994 resultados para Circumflex branch


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OBJECTIVE: To analyze the incidence of intraventricular and atrioventricular conduction defects associated with acute myocardial infarction and the degree of in hospital mortality resulting from this condition during the era of thrombolytic therapy. METHODS: Observational study of a cohort of 929 consecutive patients with acute myocardial infarction. Multivariate analysis by logistic regression. Was used. RESULTS: Logistic regression showed a greater incidence of bundle branch block in male sex (odds ratio = 1.87, 95% CI = 1.02-3.42), age over 70 years (odds ratio = 2.31, 95% CI = 1.68-5.00), anterior localization of the infarction (odds ratio = 1.93, 95% CI = 1.03-3.65). There was a greater incidence of complete atrioventricular block in inferior infarcts (odds ratio = 2.59, 95% CI 1.30-5.18) and the presence of cardiogenic shock (odds ratio = 3.90, 95% CI = 1.43-10.65). Use of a thrombolytic agent was associated with a tendency toward a lower occurrence of bundle branch block (odds ratio = 0.68) and a greater occurrence of complete atrioventricular block (odds ratio = 1.44). The presence of bundle branch block (odds ratio = 2.45 95% , CI = 1.14-5.28) and of complete atrioventricular block (odds ratio = 13.59, 95% CI = 5.43-33.98) was associated with a high and independent probability of inhospital death. CONCLUSION: During the current era of thrombolytic therapy and in this population, intraventricular disturbances of electrical conduction and complete atrioventricular block were associated with a high and independent risk of inhospital death during acute myocardial infarction.

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OBJECTIVE: To analyze the relationship between myocardial bridges and the anterior interventricular branch (anterior descending) of the left coronary artery. METHODS: The study was carried out with postmortem material, and methods of dissection and observation were used. We assessed the perimeter of the anterior interventricular branch of the left coronary artery using a pachymeter, calculated its proximal and distal diameters in relation to the myocardial bridge, and also its diameter under the myocardial bridge in 30 hearts. We also observed the position of the myocardial bridge in relation to the origin of the anterior interventricular branch. RESULTS: The diameters of the anterior interventricular branch were as follows: the mean proximal diameter was 2.76±0.76 mm; the mean diameter under the myocardial bridge was 2.08±0.54 mm; and the mean distal diameter was 1.98±0.59 mm. In 33.33% (10/30) of the cases, the diameter of the anterior interventricular branch under the myocardial bridge was lower than the diameter of the anterior interventricular branch distal to the myocardial bridge. In 3.33% (1/30) of the cases, an atherosclerotic plaque was found in the segment under the myocardial bridge. The myocardial bridge was located in the middle third of the anterior interventricular branch in 86.66% (26/30) of the cases. CONCLUSION: Myocardial bridges are more frequently found in the middle third of the anterior interventricular branch of the left coronary artery. The diameter of the anterior interventricular branch of the left coronary artery under the myocardial bridge may be smaller than after the bridge. Myocardial bridges may not provide protection against the formation of atherosclerotic plaque inside the anterior interventricular branch of the left coronary artery.

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Abstract Background: Functional tests have limited accuracy for identifying myocardial ischemia in patients with left bundle branch block (LBBB). Objective: To assess the diagnostic accuracy of dipyridamole-stress myocardial computed tomography perfusion (CTP) by 320-detector CT in patients with LBBB using invasive quantitative coronary angiography (QCA) (stenosis ≥ 70%) as reference; to investigate the advantage of adding CTP to coronary computed tomography angiography (CTA) and compare the results with those of single photon emission computed tomography (SPECT) myocardial perfusion scintigraphy. Methods: Thirty patients with LBBB who had undergone SPECT for the investigation of coronary artery disease were referred for stress tomography. Independent examiners performed per-patient and per-coronary territory assessments. All patients gave written informed consent to participate in the study that was approved by the institution’s ethics committee. Results: The patients’ mean age was 62 ± 10 years. The mean dose of radiation for the tomography protocol was 9.3 ± 4.6 mSv. With regard to CTP, the per-patient values for sensitivity, specificity, positive and negative predictive values, and accuracy were 86%, 81%, 80%, 87%, and 83%, respectively (p = 0.001). The per-territory values were 63%, 86%, 65%, 84%, and 79%, respectively (p < 0.001). In both analyses, the addition of CTP to CTA achieved higher diagnostic accuracy for detecting myocardial ischemia than SPECT (p < 0.001). Conclusion: The use of the stress tomography protocol is feasible and has good diagnostic accuracy for assessing myocardial ischemia in patients with LBBB.

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The RuvA and RuvB proteins of Escherichia coli, which are induced in response to DNA damage, are important in the formation of heteroduplex DNA during genetic recombination and related recombinational repair processes. In vitro studies show that RuvA binds Holiday junctions and acts as a specificity factor that targets the RuvB ATPase, a hexameric ring protein, to the junction. Together, RuvA and RuvB promote branch migration, an ATP-dependent reaction that increases the length of the heteroduplex DNA. Electron microscopic visualization of RuvAB now provides a new insight into the mechanism of this process. We observe the formation of a tripartite protein complex in which RuvA binds the crossover and is sandwiched between two hexameric rings of RuvB. The Holliday junction within this complex adopts a square-planar structure. We propose a molecular model for branch migration, a unique feature of which is the role played by the two oppositely oriented RuvB ring motors.

