Diagnostic lacunae and implications of an automated implantable cardioverter defibrillator implantation in a child with type 3 Long QT (LQT3) syndrome.

A diagnosis of congenital long QT interval syndrome based on history and electrocardiogram was made in a child in the absence of readily available genetic testing. A genotype 3 (LQT3) was suspected after exclusion of other variants as the child was non-responsive to beta-blocker and sodium channel blocker medication. As the child continues to show episodic bradycardia, polymorphic ventricular ectopy, and T-wave alternans, a single-chamber automated implantable cardioverter-defibrillator implantation was done successfully. This report highlights how the diagnosis of LQT3 was arrived at as well as the anesthetic challenges in the management of patients with LQTS.

Oral ascorbic acid in combination with beta-blockers is more effective than beta-blockers alone in the prevention of atrial fibrillation after coronary artery bypass grafting.

Because adrenergic beta antagonists are not sufficient to prevent atrial fibrillation after coronary artery bypass grafting, this prospective, randomized trial was designed to evaluate the effects of ascorbic acid as an adjunct to beta-blockers. Fifty patients formed our ascorbic acid group, and another 50 patients formed our control group. All patients were older than 50 years, were scheduled to undergo coronary artery bypass grafting, and had been treated with beta-blockers for at least 1 week before surgery. The mean age of the population was 60.19+/-7.14 years; 67% of the patients were men. Patients in the ascorbic acid group received 2 g of ascorbic acid on the night before the surgery and 1 g twice daily for 5 days after surgery. Patients in the control group received no ascorbic acid. Patients in both groups continued to receive beta-blockers after surgery. Telemetry monitoring was performed in the intensive care unit, and Holter monitoring was performed for 4 days thereafter. The incidence of postoperative atrial fibrillation was 4% in the ascorbic acid group and 26% in the control group (odds ratio, 0.119; 95% confidence interval, 0.025-0.558, P = 0.002). We conclude that ascorbic acid is effective, in addition to being well-tolerated and relatively safe. Therefore, it can be prescribed as an adjunct to beta-blockers for the prophylaxis of post-bypass atrial fibrillation.

ZP123 reduces energy required for defibrillation by preventing connexin43 remodeling during prolonged ventricular fibrillation in swine.

In ventricular fibrillation, the uncoupling of gap junctions slows conduction velocity and increases action-potential dispersion, which slows and diminishes defibrillation. We studied how the peptide ZP123, a gap-junction enhancer, might lower defibrillation-energy requirements during ventricular fibrillation in live pigs. We randomly assigned 33 pigs into 3 groups: ZP123 (receiving a 1-µg/kg bolus and 10 µg/kg/hr of ZP123), control (receiving saline solution), and sham (undergoing a sham operation). After a 30-min administration of agents, ventricular fibrillation was induced and left untreated for 8 min. Biphasic defibrillation of 50 J was increased by 50-J increments as necessary. Defibrillation-energy requirements were defined as the lowest energy required to achieve defibrillation. Electrocardiographic values were obtained before and after the administration of agents. Western blot and immunofluorescence analyses were performed on ventricular myocardial samples. All but one pig survived. The ZP123 treatment did not alter electrocardiographic variables. In the ZP123 group, the average required defibrillation energy was lower than that in the control group (327.28±269.6 vs 610±192.64 J; P=0.015), and the cumulative percentage of successful defibrillation at upper energy levels was higher (P<0.05). Supraventricular rhythm occurred more often in the ZP123 group than in the control group (72.7% vs 50%, P=0.042). Western-blot and immunofluorescence results showed that ZP123 did not alter the total amount of connexin43 but did prevent its dephosphorylation. We conclude that ZP123 can reduce defibrillation-energy requirements by preventing connexin43 remodeling during prolonged ventricular fibrillation.

Syncope, widened QRS interval, and left ventricular systolic depression: coincident with propafenone therapy for atrial fibrillation.

We report the case of a 46-year-old man who developed syncope, a widened QRS interval, and depressed left ventricular systolic function during propafenone therapy for atrial fibrillation. These acute findings may have been consequent to an increased dosage of propafenone combined with heavy alcohol consumption that led to decreased metabolism of propafenone. In addition, propafenone is known to interfere with liver function, although this patient's test results showed scant evidence of liver abnormalities. Yet another possible factor is the genetic spectrum in the metabolism of propafenone and other class I antiarrhythmic agents. When propafenone is prescribed, we recommend advising patients that alcohol consumption and interactions with other drugs can lead to increased levels of the antiarrhythmic agent, with resultant toxicity that can lead to adverse cardiovascular effects. Patients taking propafenone should also undergo periodic liver function testing. Finally, attention should be paid to voluntary or official recalls of specific antiarrhythmic medications that are of unreliable quality or potency.