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PubMed2002

Extreme pathway lengths and reaction participation in genome-scale metabolic networks.

Extreme pathways are a unique and minimal set of vectors that completely characterize the steady-state capabilities of genome-scale metabolic networks. A framework is provided to mathematically characterize extreme pathway length and to study how individual reactions participate in the extreme pathway structure of a network. The length of an extreme pathway is the number of reactions that comprise it. Reaction participation is the percentage of extreme pathways that utilize a given reaction. These properties were computed for the production of individual amino acids and protein production in Helicobacter pylori and individual amino acid production in Haemophilus influenzae. Reaction participation classifies the reactions into groups that are always, sometimes, or never utilized for the production of a target product. The utilized reactions can be further grouped into correlated subsets of reactions, some of which are non-obvious, and which may, in turn, suggest regulatory structure. The length of the extreme pathways did not correlate with product yield or chemical complexity. The distributions of extreme pathway lengths in H. pylori were also very different from those in H. influenzae, showing a distinct systemic difference between the two organisms, despite overall similar metabolic networks. Reaction participation and extreme pathway lengths thus serve to elucidate systemic biological features.

Computational Biology↗
PubMed1992

Coordinate regulation of cytochrome and alternative pathway respiration in tobacco.

In suspension cells of NT1 tobacco (Nicotiana tabacum L. cv bright yellow), inhibition of the cytochrome pathway of respiration with antimycin A induced a large increase in the capacity of the alternative pathway over a period of approximately 12 h, as confirmed in both whole cells and isolated mitochondria. The increase in alternative pathway capacity required de novo RNA and protein synthesis and correlated closely with the increase of a 35-kD alternative oxidase protein. When the cytochrome pathway of intact cells was inhibited by antimycin A, respiration proceeded exclusively through the alternative pathway, reached rates significantly higher than before antimycin A addition, and was not stimulated by p-trifluoromethoxycarbonylcyanide (FCCP). When inhibition of the cytochrome pathway was relieved, alternative pathway capacity and the level of the 35-kD alternative oxidase protein declined. Respiration rate also declined and could once again be stimulated by FCCP. These observations show that the capacities of the mitochondrial electron transport pathways can be regulated in a coordinate fashion.

Journal Article↗
PubMed2004

Two distinct signaling pathways participate in auxin-induced swelling of pea epidermal protoplasts.

Protoplast swelling was used to investigate auxin signaling in the growth-limiting stem epidermis. The protoplasts of epidermal cells were isolated from elongating internodes of pea (Pisum sativum). These protoplasts swelled in response to auxin, providing the clearest evidence that the epidermis can directly perceive auxin. The swelling response to the natural auxin IAA showed a biphasic dose response curve but that to the synthetic auxin 1-naphthalene acetic acid (NAA) showed a simple bell-shaped dose response curve. The responses to IAA and NAA were further analyzed using antibodies raised against ABP1 (auxin-binding protein 1), and their dependency on extracellular ions was investigated. Two signaling pathways were resolved for IAA, an ABP1-dependent pathway and an ABP1-independent pathway that is much more sensitive to IAA than the former. The response by the ABP1 pathway was eliminated by anti-ABP1 antibodies, had a higher sensitivity to NAA, and did not depend on extracellular Ca(2+). In contrast, the response by the non-ABP1 pathway was not affected by anti-ABP1 antibodies, had no sensitivity to NAA, and depended on extracellular Ca(2+). The swelling by either pathway required extracellular K(+) and Cl(-). The auxin-induced growth of pea internode segments showed similar response patterns, including the occurrence of two peaks in the dose response curve for IAA and the difference in Ca(2+) requirements. It is suggested that two signaling pathways participate in auxin-induced internode growth and that the non-ABP1 pathway is more likely to be involved in the control of growth by constitutive concentrations of endogenous auxin.

Calcium↗
PubMed1997

The Regulation of Electron Partitioning between the Cytochrome and Alternative Pathways in Soybean Cotyledon and Root Mitochondria.

