Acute Hemodynamic and Tissue Effects of Cryoballoon Ablation on Pulmonary Vessels: The IVUS‐Cryo Study. Issue 6 (June 2017)

• Record Type: Journal Article
• Authors: Baran, Jakub; Lewandowski, Paweł; Smarż, Krzysztof; Sikorska, Agnieszka; Zaborska, Beata; Kułakowski, Piotr
• Is Part Of: Journal of the American Heart Association. Volume 6:Issue 6(2017)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2017-06
• Subjects: atrial fibrillation -- collateral damage -- cryoballoon ablation; Heart -- Diseases -- Periodicals; Cardiovascular system -- Diseases -- Periodicals; Cerebrovascular disease -- Periodicals; Cardiology -- Periodicals; 616.1
• DOI: 10.1161/JAHA.117.005988
• Languages: English
• ISSNs: 2047-9980

Abstract

Abstract : Background: Cryoballoon‐based pulmonary vein isolation (CB‐PVI) has been widely used for the treatment of atrial fibrillation. Although generally safe and effective, the procedure may be associated with pulmonary vein (PV) stenosis and bronchial or esophageal injury. The mechanisms leading to these complications have not been studied in detail. Our aim was to examine acute effects of cryoballoon on the pulmonary vessel and right heart pressures as well as PV wall morphology. Methods and Results: In 8 patients (5 men, mean age 55±14 years) undergoing CB‐PVI, pressure in each PV was measured by catheter located inside the PV directly before and after CB‐PVI. The right atrial, right ventricular, and pulmonary artery pressures as well as pulmonary arterial wedge capillary pressure in the pulmonary artery branch corresponding to target PV were also measured. Morphological changes in PVs were assessed using intravascular ultrasonography. There were no significant differences in PV pressures before and after ablation. The pulmonary arterial wedge capillary pressure significantly increased during cryoapplication (left superior: 20±10 versus 29±8.5 mm Hg, P =0.004; left inferior: 24±10 versus 32±6 mm Hg, P =0.012; right superior: 25±9 versus 35±10 mm Hg, P =0.002; right inferior: 24±10 versus 37±12 mm Hg, P =0.0036). The right atrial and pulmonary artery pressures increased significantly after CB‐PVI (9±6 versus 13±8 mm Hg, P =0.004, and 20±9 versus 24±10 mm Hg, P =0.048, respectively). Intravascular ultrasonography showed acute edema and dissection‐like changes causing relative lumen narrowing in 90% of PVs. Conclusions: CB‐PVI causes significant rise in pulmonary artery and right atrial pressures as well as PV wall damage. The clinical significance of these findings warrants further investigations.