Citations

Pulmonary vein stenosis (PVS) is a known complication after catheter ablation of arrhythmias. Surprisingly, little information is available on its manifestations in the lung. We describe the case of a 39-year-old woman who presented from an outside hospital with worsening shortness of breath after catheter ablation of pulmonary veins for atrial fibrillation. After an initial diagnosis of pneumonia and its nonimprovement with antibiotics, a surgical lung biopsy was done and interpreted as nonspecific interstitial pneumonia (NSIP) with vascular changes consistent with pulmonary arterial hypertension. Later, she was admitted to our institution where a transthoracic echocardiogram (TTE) and subsequent computed tomography (CT) angiogram of the heart showed severe stenosis of all four pulmonary veins. The previous lung biopsy was rereviewed and reinterpreted as severe parenchymal congestion mimicking NSIP. Our case demonstrates that PVS is an underrecognized complication of catheter ablation, and increased awareness among both clinicians and pathologists is necessary to avoid misdiagnosis.

The mechanisms by which bacteria colonize and damage ciliated epithelium are important in understanding the pathophysiology of rhinitis, sinusitis, and otitis. Bacteria that have the ability to impair mucociliary clearance would be at an advantage in establishing infection of ciliated surfaces. This study investigates the effect of Hemophilus Influenzae, Streptococcus pneumoniae, Brahmanella catarralis, and Staphylococcus epidermidis on the ciliary activity of normal ciliated nasal epithelium in human beings. Ciliary activity of the nasal epithelium in the presence of each pathogen was assessed for more than 240 minutes with a photometric method of ciliary beat frequency (CBF) measurement. H. influenzae exerted significant effects on ciliary activity, with a 46% decrease in the CBF by 4 hours (with bacteria‐containing broth) and a 32% decrease with bacteria‐free filtrate. S. epidermidis decreased CBF by 44% with the bacterial broth. A sterile cell‐free filtrate had no significant effect. S. pneumoniae and B. catarralis had no significant effect on CBF within a 240‐minute period. H. influenzae and S. epidermidis disrupted normal synchronous ciliary motion, causing adjacent cilia to beat at different rates.

Background There is significant practice variation in oral anticoagulation ( OAC ) use following catheter ablation for atrial fibrillation. It is not clear whether the risk of cardioembolism increases after discontinuation of OAC following catheter ablation. Methods and Results We identified 6886 patients within a large national administrative claims database who underwent catheter ablation for atrial fibrillation between January 1, 2005, and September 30, 2014. We assessed the effect of time off of OAC by CHA 2 DS 2 ‐ VAS c score (after adjusting for other comorbidities) on risk of cardioembolism, using Cox proportional hazards models. There was an increase in the use of non–vitamin K OAC after ablation from 0% in 2005 to 69.8% in 2014. OAC discontinuation was high, with only 60.5% and 31.3% of patients remaining on OAC at 3 and 12 months, respectively. The rate of discontinuation was higher in low‐risk patients (82% versus 62.5% at 12 months for CHA 2 DS 2 ‐ VAS c 0–1 versus ≥2, respectively; P <0.001). Stroke occurred in 1.4% of patients with CHA 2 DS 2 ‐ VAS c ≥2 and 0.3% of those with CHA 2 DS 2 ‐ VAS c 0 or 1 over the study follow‐up. The risk of cardioembolism in the first 3 months after ablation was increased among those with any time off OAC (hazard ratio 8.06 [95% CI 1.53–42.3], P <0.05). The risk of cardioembolism beyond 3 months was increased with OAC discontinuation among high‐risk patients (hazard ratio 2.48 [95% CI 1.11–5.52], P <0.05) but not low‐risk patients. Conclusion The overall risk of stroke in postablation patients is low; however, OAC discontinuation after ablation is common and is associated with increased risk of cardioembolism for all patients within the first 3 months and for high‐risk patients in the long term. Continuing OAC for at least 3 months in all patients and indefinitely in high‐risk patients appears to be the safest strategy.