The regulation of electron partitioning between the cytochrome (Cyt) and alternative pathways in soybean (Glycine max L. cv Ransom) mitochondria in the absence of added inhibitors has been studied using the oxygen isotope fractionation technique. This regulation can depend on several factors, including the amount of alternative oxidase protein, the redox status of the alternative oxidase regulatory sulfhydryl-disulfide system, the degree of activation by [alpha]-keto acids, and the concentration and redox state of the ubiquinone pool. We studied electron partitioning onto the alternative pathway in mitochondria isolated from etiolated and light-grown cotyledons and roots to ascertain how these factors interact in different tissues. In light-grown cotyledon mitochondria there is some partitioning to the alternative pathway in state 4, which is increased dramatically by either pyruvate or dithiothreitol. In etiolated cotyledon mitochondria, the alternative pathway shows little ability to compete for electrons with the Cyt pathway under any circumstances. In root mitochondria, control of alternative pathway activity is exercised by both the ubiquinone pool and the regulatory sulfhydryl-disulfide system. In addition, oxygen isotope fractionation by the Cyt and alternative pathways in mitochondria were identical to the fractionation for the respective pathways seen in intact tissue, suggesting that residual respiration is not present in the absence of inhibitors.

Journal Article↗
PubMed1990

Induction of the 4-aminobutyrate and urea-catabolic pathways in Saccharomyces cerevisiae. Specific and common transcriptional regulators.

In the yeast Saccharomyces cerevisiae, induction of the 4-aminobutyrate-catabolic pathway by 4-aminobutyrate requires two positive regulatory factors, encoded by the UGA3 and the UGA35 genes respectively. In addition to this, expression of one gene of this pathway, namely the UGA4 gene encoding the 4-aminobutyrate-specific permease, is controlled negatively by the product of the UGA43 gene [Vissers, S., André, B., Muyldermans, F. & Grenson, M. (1989) Eur. J. Biochem. 181, 357-361]. We show here that the products of two of these regulatory genes, UGA35 and UGA43, also control the expression of the genes encoding the urea-catabolic pathway, although the 4-aminobutyrate and urea-catabolic pathways are synthesised under specific conditions and do not share any enzymatic step or metabolite: the UGA35 pathways are synthesised under specific conditions and do not share any enzymatic step or metabolite: the UGA35 gene is shown to be identical to the DURL gene which was previously identified as a positive regulatory factor of the urea-catabolic pathway; the UGA43 gene product is shown to behave like a negative regulatory factor of this pathway. In contrast to UGA35/DURL and UGA43, the positive regulatory factors encoded by the UGA3 gene and the previously identified DURM gene specifically control 4-aminobutyrate and urea catabolisms respectively. Northern hybridization experiments suggest that the UGA35/DURL and UGA43 common regulatory factors act at the transcriptional level. Our results show that the expression of two biochemically distinct nitrogenous catabolisms, as triggered by their respective inducers, seems to involve multiple regulatory factors, some of which are common to the two catabolic pathways.

Aminobutyrates↗
PubMed2006

Developmental signalling pathways in lung cancer.

Hedgehog, Notch and Wnt signalling are all essential for axial patterning and progenitor cell fates in signalling pathways conserved from flies to humans. Aberrant activation of these pathways is observed in a wide variety of cancers, suggesting that these embryonic signalling pathways contribute in a fundamental way to the evolution and maintenance of a malignant phenotype. Because all three of these pathways participate in lung development, recent studies have begun to explore the connection between lung development, airway epithelial repair and lung cancer. Development, repair and malignant transformation of the neuroendocrine lineage are all accompanied by aberrant Hedgehog pathway activation, whereas Notch and Wnt signalling may be important in other airway cell types. Small molecule targeting of these pathways may provide therapeutic opportunities in lung cancer. The plant-derived alkaloid cyclopamine is a naturally occurring Hedgehog pathway inhibitor that shows therapeutic promise in small cell lung cancer, a highly aggressive neuroendocrine tumour. A more detailed understanding of how embryonic signalling pathways participate in airway epithelial repair and tumourigenesis may reveal more novel therapeutic vulnerabilities in lung cancer.

Animals↗
PubMed2006

Anaplasma phagocytophilum delays spontaneous human neutrophil apoptosis by modulation of multiple apoptotic pathways.

