Ablation catheter orientation: In vitro effects on lesion size and in vivo analysis during PVI for atrial fibrillation.

BACKGROUND: Catheter-delivered radiofrequency (RF) lesion formation is a complex phenomenon, and few studies have explored the effect of catheter orientation on lesion size and catheter orientation behavior during pulmonary vein isolation (PVI) procedures. We evaluated the influence of catheter orientation on lesion dimensions in an in vitro experimental setting and investigated the catheter orientation behavior during PVI. METHODS AND RESULTS: 72 lesions were created in vitro on a porcine heart using a contact force catheter in a parallel, oblique, and perpendicular tip to tissue orientation. The superficial lesion length (SLL) increased shifting the catheter from perpendicular to parallel orientation. The intratissue absolute maximal lesion length (AML) was greater with an oblique catheter orientation. The lesion depth (LD) and the superficial lesion width (SLW) resulted similar with any orientation. Data from 21 PVI procedures in patients with paroxysmal atrial fibrillation using the "wide antral circumferential RF ablation" (WACA) technique were retrospectively analyzed. The mean contact angle among 1130 RF lesions was 28 ± 20°. A prevalent parallel orientation was noted in the anterior WACA segments, whereas it resulted more perpendicular in the posterior segments. Significant differences in catheter orientation between the three operators were found only in few WACA segments. CONCLUSIONS: In an in vitro setting, catheter orientation affects SLL and AML, but not LD and SLW. During PVI procedures, catheter orientation resulted mostly parallel to the endocardium. Catheter orientation varied among different WACA segments, but only small differences were found between three operators when considering similar WACA segments.

A Nonfluoroscopic Technique for Coronary Arteries Three-Dimensional Mapping during Epicardial Ventricular Tachycardia Ablation.

When performing epicardial ablation of ventricular tachycardia (VT), caution must be taken not to damage the coronary arteries. We report a case in which a new, nonfluoroscopic technique for incorporating an accurate, real-time reconstruction of the main coronary vessels into a three-dimensional electroanatomic map was used for epicardial VT ablation.

Radiofrequency ablation of drug-refractory atrial fibrillation: an observational study comparing 'ablate and pace' with pulmonary vein isolation.

AIMS: To compare clinical characteristics, procedure complexity, acute and long-term outcome of 'ablate and pace' (A&P) with pulmonary vein isolation (PVI) in patients with drug-refractory atrial fibrillation (AF). So far, only few small studies have compared the two procedures. METHODS AND RESULTS: We analysed retrospectively a cohort of symptomatic consecutive patients with drug-refractory AF. Group 1 included 100 patients treated with A&P and Group 2 included 144 patients treated with PVI. Group 1 patients were older (74 +/- 8 vs. 56 +/- 9 years; P < 0.0001), had lower left ventricular ejection fraction (50 +/- 13% vs. 59 +/- 7%; P < 0.05), and a lower prevalence of paroxysmal AF (46% vs. 65%; P < 0.05). Acute success was not statistically different (98% vs. 92.3%, P = ns). Group 1 patients had shorter procedure time and lower radiation exposure with respect to Group 2 patients (70 +/- 15 vs. 204 +/- 58 min, and 8 +/- 4 vs. 57 +/- 22 min; P < 0.0001, respectively). After a median follow-up of 29 months (I, III quartile; 15, 40 months) vs. 25 months (I, III quartile; 8, 36 months) (P = ns), all the patients in Group 1 were free of symptomatic AF, while 113 patients (79%) of Group 2 were in stable sinus rhythm (P < 0.0001). Persistent or permanent AF has been documented in 58 patients (58%) of Group 1 vs. 11 (8%) of Group 2 (P < 0.0001). CONCLUSION: In this series (i) patients treated with A&P and PVI for drug-refractory AF showed significant differences in clinical profile; (ii) A&P is a shorter and less complex procedure, but is associated with a higher rate of persistent AF; (iii) symptomatic recurrences of paroxysmal AF were more frequent in PVI group. Randomized studies appear necessary to identify the best strategy in selected cases.

Overexpression of tumor necrosis factor (TNF)alpha and TNFalpha receptor I in human viral myocarditis: clinicopathologic correlations.

Proinflammatory cytokines, including tumor necrosis factor (TNF)alpha, have been recognized as important physiopathogenetic factors in the initiation and continuation of inflammatory cardiomyopathies. Experimental and preliminary human studies have demonstrated that TNFalpha plays a crucial role in enteroviral-induced myocarditis. In this study, we investigated the expression of TNFalpha and both its receptors (TNFRI and TNFRII) in both viral and nonviral myocarditis. Myocardial expression of TNFalpha was then correlated with different clinical and pathologic findings. TNFalpha expression was investigated in endomyocardial biopsies obtained from 38 patients with myocarditis and from eight control subjects by using reverse transcriptase-polymerase chain reaction (PCR) and immunohistochemistry. Viral etiology was diagnosed by PCR in 20 cases: enterovirus in seven, Epstein-Barr virus in four, hepatitis C virus in three, adenovirus in two, influenza virus in two, cytomegalovirus in one, and double infection adenovirus and enterovirus in one. Immunohistochemistry was also used to analyze both TNFalpha receptors (RI and RII). A semiquantitative analysis was employed (score 0-3) for necrosis, inflammation, fibrosis and immunohistochemical findings. TNFalpha mRNA and TNFalpha protein were significantly more present in viral myocarditis than in nonviral myocarditis (16/20 vs 3/18, P=0.001). Remarkable immunostaining was observed for both receptors, particularly TNFRI. Histological analysis revealed that myocardial necrosis (mean score 1.89 vs 1.15, P=0.01) and cellular infiltration (mean score 2.26 vs 1.78, P=0.05) were more prominent in TNFalpha-positive cases. Among TNFalpha-positive cases, the greater TNFalpha mRNAs, the more impaired was cardiac function. Our findings suggest that the expression of TNFalpha may play an important role in the pathogenesis of viral myocarditis of any etiology and may influence the severity of cardiac dysfunction. Cytokine effects are more strictly linked to overexpression of TNFRI.