BackgroundRhythm outcomes after the pulmonary vein isolation (PVI) using the cryoballoon (CB) are reported to be excellent. However, the lesions after CB ablation have not been well discussed. We sought to characterize and compare the lesion formation after CB ablation with that after radiofrequency (RF) ablation.MethodsA total of 42 consecutive patients who underwent PVI were enrolled (29 in the CB group and 13 in the RF group). The PVI lesions were assessed by late gadolinium enhancement magnetic resonance imaging 1–3 months after the PVI. The region around the PVs was divided into eight segments: roof, anterior‐superior, anterior‐carina, anterior‐inferior, bottom, posterior‐inferior, posterior‐carina, and posterior‐superior segment. The lesion width and lesion gap in each segment were compared between the two groups. Lesion gaps were defined as no‐enhancement sites of >4 mm.ResultsAs compared to the RF group, the overall lesion width was significantly wider and lesion gaps significantly fewer at the anterior‐superior segment of the left PV (LAS) and anterior‐inferior segment of the right PV (RAI) in the CB group (lesion width: 8.2 ± 2.2 mm vs 5.6 ± 2.0 mm, P = .001; lesion gap at LAS: 7% vs 38%, P = .02; lesion gap at RAI: 7% vs 46%, P = .006).ConclusionsThe PVI lesions after CB ablation were characterized by extremely wider and more continuous lesions than those after RF ablation.
A 51‐year‐old male with dextrocardia and situs inversus underwent catheter ablation for paroxysmal atrial fibrillation. Because the procedure through the trans‐septal approach was impossible due to the inferior vena cava continuity with azygos vein, we performed pulmonary vein isolation using magnetic navigation system through the retrograde trans‐aortic approach. Superior and inferior left‐sided and superior right‐sided pulmonary veins could be isolated which was confirmed by the ablation catheter. The patient was free from atrial fibrillation episode at the 12 months follow‐up except only one palpitation episode lasting nearly 12 hours at 9 months after the ablation.
A 77-year-old man developed pulmonary tumor thrombotic microangiopathy (PTTM) 2 days after undergoing transurethral resection for urothelial carcinoma (G3) of the urinary bladder and died of respiratory failure 6 days later. Histological findings demonstrated marked intimal fibrocellular proliferation, fibrin thrombi, and both cancer cells and fibrin thrombi in the arteries of the lungs, findings consistent with PTTM. Prominent stenosis in arteries smaller than 300 μm was also seen. The Ki-67 labeling index of primary and metastasized cancer cells was 62.4 % and 70.2 %, respectively. The membranes of metastasized cancer cells expressed E-cadherin, similar to membranes in the urinary bladder. An aggressive PTTM course is affected by intimal fibrocellular proliferation and the high cell proliferation of cancer cells. Furthermore, prominent stenosis in small arteries and membranous staining of E-cadherin of metastasized cells suggest that cancer cells formed clusters by maintaining adhesion molecules and migrated into the arteries of the lungs, where they easily caused damage to the endothelium of small arteries, in contrast to dispersed cancer cells.
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