Anaplasma phagocytophilum infects human neutrophils and inhibits the intrinsic pathway of spontaneous neutrophil apoptosis by protecting mitochondrial membrane integrity. In the present study, we investigated the molecular signalling of the extrinsic pathway and the interaction between the intrinsic and extrinsic pathways in the inhibition of spontaneous human neutrophil apoptosis by A. phagocytophilum. Cell surface Fas clustering during spontaneous neutrophil apoptosis was significantly blocked by A. phagocytophilum infection. The cleavage of pro-caspase 8, caspase 8 activation and the cleavage of Bid, which links the intrinsic and extrinsic pathways, in the extrinsic pathway of spontaneous neutrophil apoptosis were inhibited by A. phagocytophilum infection. Inhibition of this pathway was active as the cleavage of pro-caspase 8 and Bid in anti-Fas-induced neutrophil apoptosis was also inhibited by A. phagocytophilum infection. Likewise, A. phagocytophilum infection inhibited the pro-apoptotic Bax translocation to mitochondria, activation of caspase 9, the initiator caspase in the intrinsic pathway, and the degradation of a potent caspase inhibitor, X-chromosome-linked inhibitor of apoptosis protein (XIAP), during spontaneous neutrophil apoptosis. These data point to a novel mechanism induced by A. phagocytophilum involving both extrinsic and intrinsic pathways to ensure to delay the apoptosis of host neutrophils.

Anaplasma phagocytophilum↗
PubMed2004

The phosphatidylinositol-3 kinase pathway regulates bladder cancer cell invasion.

OBJECTIVES: To investigate the role of the phosphatidylinositol (PI)-3 kinase pathway in the invasion of bladder cancer cell lines, and to assess the activation of this pathway in primary human bladder tumours. MATERIALS AND METHODS: Human bladder cancer cells were treated with pathway specific inhibitors or were transfected with PI-3 kinase pathway components. The invasion of cultured bladder cancer cells was analysed by an invasion assay. Bladder cancer cells lines and primary human bladder tumours were analysed for pathway activation by western blotting. RESULTS: A specific inhibitor of PI-3 kinase enzyme activity, Ly294002, potently suppressed the invasive properties of three highly invasive bladder tumour cell lines. Restoration of the PTEN gene to invasive UM-UC-3 bladder tumour cells or expression of a dominant-negative version of the PI-3 kinase target, Akt, also potently inhibited invasion, indicating a central role for the PI-3 kinase/Akt pathway in this process. In addition, 55% of primary tumours from patients with bladder cancer had markedly high levels of phosphorylated Akt. CONCLUSION: Pharmacological or biochemical inhibition of the PI-3 kinase pathway drastically reduced the invasive capacity of bladder cancer cell lines; over half of primary human bladder tumours had high Akt phosphorylation, suggesting that the aberrant activation of this pathway may contribute to the invasion of a significant subset of bladder cancers.

Cell Line, Tumor↗
PubMed1999

A non-capacitative pathway activated by arachidonic acid is the major Ca2+ entry mechanism in rat A7r5 smooth muscle cells stimulated with low concentrations of vasopressin.

1. Depletion of the Ca2+ stores of A7r5 cells stimulated Ca2+, though not Sr2+, entry. Vasopressin (AVP) or platelet-derived growth factor (PDGF) stimulated Sr2+ entry. The cells therefore express a capacitative pathway activated by empty stores and a non-capacitative pathway stimulated by receptors; only the former is permeable to Mn2+ and only the latter to Sr2+. 2. Neither empty stores nor inositol 1,4,5-trisphosphate (InsP3) binding to its receptors are required for activation of the non-capacitative pathway, because microinjection of cells with heparin prevented PDGF-evoked Ca2+ mobilization but not Sr2+ entry. 3. Low concentrations of Gd3+ irreversibly blocked capacitative Ca2+ entry without affecting AVP-evoked Sr2+ entry. After inhibition of the capacitative pathway with Gd3+, AVP evoked a substantial increase in cytosolic [Ca2+], confirming that the non-capacitative pathway can evoke a significant increase in cytosolic [Ca2+]. 4. Arachidonic acid mimicked the effect of AVP on Sr2+ entry without stimulating Mn2+ entry; the Sr2+ entry was inhibited by 100 microM Gd3+, but not by 1 microM Gd3+ which completely inhibited capacitative Ca2+ entry. The effects of arachidonic acid did not require its metabolism. 5. AVP-evoked Sr2+ entry was unaffected by isotetrandrine, an inhibitor of G protein-coupled phospholipase A2. U73122, an inhibitor of phosphoinositidase C, inhibited AVP-evoked formation of inositol phosphates and Sr2+ entry. The effects of phorbol esters and Ro31-8220 (a protein kinase C inhibitor) established that protein kinase C did not mediate the effects of AVP on the non-capacitative pathway. An inhibitor of diacylglycerol lipase, RHC-80267, inhibited AVP-evoked Sr2+ entry without affecting capacitative Ca2+ entry or release of Ca2+ stores. 6. Selective inhibition of capacitative Ca2+ entry with Gd3+ revealed that the non-capacitative pathway is the major route for the Ca2+ entry evoked by low AVP concentrations. 7. We conclude that in A7r5 cells, the Ca2+ entry evoked by low concentrations of AVP is mediated largely by a non-capacitative pathway directly regulated by arachidonic acid produced by the sequential activities of phosphoinositidase C and diacylglycerol lipase.

