An Electrical Storm Is Coming!: Ventricular Storm Case Study.

A 65-year-old man presented to the emergency department (ED) for evaluation of epigastric and chest pain. On presentation, a 12-lead electrocardiogram revealed a patient in rapid atrial fibrillation (AFib) with anteroseptal myocardial infarction. Treatment of ST-elevation myocardial infarction (STEMI) and rapid AFib were initiated, and the patient was flown to a regional percutaneous coronary intervention center. Two weeks later, the patient presented to the same ED with a LifeVest external defibrillator (Zoll Medical, Chelmsford, MA). The patient received electrical shock in excess of 10 times from the LifeVest prior to ED arrival where he promptly developed ventricular tachycardia (VT). After cardioversion, the VT storm persisted and required multiple cardioversions, resuscitation, intubation, and transfer back to a tertiary cardiac center for electrophysiology studies and internal cardiac defibrillator placement. This case explores the course of a patient's anteroseptal infarction, utilization and description of the LifeVest external defibrillator, and the subsequent visit to the ED in VT storm. It provides insight into the team approach, decision-making process, and managing a complex medical illness. Furthermore, it helps identify methods for emergency providers to improve their approach in both complex and rare cases.

Refractory Ventricular Fibrillation Successfully Cardioverted With Dual Sequential Defibrillation.

BACKGROUND: Current guidelines for the treatment of adult patients in cardiac arrest are supplied by the American Heart Association through basic life support and advanced cardiovascular life support (ACLS) provider courses. When treatments defined by the ACLS guidelines are unsuccessful in terminating a lethal dysrhythmia, the use of alternative strategies may prove useful. In this case, two defibrillators were used to deliver a greater than normal energy waveform over an extended time interval to return a patient to a normal sinus rhythm. CASE REPORT: A 56-year-old woman presented to the emergency department with complaints of chest pain, nausea, and vomiting. The patient's initial work-up, including an electrocardiogram and cardiac troponin, did not show evidence of acute ischemia, and she was admitted to the observation unit for further evaluation. While in the emergency department, the patient developed ventricular fibrillation, and ACLS was initiated. After four unsuccessful defibrillation attempts, a second defibrillator was placed on the patient, and the two were activated almost simultaneously. The patient had immediate return of spontaneous circulation, underwent cardiac catheterization, and was discharged home 1 week later. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: This case shows that dual sequential defibrillation may be a successful method for terminating refractory ventricular fibrillation. Further investigation on cardiac resuscitation should be conducted to standardize the dual sequential defibrillation delivery procedure. Until such guidelines are established, physicians should take this treatment into consideration when standard ACLS measures have failed to successfully terminate refractory ventricular fibrillation.

A common variant in the patatin-like phospholipase 3 gene (PNPLA3) is associated with fatty liver disease in obese children and adolescents.

UNLABELLED: The genetic factors associated with susceptibility to nonalcoholic fatty liver disease (NAFLD) in pediatric obesity remain largely unknown. Recently, a nonsynonymous single-nucleotide polymorphism (rs738409), in the patatin-like phospholipase 3 gene (PNPLA3) has been associated with hepatic steatosis in adults. In a multiethnic group of 85 obese youths, we genotyped the PNLPA3 single-nucleotide polymorphism, measured hepatic fat content by magnetic resonance imaging and insulin sensitivity by the insulin clamp. Because PNPLA3 might affect adipogenesis/lipogenesis, we explored the putative association with the distribution of adipose cell size and the expression of some adipogenic/lipogenic genes in a subset of subjects who underwent a subcutaneous fat biopsy. Steatosis was present in 41% of Caucasians, 23% of African Americans, and 66% of Hispanics. The frequency of PNPLA3(rs738409) G allele was 0.324 in Caucasians, 0.183 in African Americans, and 0.483 in Hispanics. The prevalence of the G allele was higher in subjects showing hepatic steatosis. Surprisingly, subjects carrying the G allele showed comparable hepatic glucose production rates, peripheral glucose disposal rate, and glycerol turnover as the CC homozygotes. Carriers of the G allele showed smaller adipocytes than those with CC genotype (P = 0.005). Although the expression of PNPLA3, PNPLA2, PPARγ2(peroxisome proliferator-activated receptor gamma 2), SREBP1c(sterol regulatory element binding protein 1c), and ACACA(acetyl coenzyme A carboxylase) was not different between genotypes, carriers of the G allele showed lower leptin (LEP)(P = 0.03) and sirtuin 1 (SIRT1) expression (P = 0.04). CONCLUSION: A common variant of the PNPLA3 gene confers susceptibility to hepatic steatosis in obese youths without increasing the level of hepatic and peripheral insulin resistance. The rs738409 PNPLA3 G allele is associated with morphological changes in adipocyte cell size.