ObjectiveGuidelines state that verapamil is contraindicated in infants. This is based on reports of cardiovascular collapse and even death after rapid intravenous administration of verapamil in infants with supraventricular tachycardia (SVT). We wish to challenge this contraindication for the specific indication of verapamil sensitive ventricular tachycardia (VSVT) in infants.DesignRetrospective case series and critical literature review.SettingHospitals within New Zealand.PatientsWe present a series of three infants/young children with VSVT or ‘fascicular VT’.ResultsThree children aged between 8 days and 2 years presented with tachycardia 200–220 beats per minute with right bundle brunch block and superior axis. Adenosine failed to cardiovert and specialist review diagnosed VSVT. There were no features of cardiovascular shock. Verapamil was given as a slow infusion over 10–30 min (rather than as a push) and each successfully cardioverted without incident. Critical review of the literature reveals that cardiovascular collapses were associated with a rapid intravenous push in cardiovascularly compromised infants and/or infants given other long-acting antiarrhythmics prior to verapamil.ConclusionsVerapamil is specifically indicated for the treatment of fascicular VT, and for this indication should be used in infancy, as well as in older children, as first-line treatment or after failure of adenosine raises suspicion of the diagnosis. We outline how to distinguish this tachycardia from SVT and propose a strategy for the safe intravenous slow infusion of verapamil in children, noting that extreme caution is necessary with pre-existing ventricular dysfunction.

In children, 25OHD levels are not affected by acute bacterial infections; 25OHD levels taken during acute bacterial infection are representative of baseline levels. 25OHD levels collected during acute bacterial infection provide reliable information for case-control studies.

Background Isolated cardiac arrhythmia due to a variant in CACNA1C is of recent knowledge. Most reports have been of singleton cases or of quite small families, and estimates of penetrance and expressivity have been difficult to obtain. We here describe a large pedigree, from which such estimates have been calculated. Methods We studied a five‐generation family, in which a CACNA1C variant c.2573G>A p.Arg858His co‐segregates with syncope and cardiac arrest, documenting electrocardiographic data and cardiac symptomatology. The reported patients/families from the literature with CACNA1C gene variants were reviewed, and genotype–phenotype correlations are drawn. Results The range of phenotype in the studied family is wide, from no apparent effect, through an asymptomatic QT interval prolongation on electrocardiography, to episodes of presyncope and syncope, ventricular fibrillation, and sudden death. QT prolongation showed inconsistent correlation with functional cardiology. Based upon analysis of 28 heterozygous family members, estimates of penetrance and expressivity are derived. Conclusions These estimates of penetrance and expressivity, for this specific variant, may be useful in clinical practice. Review of the literature indicates that individual CACNA1C variants have their own particular genotype–phenotype correlations. We suggest that, at least in respect of the particular variant reported here, “arrhythmogenic channelopathy” may be a more fitting nomenclature than long QT syndrome.