Animals↗
PubMed1995

Initial onset of accessory pathway-mediated and atrioventricular node reentrant tachycardia after age 65: clinical features, electrophysiologic characteristics, and possible facilitating factors.

OBJECTIVE: To evaluate the clinical features electrophysiologic characteristics, and possible facilitating factors in older patients (> or = 65 years) with initial onset of accessory pathway-mediated and atrioventricular (AV) node reentrant tachycardia. DESIGN: Of the patients undergoing electrophysiologic study and radiofrequency catheter ablation of accessory pathway-mediated and AV node reentrant tachycardia at this institution, patients with initial tachyarrhythmia after age 65 years were compared with those presenting initially before age 30. SETTING: A tertiary medical center for the general public. PARTICIPANTS: Sixty-six patients had their initial symptoms after age 65: Group I, 32 patients with accessory pathway-mediated tachycardia, and Group II, 34 patients with AV node reentrant tachycardia. Four-hundred forty patients had their initial symptoms before age 30: Group III, 283 with accessory pathway mediated tachyarrhythmia, and Group IV, 157 with AV node reentrant tachycardia. INTERVENTION: All patients underwent electrophysiological study to determine the mechanisms of tachyarrhythmia, and radiofrequency catheter ablation for treatment of tachycardia. RESULTS: (1) Older patients with initial arrhythmia had incidence of critical clinical manifestations, including tachyarrhythmia-related syncope and cardioversion, similar to those with initial arrhythmia at a younger age. (2) Patients in Group III, showed anterograde effective refractory period (ERP) of the AV node (P = .432), longer anterograde ERP of the accessory pathway (P = .004), and greater difference of the anterograde ERP between the AV node and the accessory pathway (D-ERP) (P = .003) similar to patients in group I. In Group II, the ERP and Wenckebach cycle length of the retrograde fast pathway was significantly longer than in Group IV (P = .037 and P < .001, respectively), and a greater percentage of patients in Group II than in Group IV AV node reentrant tachycardia needed isoproteronol to facilitate the induction of reentrant tachycardia (P = .034). (3) Patients in Group I and Group II had a higher incidence of supraventricular and ventricular ectopic activity than those in Group III (P = .002 and P = .005, respectively) and Group IV (P = .024 and P = .012, respectively) in 24-hour ambulatory electrocardiograms. CONCLUSION: The initial onset of accessory pathway-mediated tachycardia after age 65 may be caused by changes of electrophysiologic properties (greater D-ERP) as well as increased supraventricular and ventricular ectopic activity. Influence of the autonomic nervous system, rather than changes of conduction properties in the AV node, and increase in ectopic activity may contribute to the new onset of AV node reentrant tachycardia in older adults. The choice of antiarrhythmic drugs and radiofrequency ablation require attention to the clinical profile and facilitating factors of reentrant tachycardia in this group of patients.

Adult↗
PubMed1992

Radiofrequency ablation of accessory pathways: characteristics of transiently and permanently effective pulses.

