Cross-sectional imaging obtained immediately following radiofrequency atrial fibrillation ablation does not predict endoscopic evidence of esophageal injury.

BACKGROUND: Radiofrequency atrial fibrillation ablation (AFA) is commonly performed in patients with atrial fibrillation. It is imperative to develop a strategy for the early detection of esophageal lesions secondary to AFA. The current protocol is to obtain cross-sectional imaging before and immediately after the procedure. If patients have evidence of esophageal inflammation, they undergo esophagogastroduodenoscopy (EGD). We hypothesized that esophageal abnormalities seen on imaging immediately post-ablation are a poor predictor of the damage seen during EGD. METHODS: Patients referred for EGD following AFA from 1/2009 to 11/2010 were included. Two endoscopists reviewed and scored the EGD images. Two radiologists reviewed the post-AFA imaging studies. For computed tomography (CT) scans, esophageal inflammation was scored from 0 to 2. For T2 and delayed magnetic resonance imaging (MRI) pictures, esophageal enhancement was scored from 0 to 2, with the circumference involved as 0, <50%, or >50%, and the length of esophageal enhancement in mm. RESULTS: In total, 76 patients were included; 22 patients had only endoscopic images and 54 had both endoscopic and radiologic images for review. Of the post-AFA imaging studies, 16 were CTs and 60 were MRIs. The kappa score for the inter-rater agreement of esophageal inflammation on EGD was 0.4584 (moderate). For MRIs, the kappa scores for T2 images were 0.1980 and 0.2857 for edema and circumference, respectively. For delayed images, the kappa scores were 0.2687 and 0.3101 for edema and circumference, respectively. The kappa scores were negative between EGD score by T2 edema (-0.2104) and circumference (-0.2212), and between EGD score and delayed edema (-0.0588) and circumference (-0.0446). When measures were treated as dichotomous, the overall agreement between CT measures and EGD scores was kappa = 0, for T2 measures and EGD kappa = -0.2963, 95% confidence interval (CI) (-0.5643, -0.0282), and between delayed measures kappa = -0.0244, 95% CI (-0.1420, -0.0932). CONCLUSIONS: There was no agreement between immediate imaging and the endoscopic findings of esophageal inflammation after AFA. A longer period of time between AFA and obtaining an imaging study may be useful in detecting patients with significant esophageal injury who should undergo EGD to assess for complications of AFA. Further studies are needed in order to determine the best modalities and optimal timing to detect post-AFA esophageal damage in an attempt to prevent the formation of atrial-esophageal fistulas.

Ticagrelor Use in Acute Myocardial Infarction: Balancing Evidence-Based Medicine with Affordability.

STUDY OBJECTIVE: Data from randomized controlled trials support a mortality benefit with ticagrelor versus clopidogrel among patients with acute myocardial infarction (AMI). Many healthcare providers preferentially treat patients with AMI with ticagrelor. The goal of this study was to determine the association between out-of-pocket drug costs and ticagrelor continuation compared with switching to clopidogrel among patients hospitalized for AMI, following a pharmacist-led discussion on outpatient co-payment costs for ticagrelor. DESIGN: Retrospective cohort study. SETTING: A tertiary care academic medical center. PATIENTS: Patients hospitalized with AMI between February 15, 2015 and January 23, 2017, who were loaded with ticagrelor on presentation. MAIN RESULTS: Of 143 patients with AMI loaded with ticagrelor, 70 (49%) switched to clopidogrel after cost discussion. The median monthly ticagrelor co-payment was $268.29 (interquartile range [IQR] $45-$350) for switchers, versus $18 (IQR $6-$24) for non-switchers (p<0.001). Patients with co-payments of $100/month or more were 3.4 times more likely to switch to clopidogrel (relative risk 3.41, 95% confidence interval 2.12 to 5.47), compared with patients with co-payments of less than $100/month. CONCLUSIONS: Following a discussion of outpatient costs, half of patients with AMI switched from ticagrelor to clopidogrel when given the choice.

Carcinoid Syndrome-Induced Ventricular Tachycardia.

Introduction. Carcinoid tumors are rare neuroendocrine malignancies that secrete multiple bioactive substances. These bioactive substances are responsible for the carcinoid syndrome characterized by diarrhea, flushing, syncope, and right-sided valvular heart disease. Previous case reports have described carcinoid syndrome associated with coronary vasospasm and the well-characterized carcinoid heart disease. Case. Our patient is a 73-year-old female with complex past medical history most notable for metastatic carcinoid tumors diagnosed in 2013-05. She initially presented in 2014-09 with syncope and dizziness associated with sinus pause on an event monitor. She received a pacemaker given normal left ventricular function and was discharged. However, she was readmitted with similar symptoms corresponding to multiple episodes of ventricular tachycardia. She was started on high-dose beta blockade and has had no recurrence of arrhythmia over a follow-up period of 12 months. Conclusion. We hypothesize that the patient's ventricular tachycardia was mediated by the multiple bioactive substances secreted by her carcinoid tumors. Her carcinoid tumor biomarkers were elevated and other explanations for arrhythmia were investigated and ruled out. To our knowledge, this is the first case of ventricular tachycardia mediated by carcinoid syndrome and suppressed by beta-blocker. Further investigation into this relationship is needed.