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Cryptic exons or pseudoexons are typically activated by point mutations that create GT or AG dinucleotides of new 5' or 3' splice sites in introns, often in repetitive elements. Here we describe two cases of tetrahydrobiopterin deficiency caused by mutations improving the branch point sequence and polypyrimidine tracts of repeat-containing pseudoexons in the PTS gene. In the first case, we demonstrate a novel pathway of antisense Alu exonization, resulting from an intronic deletion that removed the poly(T)-tail of antisense AluSq. The deletion brought a favorable branch point sequence within proximity of the pseudoexon 3' splice site and removed an upstream AG dinucleotide required for the 3' splice site repression on normal alleles. New Alu exons can thus arise in the absence of poly(T)-tails that facilitated inclusion of most transposed elements in mRNAs by serving as polypyrimidine tracts, highlighting extraordinary flexibility of Alu repeats in shaping intron-exon structure. In the other case, a PTS pseudoexon was activated by an A>T substitution 9 nt upstream of its 3' splice site in a LINE-2 sequence, providing the first example of a disease-causing exonization of the most ancient interspersed repeat. These observations expand the spectrum of mutational mechanisms that introduce repetitive sequences in mature transcripts and illustrate the importance of intronic mutations in alternative splicing and phenotypic variability of hereditary disorders.

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The second Annual Report of Dental Branch

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The second Annual Report of Dental Branch

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During genetic recombination a heteroduplex joint is formed between two homologous DNA molecules. The heteroduplex joint plays an important role in recombination since it accommodates sequence heterogeneities (mismatches, insertions or deletions) that lead to genetic variation. Two Escherichia coli proteins, RuvA and RuvB, promote the formation of heteroduplex DNA by catalysing the branch migration of crossovers, or Holliday junctions, which link recombining chromosomes. We show that RuvA and RuvB can promote branch migration through 1800 bp of heterologous DNA, in a reaction facilitated by the presence of E.coli single-stranded DNA binding (SSB) protein. Reaction intermediates, containing unpaired heteroduplex regions bound by SSB, were directly visualized by electron microscopy. In the absence of SSB, or when SSB was replaced by a single-strand binding protein from bacteriophage T4 (gene 32 protein), only limited heterologous branch migration was observed. These results show that the RuvAB proteins, which are induced as part of the SOS response to DNA damage, allow genetic recombination and the recombinational repair of DNA to occur in the presence of extensive lengths of heterology.

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Fanconi anemia (FA) is a genetically heterogeneous chromosome instability syndrome associated with congenital abnormalities, bone marrow failure, and cancer predisposition. Eight FA proteins form a nuclear core complex, which promotes tolerance of DNA lesions in S phase, but the underlying mechanisms are still elusive. We reported recently that the FA core complex protein FANCM can translocate Holliday junctions. Here we show that FANCM promotes reversal of model replication forks via concerted displacement and annealing of the nascent and parental DNA strands. Fork reversal by FANCM also occurs when the lagging strand template is partially single-stranded and bound by RPA. The combined fork reversal and branch migration activities of FANCM lead to extensive regression of model replication forks. These observations provide evidence that FANCM can remodel replication fork structures and suggest a mechanism by which FANCM could promote DNA damage tolerance in S phase

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OBJECTIVES: The aim of this study was to evaluate new electrocardiographic (ECG) criteria for discriminating between incomplete right bundle branch block (RBBB) and the Brugada types 2 and 3 ECG patterns. BACKGROUND: Brugada syndrome can manifest as either type 2 or type 3 pattern. The latter should be distinguished from incomplete RBBB, present in 3% of the population. METHODS: Thirty-eight patients with either type 2 or type 3 Brugada pattern that were referred for an antiarrhythmic drug challenge (AAD) were included. Before AAD, 2 angles were measured from ECG leads V(1) and/or V(2) showing incomplete RBBB: 1) α, the angle between a vertical line and the downslope of the r'-wave, and 2) β, the angle between the upslope of the S-wave and the downslope of the r'-wave. Baseline angle values, alone or combined with QRS duration, were compared between patients with negative and positive results on AAD. Receiver-operating characteristic curves were constructed to identify optimal discriminative cutoff values. RESULTS: The mean β angle was significantly smaller in the 14 patients with negative results on AAD compared to the 24 patients with positive results on AAD (36 ± 20° vs. 62 ± 20°, p < 0.01). Its optimal cutoff value was 58°, which yielded a positive predictive value of 73% and a negative predictive value of 87% for conversion to type 1 pattern on AAD; α was slightly less sensitive and specific compared with β. When the angles were combined with QRS duration, it tended to improve discrimination. CONCLUSIONS: In patients with suspected Brugada syndrome, simple ECG criteria can enable discrimination between incomplete RBBB and types 2 and 3 Brugada patterns.