Concomitant Wolff-Parkinson-White and Atrioventricular Nodal Reentrant Tachycardia: Which Pathway to Ablate?

BACKGROUND: Atrioventricular nodal reentrant tachycardia (AVNRT) is the most common form of supraventricular tachycardia. In contrast, Wolff-Parkinson-White (WPW) pattern consists of an accessory pathway, which may result in the development of ventricular arrhythmias. Frequent tachycardia caused by AVNRT and accessory pathways may play a role in left ventricular systolic dysfunction. CASE REPORT: A 54-year-old man presented with palpitations and acute decompensated congestive heart failure. His baseline EKG showed Wolff-Parkinson-White (WPW) pattern. While hospitalized, he had an episode of atrioventricular nodal reentrant tachycardia (AVNRT). He underwent radiofrequency catheter ablation for AVNRT, and his accessory pathway was also ablated even though its conduction was found to be weak. He was clinically doing well on follow-up visit, with resolution of his heart failure symptoms and normalization of left ventricular function on echocardiography. CONCLUSIONS: This case raises the question whether the accessory pathway plays a role in the development of systolic dysfunction, and if there is any role for ablation in patients with asymptomatic WPW pattern.

Current advances in endovascular therapy for infrapopliteal artery disease.

Peripheral arterial disease (PAD) is a systemic disease with significant morbidity and mortality. A substantial number of patients with PAD have infrapopliteal disease; however, diagnosis based solely on symptoms and ankle-brachial index can lead to delayed or missed opportunities to provide improved quality of life and limb salvage, and potentially reduce mortality. Advances in techniques and devices, and modification of classification systems have shown that an endovascular approach should be the primary therapeutic option for critical limb ischemia resulting from infrapopliteal disease.

Hyperacute drug-induced hepatitis with intravenous amiodarone: case report and review of the literature.

Amiodarone is a benzofuran class III antiarrhythmic drug used to treat a wide spectrum of ventricular tachyarrhythmias. The parenteral formulation is prepared in polysorbate 80 diluent. We report an unusual case of acute elevation of aminotransaminase concentrations after the initiation of intravenous amiodarone. An 88-year-old Caucasian female developed acute hepatitis and renal failure after initiating intravenous amiodarone for atrial fibrillation with a rapid ventricular response in the setting of acutely decompensated heart failure and hepatic congestion. Liver transaminases returned to baseline within 7 days after discontinuing the drug. Researchers hypothesized that this type of injury is related to liver ischemia with possible superimposed direct drug toxicity. The CIOMS/RUCAM scale identifies our patient's acute hepatitis as a highly probable adverse drug reaction. Future research is needed to understand the mechanisms by which hyperacute drug toxicity occurs in the setting of impaired hepatic perfusion and venous congestion.

Modulation of sensory inputs and ectopic presence of Schwann cells depend upon the route and duration of nerve growth factor administration.

Nerve growth factor (NGF) ameliorates deficits in models of cholinergic hypofunction. However, notable adverse effects of intracerebroventricular (ICV) infusion of NGF include weight loss, Schwann cell hyperplasia (SCH), and aberrant sensory and sympathetic sprouting. In order to maintain efficacy on the cholinergic basal forebrain (CBF) and minimize these detrimental effects, intraparenchymal NGF infusion was compared with ICV administration to assess morphological and functional measures. NGF was delivered intraparenchymally (Intra-NGF) or intracerebroventricularly (ICV-NGF) for 3 and 6 months. Hypertrophy of cholinergic nucleus basalis neurons at 3 and 6 months was not different between both routes of administration, indicating similar efficacy for the CBF. SCH surrounding the medulla was observed in both Intra- and ICV-NGF animals due to the widespread distribution of NGF from the infusion site. The thickness of SCH reached a plateau at 3 months in ICV-NGF animals, while further proliferation occurred in Intra-NGF animals. More importantly, ectopic Schwann cells and aberrant sensory and sympathetic sprouting within the medulla oblongata were found solely in ICV-NGF animals. Differential changes in sensory processing were evident by an exaggerated response to acoustic stimuli in Intra-NGF animals and a decrease in thermal pain threshold in ICV-NGF-treated animals. Intra-NGF treatment did not produce the reduction in body weight exhibited by ICV-NGF-treated rats. These results indicate that different routes of NGF administration are identically efficacious for CBF neurons, but differentially modulate behaviors and structures leading to distinct profiles of adverse effects. Thus, current trophic factor delivery methods require further refinement to abolish detrimental effects.