The purpose of this study was to characterize and compare the radiofrequency current applications that produced permanent or transient accessory pathway conduction block. One hundred fifty-two radiofrequency energy applications that induced permanent (permanently effective pulses, n = 48) or transient (transiently effective pulses, n = 104) accessory pathway block in 57 patients with 60 accessory pathways were analyzed. The time from the onset of current application to disappearance of preexcitation or termination of supraventricular tachycardia by permanently effective pulses was 1-15 seconds (mean 3.6 +/- 3.8 sec) compared to 2-29 seconds (mean 11.5 +/- 7.5 sec) by transiently effective pulses (P less than 0.01). After transiently effective pulses that induced block in accessory pathway, conduction resumed within 5 minutes while induced block by permanently effective pulses persisted in 44 of 48 patients (92%) during follow-up of 11 +/- 12 months. The accessory pathway conduction returned in the remaining four patients after ablation 2 weeks to 7 months. After transiently effective pulses, 41 impulses were delivered to the same site using a higher power output (n = 32) and/or longer energy delivery duration (n = 20) without new mapping of accessory pathway location. Thirty-six of these impulses again resulted in transient accessory pathway block, four had no effect, only one impulse induced a permanent block in the accessory pathway. Pulses with higher power outputs tended to induce transient effects more frequently than pulses with lower energy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Effect of pacing site on the atrial electrogram at target sites for slow pathway ablation in patients with atrioventricular nodal reentrant tachycardia.

Atrial electrograms recorded from target sites during radiofrequency catheter ablation of the slow atrioventricular (AV) nodal pathway are often fractionated and may be associated with a late, high frequency component (the slow pathway potential). The purpose of the current study was to assess the effects of slow pathway ablation on the morphology of the atrial electrogram and to determine whether target site electrograms display direction dependent changes in morphology during atrial pacing maneuvers. Twenty-six patients with typical AV nodal reentry had electrograms recorded from target sites before and after successful ablation of the slow AV nodal pathway and during pacing from the high right atrium and distal coronary sinus at cycle lengths of 500 and 300 msec. There was no significant change in the duration or degree of fractionation of the atrial electrogram as the result of slow pathway ablation. In contrast, the duration and degree of fractionation were less when pacing from the coronary sinus compared with sinus rhythms or right atrial pacing. Pacing rate did not affect electrogram morphology. These data suggest that the morphology of the slow pathway target site electrogram is dependent on the direction of atrial activation and that the "slow pathway potential" does not represent activation of an anatomically discrete pathway.

Adult↗
PubMed2000

Atrioventricular nodal reentry tachycardia: slow pathway ablation using the transseptal approach.

Four hundred twenty consecutive patients with symptomatic slow/fast atrioventricular nodal reentry tachycardia had attempted slow pathway radiofrequency ablation. All patients had successful slow pathway ablation and no inducible tachycardia after ablation using the standard right-sided approach except for three patients. The three unsuccessful patients had inducible slow/fast atrioventricular nodal tachycardia after attempted right-sided posterior and inferoposterior anatomic ablative techniques and with slow pathway potential electrogram guidance. Lesions were also delivered linearly in the triangle of Koch and within the coronary sinus ostium. A transseptal puncture was performed and slow pathway ablation was obtained in each of these patients. Ablation was performed from the septal mitral valve annulus, anterior to the os of the coronary sinus and inferior to the His-bundle catheter with elimination of slow pathway conduction. Prior to the ablation, two of the three patients exhibited initiation of tachycardia with a double fast/slow antegrade response, and all three patients had long AH intervals (mean 378 ms) during slow pathway conduction. These electrophysiological findings may be consistent with a large area of slow pathway conduction that may include the left atrial septum not approachable by conventional right-sided ablative techniques. Slow pathway ablation to eliminate atrioventricular nodal reentry tachycardia at times may require a left atrial/transseptal approach when conventional right-sided techniques are ineffective.

Adult↗
PubMed2000

Multiple AV nodal pathways with multiple peaks in the RR interval histogram of the Holter monitoring ECG during atrial fibrillation.

