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BACKGROUND: Left-sided ablation, targeting left inferior AV nodal extensions, is thought to be necessary for success in a small proportion of atrioventricular nodal re-entrant tachycardia (AVNRT) ablations; however Indian data are scarce in this regard. METHODS: Consecutive cases of AVNRT undergoing slow pathway ablation in a single centre over an 18-month period were retrospectively analyzed. Left-sided ablation at the posteroseptal mitral annulus was performed if right-sided ablation failed to abolish AVNRT. RESULTS: From January 2017 to June 2018, out of 215 consecutive supraventricular tachycardia (SVT) cases, 154 (71.6%) were AVNRT (47.1 ± 13.1 years, 46.1% male). Trans-septal ablation was required in 5 (3.2%) cases (mean age 48.8 ± 9.4 years; 4 female, 1 male); all with typical (slow-fast) form of AVNRT. Compared with cases needing only right-sided ablation, radiofrequency time (50.8 ± 16.9 vs. 9.9 ± 8.5 min; p = 0.005) and procedure time (166.0 ± 35.0 vs 79.6 ± 35.9 min; p = 0.004) were significantly longer for trans-septal cases, while baseline intervals and tachycardia cycle length were not significantly different. Junctional ectopy was seen in only 2 of the 5 cases during left-sided ablation, but acute success (non-inducibility) was obtained in 3 cases. There were no instances of AV block. Over mean follow-up of 12.2 ± 4.0 months, clinical recurrence of AVNRT occurred in one case, while others remained arrhythmia-free without medication. CONCLUSION: Left-sided ablation was required in a small proportion of AVNRT ablations. Trans-septal approach targeting the posteroseptal mitral annulus was safe and yielded good mid-term clinical success.
RESUMO
<p><b>INTRODUCTION</b>Recently, there has been increasing evidence that genetic variation in the angiotensin-converting enzyme (ACE) plays an important role in myocardial infarction. Therefore, the present study was carried out with the aim of investigating the association of the ACE gene insertion/deletion (I /D) polymorphism and its levels in myocardial infarction patients and their first-degree relatives (FDRs).</p><p><b>METHODS</b>206 patients with myocardial infarction, 168 FDRs and 210 control subjects were enrolled in the study. ACE I /D polymorphism was determined using the polymerase chain reaction method. Serum ACE levels were measured using the photometric method.</p><p><b>RESULTS</b>The DD genotype and ACE activity were significantly higher in patients (p-value is 0.00006 and 0.0001, respectively) and FDRs (p-value is 0.003 and 0.04, respectively) compared with the controls.</p><p><b>CONCLUSION</b>ACE DD genotype and ACE levels are important risk factors for myocardial infarction. This study indicates that the higher frequency of the DD genotype and ACE levels observed in FDRs may increase susceptibility to developing myocardial infarction.</p>