1.
Compound heterozygous mutations in the SCN5A-encoded Nav1.5 cardiac sodium channel resulting in atrial standstill and His-Purkinje system disease.
Baskar, S, Ackerman, MJ, Clements, D, Mayuga, KA, Aziz, PF
The Journal of pediatrics. 2014;(5):1050-2
Abstract
An 11-year-old girl on evaluation for syncope was found to have progressive sinus node dysfunction and His-Purkinje system disease with atrial standstill. Genetic analysis revealed compound heterozygous mutations of the SCN5A gene in a novel combination.
2.
Early-onset pentamidine-associated second-degree heart block and sinus bradycardia: case report and review of the literature.
Antoniou, T, Gough, KA
Pharmacotherapy. 2005;(6):899-903
Abstract
Although various manifestations of pentamidine-induced cardiotoxicity have been reported, to our knowledge, second-degree heart block associated with this agent has not been described. In addition, cardiac adverse effects usually develop after at least 6 days of therapy. We describe a 54-year-old, human immunodeficiency virus-positive man with a history of sulfonamide allergy who received treatment with pentamidine for Pneumocystis jiroveci pneumonia. After only the third dose of pentamidine, it was noted that the patient's heart rate had decreased to 48 beats/minute. Subsequently, five episodes of Wenckebach (Mobitz type 1) heart block with a ventricular rate of 28 beats/minute were observed on continuous cardiac telemetry. Serum electrolyte and creatinine levels remained within normal limits. Within 4 days of discontinuing the pentamidine, the patient's heart rate stabilized at 80 beats/minute without further intervention. Clinicians should be vigilant when monitoring for cardiotoxicity in patients receiving pentamidine throughout the duration of therapy. In addition, they should continue to reserve its use for moderate-to-severe Pneumocystis jiroveci pneumonia for which trimethoprim-sulfamethoxazole is ineffective or contraindicated.