Two or more peaks on the 24-hour electrocardiogram (ECG) RR interval histogram of patients with atrial fibrillation suggests the presence multiple AV nodal pathways. The prevalence of multiple AV nodal pathways in this population is unknown. The study included 250 patients with permanent atrial fibrillation during 24-hour ECG. The number of peaks on the RR interval histogram was measured in each patient. A single peak was present in 153 patients (61%), 80 patients (32%) had two peaks, 13 patients (5%) had three, and 4 patients (2%) had four peaks. Among the 97 patients (39%) with > 1 AV nodal pathway, the estimated mean heart rate reduction by hypothetical ablation of all supernumerary AV nodal pathways with short refractory periods was 16 beats/min, from 82 to 65 beats/min. Among the overall population, 16 patients (6%) with > 1 AV nodal pathway had a mean heart rate > 100 beats/min. In this subgroup, modulation of AV node conduction by hypothetical ablation of all supernumerary AV nodal pathways with short refractory periods yielded an estimated reduction in mean heart rate of 26 +/- 15 beats/min, from 110 +/- 9 beats/min to 84 +/- 14 beats/min (P < 0.01), a 23% decrease. The presence of > 1 AV nodal pathway was suspected in 39% of all patients with permanent atrial fibrillation. The hypothetical ablation of all supernumerary AV nodal pathways with short refractory periods resulted in a clinically significant reduction in heart rate in 6% of patients in this population.

Aged↗
PubMed2005

Electrocardiographic characteristics of fasciculoventricular pathways.

INTRODUCTION: Fasciculoventricular (FV) pathways are rare variants of preexcitation, and their ECGs may be misinterpreted as Wolff-Parkinson-White syndrome with anteroseptal accessory pathways (WPW-AS). We analyzed the electrocardiographic characteristics of the patients with FV pathways to find out the different findings from WPW-AS. METHODS AND RESULTS: Five patients with FV pathways and four patients with WPW-AS who underwent electrophysiologic studies were evaluated. Intervals and amplitudes of each wave and QRS morphologies were analyzed in standard 12-lead ECGs of these patients by two independent cardiologists without the information of the electrophysiologic findings. PR intervals were longer in FV pathways (122 +/- 11.0 vs 83 +/- 21 ms, FV pathways vs WPW-AS, P = 0.017). In lead V1, narrower width of R waves (25 +/- 6 vs 45 +/- 13 ms, P = 0.037) and smaller amplitude of S waves (12.8 +/- 8.3 vs 26.6 +/- 7.4 mm, P = 0.037) were observed in FV pathways. The polarity of delta waves in V1 was flat or negative in contrast with the cases of WPW-AS in which the polarity was positive. Three of five patients had notching in the descending limb of S waves in V1, which was not observed in WPW-AS. CONCLUSION: FV pathways have different ECG characteristics from WPW-AS in PR interval and morphology of QRS complexes in lead V1 of the standard 12-lead ECG.

Adolescent↗
PubMed2005

Electrophysiological characteristics of junctional rhythm during ablation of the slow pathway in different types of atrioventricular nodal reentrant tachycardia.

BACKGROUND: Junctional rhythm (JR) is commonly observed during radiofrequency (RF) ablation of the slow pathway for atrioventricular (AV) nodal reentrant tachycardia. However, the atrial activation pattern and conduction time from the His-bundle region to the atria recorded during JR in different types of AV nodal reentrant tachycardia have not been fully defined. METHODS: Forty-five patients who underwent RF ablation of the slow pathway for AV nodal reentrant tachycardia were included; 27 patients with slow-fast, 11 patients with slow-intermediate, and 7 patients with fast-slow AV nodal reentrant tachycardia. The atrial activation pattern and HA interval (from the His-bundle potential to the atrial recording of the high right atrial catheter) during AV nodal reentrant tachycardia (HA(SVT)) and JR (HA(JR)) were analyzed. RESULTS: In all patients with slow-fast AV nodal reentrant tachycardia, the atrial activation sequence recorded during JR was similar to that of the retrograde fast pathway, and transient retrograde conduction block during JR was found in 1 (4%) patient. The HA(JR) was significantly shorter than the HA(SVT) (57 +/- 24 vs 68 +/- 21 ms, P < 0.01). In patients with slow-intermediate AV nodal reentrant tachycardia, the atrial activation sequence of the JR was similar to that of the retrograde fast pathway in 5 (45%), and to that of the retrograde intermediate pathway in 6 (55%) patients. Transient retrograde conduction block during JR was noted in 1 (9%) patient. The HA(JR) was also significantly shorter than the HA(SVT) (145 +/- 27 vs 168 +/- 29 ms, P = 0.014). In patients with fast-slow AV nodal reentrant tachycardia, retrograde conduction with block during JR was noted in 7 (100%) patients. The incidence of retrograde conduction block during JR was higher in fast-slow AV nodal reentrant tachycardia than slow-fast (7/7 vs 1/11, P < 0.01) and slow-intermediate AV nodal reentrant tachycardia (7/7 vs 1/27, P < 0.01). CONCLUSIONS: In patients with slow-fast and slow-intermediate AV nodal reentrant tachycardia, the JR during ablation of the slow pathway conducted to the atria through the fast or intermediate pathway. In patients with fast-slow AV nodal reentrant tachycardia, there was no retrograde conduction during JR. These findings suggested there were different characteristics of the JR during slow-pathway ablation of different types of AV nodal reentrant tachycardia.

