From 1996 to 2011, 57 high-risk patients with BS (35 males; mean age: 43 ± 16 years) underwent an automated implantable cardioverter defibrillator implantation at our center using propofol as induction drug of general anesthesia. Three patients had a history of spontaneous type I ECG, three had aborted sudden death, and 51 had a history of recurrent or unexplained syncope. The induction dose ranged between 0.8 mg/kg and 5.0 mg/kg (2.2 ± 0.7 mg/kg). Only one case received propofol to maintain anesthesia. The surgical procedure involved an anesthetic period of 75 ± 25 minutes. No patient developed a malignant rhythm during induction and maintenance of anesthesia. All patients were then safely discharged from the postanesthetic care unit after 1 hour. No adverse events were noticed during the recovery phase. In our study, administration of a single-dose propofol in patients with BS was safe. Nevertheless, extreme caution is still recommended when conducting general anesthesia in patients with BS, especially if BS patients are sedated with propofol for longer periods.

Background Brugada Syndrome is an inherited arrhythmogenic disease, characterized by the typical coved type ST-segment elevation in the right precordial leads from V1 through V3. The BrugadaDrugs.org Advisory Board recommends avoiding administration of propofol in patients with Brugada Syndrome. Since prospective studies are lacking, it was the purpose of this study to assess the electrocardiographic effects of propofol and etomidate on the ST- and QRS-segments. In this trial, it was hypothesized that administration of propofol or etomidate in bolus for induction of anesthesia, in patients with Brugada Syndrome, do not clinically affect the ST- and QRS-segments and do not induce arrhythmias. Methods In this prospective, double-blinded trial, 98 patients with established Brugada syndrome were randomized to receive propofol (2 to 3 mg/kg-1) or etomidate (0.2 to 0.3 mg/kg-1) for induction of anesthesia. The primary endpoints were the changes of the ST- and QRS-segment, and the occurrence of new arrhythmias upon induction of anesthesia. Results The analysis included 80 patients: 43 were administered propofol and 37 etomidate. None of the patients had a ST elevation greater than or equal to 0.2 mV, one in each group had a ST elevation of 0.15 mV. An ST depression up to −0.15mV was observed eleven times with propofol and five with etomidate. A QRS-prolongation of 25% upon induction was seen in one patient with propofol and three with etomidate. This trial failed to establish any evidence to suggest that changes in either group differed, with most percentiles being zero (median [25th, 75th], 0 [0, 0] vs. 0 [0, 0]). Finally, no new arrhythmias occurred perioperatively in both groups. Conclusions In this trial, there does not appear to be a significant difference in electrocardiographic changes in patients with Brugada syndrome when propofol versus etomidate were administered for induction of anesthesia. This study did not investigate electrocardiographic changes related to propofol used as an infusion for maintenance of anesthesia, so future studies would be warranted before conclusions about safety of propofol infusions in patients with Brugada syndrome can be determined. Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New

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The effect of apurinic/apyrimidinic (AP) sites in DNA on RNA and protein synthesis was studied in vitro using T7 coliphage DNA. Initiation of RNA synthesis by Escherichia coli RNA polymerase was synchronized and heparin was used to prevent reinitiation. When the T7 DNA contained AP sites, the rate of RNA synthesis was decreased but it remained higher than the values calculated on the assumption that an AP site in the transcribed strand is a complete block to the enzyme progression. Moreover, after the time taken by an unimpeded enzyme to go from promoter to terminator, the rate of RNA synthesis remained elevated and the number of complete RNA molecules (7000 nucleotides) continued to increase for some time. These results suggest that, if the E. coli RNA polymerase is stopped by an AP site, most often, after a pause, the enzyme resumes elongation of the RNA chain which is continuous over the AP site. Sometimes however, RNA synthesis is definitively interrupted during the pause; the probability of interruption has been estimated to be 0.3 in our experimental conditions. When a nick is placed 5' to the AP site by an AP endonuclease, the results are similar: most often, the RNA chain is synthesized without interruption past the nick in the template strand. The pause of the E. coli RNA polymerase at this combined lesion appears to be shorter than when the AP site is intact. To investigate whether a nucleotide is placed in the RNA chain in front of the AP site in the template strand by E. coli RNA polymerase, RNA synthesis was taken to completion before using this RNA for protein synthesis and measuring the activity ofgene-I product, T7 RNA polymerase. The result suggests that, after pausing, the E. coli RNA polymerase places a nucleotide in the RNA chain when passing over an AP site. The mechanism of the delayed lethality of T7 coliphages treated with monofunctional alkylating agents, which is due to the appearance of AP sites, is discussed.

