An old drug for use in the prevention of sudden infant unexpected death due to vagal hypertonia

Abstract

Reflex vagal hypertonia (RVH) has been identified as a possible cause of sudden unexpected death in infants during the first year of life. Homatropine methylbromide (HM) is an anticholinergic drug known to inhibit muscarinic acetylcholine receptors, thus affecting the parasympathetic nervous system. The aim of the present study was to investigate the effects of HM on 24-h Holter electrocardiographic signs of RVH (pre-HM treatment vs post-HM treatment; post-HM treatment vs a control group of healthy infants). A total of 50 patients (mean age, 6.1 ± 2.7 months; 28 males, 22 females; 12 born pre-term) affected by RVH were enrolled in the study. Pre-HM treatment vs post-HM treatment: statistically significant differences were detected for higher heart rate, lower heart rate, mean heart rate, longer sinusal pause, presence of advanced atrio-ventricular blocks, and systolic blood pressure (p < 0.001, p < 0.00001, p < 0.02, p < 0.00001, p < 0.05, and p < 0.04, respectively). A statistically significant correlation was revealed between HM-administered dose and both average heart rate and systolic blood pressure (r = 0.93, p < 0.0001; r = 0.94, p < 0.0001, respectively). No significant differences were detected between post-HM treatment electrocardiographic data and those of the control group. By antagonizing action of the vagus nerve of the parasympathetic system on the heart, thus increasing cardiac frequency, HM treatment appears to feature a good safety profile and be highly effective in preventing transient infantile hypervagotonia, the potential cause of several cases of sudden unexpected death during the first year of life.

The vagal ganglia transcriptome identifies candidate therapeutics for airway hyperreactivity

“…This left eight candidates (diazoxide, alverine, meprylcaine, yohimbine, atenolol, solasodine, solanine, and homatropine). Of those, only homatropine and alverine citrate were of continued interest, due to their ability to modulate vagal nerve activity ( 1 , 4 , 8 , 23 ). Because anticholinergics are currently used in asthma ( 61 ), we did not further explore homatropine.…”

A pallid paroxysmal event in children: it is vagal anoxic seizure, it is treatable, and it is not “epilepsy”

“…The article published in this journal by Bassareo et al [1] on the use of homatropine methylbromide as anticholinergic medication, in the prevention of vagal hypertonia, is a well-documented evaluation of this drug in one of the most spectacular non-epileptic symptom related to fits and fails. The strength of this article is to provide clear clinical observations of patients with increased vagal reactivity treated by homatropin.…”