno of the Mayo Clinic, Rochester, Minn.
He reviewed the cardiac pathology of 11 patients who had died during status and 22 control patients who died of known causes other than status. Eight of those who died directly as a result of status had identifiable contraction band necrosis (72%), compared with five of the controls (23%). The difference between these two groups achieved statistical significance. Dr. Manno said the mechanism for cardiac deterioration during status is speculative at this point. A 1998 study of death during status identified two mechanisms: a gradual decline in blood pressure and cardiac function in older patients, and sudden cardiac death in younger patients. “These two mechanisms may represent an imbalance between parasympathetic and sympathetic autonomic activity during status epilepticus,” Dr. Manno wrote.
Three of those in his study had seizures originating in brain areas associated with cardiorespiratory activity. “We speculate that in these patients, increased sympathetic activity may have led to the development of cardiac arrhythmia and contraction band necrosis.”
The site of the contraction bands hints at their relationship to catecholamines, he said. “These features are located in the myocardium adjacent to the insertion of the sympathetic end plates, suggesting that massive catecholamine release is the mechanism of contraction band necrosis.”
“In selected patients with refractory status epilepticus, a short-acting β-blocker could provide some cardiac protection and prevent cardiac decompensation,” he said.