An actinomycin D molecule bound to DNA sometimes stops the synthesis of RNA by Escherichia coli RNA polymerase. However, quite often, the bound antibiotic is released before the RNA polymerase detaches from the template DNA, so that the enzyme can resume, without interruption, the synthesis of the RNA chain.

helped design the study, develop the protocol, get Institutional Review Board approval, analyze the results and develop the manuscript. Kea Viaene M.D.* a : * The first two authors equally contributed to the study. This author helped design the study, develop the protocol, get Institutional Review Board approval, analyze the results and develop the manuscript. Maurizio Tosi M.D. a : This author helped design the study, develop the protocol, writing methods and editing the manuscript. Hugo Carvalho M.D. a : This author helped design the study, writing methods and editing manuscript. Patrice Forget, M.D. Ph.D. c : This author helped provide senior mentoring for study design, develop the protocol, writing and editing the manuscript. Jan Poelaert, M.D. Ph.D. a : This author helped provide senior mentoring for study design, develop the protocol, writing and editing the manuscript.

RBSUMEDe I'acide P-hydroxy-y-aminobutyrique a ete marque avec du tritium par echange selon la technique de Wilzbach. Le produit tritie a ete methyle et la dl-carnitine obtenue purifiee par chromatographie et electrophorese. Les rendements chimique et isotopique de cette operation ont etC calcules et sont commentes. La dl-carnitine tritiee a ete deshydratee en betai'ne crotonique tritiee; cette derniere a ete purifiee par chromatographie. La localisation du tritium dans ces molecules marquees est discutte.Le but de ce travail est de marquer avec du tritium, en dehors des groupes mCthyle, de la dl-carnitine et de la betai'ne crotonique.La mCthode consiste 21 exposer de l'acide P-hydroxy-y-aminobutyrique A de I'hydrogbne tritie selon la technique de Wilzbach (I), puis 21 mCthyler cet acide en dl-carnitine. La dl-carnitine est purifiCe successivement par chromatographie et Clectrophorbse continue. Une partie de la dl-carnitine tritiCe est dCshydratCe en bCtai'ne crotonique qui est 21 son tour purifike par chromatographie.Au cours de ces operations, la carnitine et la bttayne crotonique sont dosCes par le permanganate; Ieur purett est surveillee par klectrophorbse sur papier et leur radioactivite mesurCe par scintillation fiquide. Ces mCthodes ont permis d'avoir des assurances quant A la puretC radio-chimique des produits de synthbse et aussi d'estimer la valeur de la mkthode d'echange de Wilzbach en ce qui concerne le marquage au tritium du prkcurseur de la carnitine, I'acide P-hydroxy-y-aminobutyrique.(*) Ce travail a Bte subsidie par le contrat de recherche Euratom 001-61 7-RISB.

Background: Non-contact charge density (CD) mapping allows a global visualization of left atrium (LA) activation and of activation patterns during atrial fibrillation (AF). The aim of this study was to analyze, with CD mapping, the changes in persistent AF induced by pulmonary vein isolation (PVI) and LA posterior wall isolation (LAPWI). Methods: Patients undergoing PVI + LAPWI using the Arctic Front Advance PROTM cryoballoon system were included in the study. CD maps were created during AF at baseline, after PVI and after LAPWI. Three distinct activation patterns were identified in the CD maps: localized irregular activation (LIA), localized rotational activation (LRA) and focal centrifugal activation (FCA). LA maps were divided into the following regions: anterior, septal, lateral, roof, posterior, inferior. Results: Eleven patients were included, with a total of 33 maps and 198 AF regions analyzed. Global and regional AF cycle lengths significantly increased after PVI and LAPWI. Baseline analysis demonstrated higher LIA, LRA and FCA numbers in the posterior and anterior regions. After PVI, there was no change in LIA, LRA and FCA occurrence. After PVI + LAPWI, a significant decrease in LRA was observed with no difference in LIA and FCA occurrence. In the regional analysis, there was a significant reduction in the LIA number in the inferior region, in the LRA number in the roof and posterior regions and in the FCA number in the lateral region. Conclusions: A global reduction in the LRA number was observed only after PVI + LAPWI; it was driven by a reduction in rotational activity in the roof and posterior regions.