Experimental data suggest that cryoenergy is associated with less endothelial damage and thrombus formation than radiofrequency energy. This study aimed to compare the impact of pulmonary vein isolation (PVI) on the endothelial damage, myocardial damage, inflammatory response, and prothrombotic state between the two latest technologies, second-generation cryoballoon (CB2) and contact force-sensing radiofrequency catheter (CFRF) ablation. Eighty-six paroxysmal atrial fibrillation (AF) patients (55 men; 65 ± 12 years) underwent PVI with either the CB2 (n = 64) or CFRF (n = 22). Markers of the endothelial damage (L-arginine/asymmetric dimethylarginine [ADMA]), myocardial injury (creatine kinase-MB [CK-MB], troponin-T, and troponin-I), inflammatory response (high-sensitive C-reactive protein), and prothrombotic state (D-dimer, soluble fibrin monomer complex, and thrombin-antithrombin complex) were determined before and up to 24-h post-procedure. The total application time was shorter (1,460 ± 287 vs. 2,395 ± 571 [sec], p < 0.01) and total procedure time tended to be shorter (199 ± 37 vs. 218 ± 38 [min], p = 0.06) with CB2 than CFRF ablation. The amount of myocardial injury was greater (CK-MB: 45 ± 17 vs. 11 ± 3 [IU/l], p < 0.01) with CB2 than CFRF ablation. The L-arginine/ADMA ratio was lower (160 ± 51 vs. 194 ± 38, p = 0.028) after CB2 than CFRF ablation. Inflammatory and all prothrombotic markers were significantly elevated post-ablation; however, the magnitude was similar between the two groups. During a mean follow-up of 20 ± 6 months, the single-procedure AF freedom was similar between the CB2 and CFRF groups (60/64 vs. 20/22, p = 0.82). CB2-PVI produces significantly lesser endothelial damage with greater myocardial injury than CFRF-PVI; however, similar anticoagulant regimens are required during the peri-procedural periods in both technologies.
Background: The utility of pressure waveform analyses to assess pulmonary vein (PV) occlusions has been reported in cryoballoon PV isolation (CB‐PVI) using first‐generation CBs. This prospective randomized study compared the procedural and clinical outcomes of pressure‐guided and conventional CB‐PVI.
Methods and Results: Sixty patients with paroxysmal atrial fibrillation underwent CB‐PVI with 28‐mm second‐generation CBs. PV occlusions were assessed either by real‐time pressure waveforms without contrast utilization (pressure‐guided group) or contrast injections (conventional group) and randomly assigned. Before the randomization, 24 patients underwent pressure‐guided CB‐PVIs. In the derivation study, a vein occlusion was obtained in 88/96 (91.7%) PVs among which 86 (97.7%) were successfully isolated by the application. In the validation study, the nadir balloon temperature and total freezing time did not significantly differ per PV between the two groups. The positive predictive value of the vein occlusion for predicting successful acute isolations was similar (93 of 103 [90.2%] and 89 of 98 [90.8%] PVs; P = 1.000), but the negative predictive value was significantly higher in pressure‐guided than angiographical occlusions (14 of 17 [82.3%] vs 7 of 22 [31.8%]; P = .003). Both the procedure (57.7 ± 14.2 vs 62.6 ± 15.8 minutes; P = .526) and fluoroscopic times (16.3 ± 6.4 vs 20.1 ± 6.1; P = .732) were similar between the two groups, however, the fluoroscopy dose (130.6 ± 97.7 vs 353.2 ± 231.4 mGy; P < .001) and contrast volume used (0 vs 17.5 ± 7.7 mL; P < .001) were significantly smaller in the pressure‐guided than conventional group. During 27.8 (5‐39) months of follow‐up, the single procedure arrhythmia freedom was similar between the two groups (P = .438).
Conclusions: Pressure‐guided second‐generation CB‐PVIs were similarly effective and as safe as conventional CB‐PVIs. This technique required no contrast utilization and significantly reduced radiation exposure more than conventional CB‐PVIs.
Patients presenting with aborted cardiac arrest who display early repolarization generally are diagnosed with early repolarization syndrome. Therapeutic hypothermia is a standard strategy to improve neurological outcome in comatose patients after cardiac arrest. We present here a patient in whom therapeutic hypothermia exacerbated the J-wave amplitude and morphology, which resulted in episodes of refractory ventricular fibrillation.
Introduction: Despite the characteristic electrocardiogram (ECG) findings of early activation during ventricular tachyarrhythmias (VAs) and/or excellent pacemapping in the right ventricular outflow tract (RVOT), some VAs may require additional, left-sided ablation for a cure. Methods and Results: This study included five patients with idiopathic VAs whose QRS morphologies were highly suggestive of an RVOT origin. The ECG characteristics and intracardiac electrocardiograms during catheter ablation were assessed. In all patients, the clinical VAs had an LBBB QRS morphology and inferior axis with a precordial R/S transition through leads V3-V5, and negative components in lead I. The earliest activation during the VAs (local electrogram-QRS interval = −34 ± 6.8 ms) and excellent pacemapping were obtained at the posterior portion of the RVOT just beneath the pulmonary valve. However, ablation at those sites failed, and the QRS morphology of the VAs changed. During left-sided OT mapping, the earliest activation was found at sites just contralateral to the initially ablated sites of the RVOT (junction of the left and right coronary cusps = 2, left coronary cusp = 3). In spite of the late activation time and poor pacemapping scores, catheter ablation at those sites cured the VAs. Those successful sites were also near the transitional zone from the great cardiac vein to the anterior interventricular vein (GCV-AIV). Conclusions: Some VAs, highly suggestive of having RVOT origins, require catheter ablation in the left-sided OT near the initially ablated RVOT site. Those VAs have the same ECG characteristics and might have intramural origins in the superobasal LV surrounded by the RVOT, LVOT, and GCV-AIV.
Background--The relationship between the serum levels of matrix metalloproteinase (MMP) and tissue inhibitors of MMP (TIMP) and left ventricular (LV) reverse remodeling (LV-RR) after an acute myocardial infarction (AMI) has not been sufficiently examined.Methods and Results--In 25 patients with successful reperfusion after an AMI and 15 normal control subjects, the serum MMP-2 and TIMP-2 levels were measured on days 1, 2, 3, and 7 and at 1 and 6 months after the AMI onset. LV-RR was defined as a >15% decrease in the LV end-systolic volume index at 6 months after the AMI. The MMP-2 level on day 1 and TIMP-2 levels throughout the study period were comparable between the patients with and without LV-RR. The MMP-2 on day 7 (P<0.05) and the changes in the MMP-2 from day 1 to day 7 (ΔMMP-2; P<0.01) were lower in patients with than in those without LV-RR. The ΔMMP-2 was strongly correlated with the changes in the LV volume and ejection fraction from 1 month to 6 months after the AMI. The ΔMMP-2 value of <À158.5 ng/mL predicted LV-RR with a high accuracy (91.7% sensitivity and 76.9% specificity; area under the curve=0.82).Conclusions--Changes in MMP-2 are associated with LV-RR after an AMI. The DMMP-2 might be a useful predictor of subsequent
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