Analysis of Variance↗
PubMed1995

Effect of isoproterenol on accessory pathways without overt retrograde conduction.

INTRODUCTION: Absence of overt retrograde accessory pathway conduction may be related to low resting sympathetic tone in patients with apparent unidirectional anterogradely conducting accessory pathways (UACAP). METHODS AND RESULTS: To test this hypothesis, we studied the effect of isoproterenol on accessory pathway function and tachycardia induction in 18 patients (12 men and 6 women, ages 34 +/- 16 years [mean +/- SD]) with UACAP. After baseline study in the drug-free state, electrphysiologic testing was repeated during infusion of isoproterenol (0.5 to 1.5 micrograms/min, titrated to increase heart rate by 20%). Isoproterenol shortened the anterograde effective refractory period (398 +/- 117 vs 305 +/- 63 msec; P < 0.01; basic drive cycle length 600 msec) of the accessory pathway. However, retrograde accessory pathway conduction and atrioventricular reentrant tachycardia were exposed in only 3 (17%) patients by isoproterenol infusion. All 3 patients with retrograde accessory pathway revealed after isoproterenol had clinically documented tachycardia (supraventricular tachycardia in 2, atrial fibrillation in 1) during exercise, while none of the patients with persistent absence of retrograde accessory pathway conduction had this symptom. CONCLUSIONS: We conclude that absence of overt retrograde conduction over accessory pathways may be related to low resting sympathetic tone in some individuals. Restoration of retrograde conduction with isoproterenol is unusual and most likely to be observed in patients with clinically documented paroxysmal supraventricular tachycardia related to exercise.

Accessory Nerve↗
PubMed1998

Development and validation of an ECG algorithm for identifying accessory pathway ablation site in Wolff-Parkinson-White syndrome.

INTRODUCTION: Delta wave morphology correlates with the site of ventricular insertion of accessory AV pathways. Because lesions due to radiofrequency (RF) current are small and well defined, it may allow precise localization of accessory pathways. The purpose of this study was to use RF catheter ablation to develop an ECG algorithm to predict accessory pathway location. METHODS AND RESULTS: An algorithm was developed by correlating a resting 12-lead ECG with the successful RF ablation site in 135 consecutive patients with a single, anterogradely conducting accessory pathway (Retrospective phase). This algorithm was subsequently tested prospectively in 121 consecutive patients (Prospective phase). The ECG findings included the initial 20 msec of the delta wave in leads I, II, aVF, and V1 [classified as positive (+), negative (-), or isoelectric (+/-)] and the ratio of R and S wave amplitudes in leads III and V1 (classified as R > or = S or R < S). When tested prospectively, the ECG algorithm accurately localized the accessory pathway to 1 of 10 sites around the tricuspid and mitral annuli or at subepicardial locations within the venous system of the heart. Overall sensitivity was 90% and specificity was 99%. The algorithm was particularly useful in correctly localizing anteroseptal (sensitivity 75%, specificity 99%), and mid-septal (sensitivity 100%, specificity 98%) accessory pathways as well as pathways requiring ablation from within ventricular venous branches or anomalies of the coronary sinus (sensitivity 100%, specificity 100%). CONCLUSION: A simple ECG algorithm identifies accessory pathway ablation site in Wolff-Parkinson-White syndrome. A truly negative delta wave in lead II predicts ablation within the coronary venous system.

Adolescent↗