Pulmonary vein stenosis after catheter ablation: electroporation versus radiofrequency.

BACKGROUND: Radiofrequency ablation inside pulmonary vein (PV) ostia can cause PV stenosis. A novel alternative method of ablation is irreversible electroporation, but the long-term response of PVs to electroporation ablation is unknown. METHODS AND RESULTS: In ten 6-month-old pigs (60-75 kg), the response of PVs to circular electroporation and radiofrequency ablation was compared. Ten consecutive, nonarcing, electroporation applications of 200 J were delivered 5 to 10 mm inside 1 of the 2 main PVs, using a custom-deflectable, 18-mm circular decapolar catheter. Inside the other PV, circular radiofrequency ablation was performed using 30 W radiofrequency applications via an irrigated 4-mm ablation catheter. PV angiograms were made before ablation, immediately after ablation, and after 3-month survival. PV diameters and heart size were measured. With electroporation ablation, PV ostial diameter decreased 11±10% directly after ablation, but had increased 19±11% after 3 months. With radiofrequency ablation, PV ostial diameter decreased 23±15% directly after ablation and remained 7±17% smaller after 3 months compared with preablation diameter despite a 21±7% increase in heart size during aging from 6 to 9 months. CONCLUSIONS: In this porcine model, multiple circumferential 200-J electroporation applications inside the PV ostia do not affect PV diameter at 3-month follow-up. Radiofrequency ablation inside PV ostia causes considerable PV stenosis directly after ablation, which persists after 3 months.

Myocardial lesion depth with circular electroporation ablation.

BACKGROUND: Recently, we demonstrated the feasibility and safety of circular electroporation ablation in porcine pulmonary vein ostia, but the relationship between the magnitude of the application and lesion dimensions is still unknown. METHODS AND RESULTS: An in vivo porcine study was performed on left ventricular epicardium submerged under 10 mm of blood, using devices that mimic a 20-mm-diameter 7F circular ablation catheter. Model D contained 10 separate electrodes, whereas model M consisted of 1 circular electrode. Ablations were performed at 50, 100, and 200 J with model D and at 100 J with model M. Lesion dimensions were measured after 3-week survival. All applications resulted in smooth voltage waveforms demonstrating the absence of vapor globe formation, arcing, and a pressure wave. Applications up to 100 J with model D resulted in separate lesions under the electrodes. At 200 J, continuous deep circular lesions were created despite the use of separate electrodes. There was a significant relationship between applied current and median lesion depth, with a slope of 0.17 mm/A. At 100 J, there was no difference in lesion depth or width between models D and M. The electrodes and ablation site directly after ablation showed no signs of thermal damage. CONCLUSIONS: In an epicardial porcine model with blood around the application site, continuous circular lesions, deep enough for electric pulmonary vein isolation, were created with a single circular 200-J application. Lesions were continuous despite the use of separate electrodes. Lesion depth increased with the magnitude of the application.

Late left ventricular pseudoaneurysm formation following subacute myocardial infarction.

We describe a patient with a subacute inferior myocardial infarction who developed a pseudo-aneurysm more than 18 days after the acute event. This is an unusual case with three different complications of a myocardial infarction: Firstly, ventricular rupture is usually the result following transmural myocardial infarction without reperfusion. However, coronary angiography confirmed reperfusion after late thrombolysis in this patient. The subacute rupture could potentially be caused or aggravated by the late thrombolysis. Secondly, this patient developed a mural apical thrombus in a non-infarcted region. It seems most likely that the new infarct caused a low flow state which enhanced thrombus formation. Against expectations, this developed at the apex rather than the site of the recent inferior wall myocardial infarction. Thirdly, we documented the development of a pseudo-aneurysm more than 18 days after the myocardial infarction. This complication is rarely seen at this stage after a myocardial infarction, as most pseudo-aneurysms are formed within 7 days after a myocardial infarction. We have beautifully visualised the apical thrombus and pseudo-aneurysm with echocardiography. This report shows that serial echocardiography is a very useful tool in evaluating the patient's clinical and cardiac status in the period after a myocardial infarction.

Acute blindness as the presenting symptom of ST segment elevation myocardial infarction.

This case report shows acute blindness as the first symptom of a silent anterior wall myocardial infarction. Although uncommon, all patients with a ST segment elevation myocardial infarction and a simultaneous neurological defect need additional assessment.