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PubMed1989

The biosynthesis of the chromophore of phycocyanin. Pathway of reduction of biliverdin to phycocyanobilin.

The later stages in the pathway of biosynthesis of phycocyanobilin, the chromophore of phycocyanin, were studied by using radiolabelled intermediates. Three possible pathways from biliverdin IX-alpha to phycocyanobilin were considered. 14C-labelled samples of key intermediates in two of the pathways, 3-vinyl-18-ethyl biliverdin IX-alpha and 3-ethyl-18-vinyl biliverdin IX-alpha, were synthesized chemically and were administered to cultures of Cyanidium caldarium that were actively synthesizing photosynthetic pigments in the light. Neither of these two compounds was apparently incorporated into the phycobiliprotein chromophore, suggesting that two of the three pathways were not operative. By elimination, the results imply that the third possible pathway, which involves phytochromobilin, the chromophore of phytochrome, represents the route for biosynthesis of phycocyanobilin. Unfortunately, since 14C-labelled phytochromobilin is not available, no direct proof of this pathway could be obtained. However, if correct, the present interpretation represents a unified pathway for biosynthesis of all plant bilins, via the intermediacy of phytochromobilin.

Bilirubin↗
PubMed1991

Role of serine biosynthesis and its utilization in the alternative pathway from glucose to glycogen during the response to insulin in cultured foetal-rat hepatocytes.

The role of serine as a possible intermediate of the alternative pathway from glucose to glycogen was investigated under basal and insulin-stimulated conditions in 18-day cultured foetal-rat hepatocytes because these cells cannot use pyruvate-derived metabolites [Bismut & Plas (1989) Biochem. J. 263, 889-895]. Incubation of cells with [U-14C]glucose for 24 h led to a release of labelled serine in the medium concomitantly with a net serine production (100 nmol/24 h per culture). The rate of [14C]serine formation (close to 3 nmol/h per culture) indicated that a large part of newly formed serine originated from glucose. When short-term experiments were performed at day 2, glycogen labelling from [U-14C]serine or [U-14C]glycine, which was increased 3-fold by insulin after 2 h, evidenced their participation as glycogenic precursors. When a double-isotope procedure with [U-14C,3-3H]glucose was used, the direct and the alternative pathways from glucose were found to contribute to glycogenesis by 75 and 25% respectively. Cycloserine (18 mM), a transaminase inhibitor, strongly inhibited glycogen labelling from [U-14C] serine while producing a 70% increase in glucose incorporation by the alternative pathway, in both the presence and the absence of insulin. The inhibitor had no effect on the direct pathway from glucose to glycogen. Supplementation with 1 mM-hydroxypyruvate, a serine-derived metabolite, did not affect direct glucose incorporation, whereas the alternative pathway was stimulated whether insulin was present or not. These results indicate that the sequence glucose----serine----glycogen is operative in cultured foetal hepatocytes. The alternative pathway interferes with hydroxypyruvate utilization, and is likely mediated by the serine aminotransferase pathway, independently of the acute glycogenic action of insulin.

Animals↗
PubMed1991

Calculation of control coefficients of metabolic pathways. A flux-oriented graph-theoretic approach.

Within the premises of the flux-oriented theory of Crabtree & Newsholme [(1987) Biochem. J. 247, 113-120], I have used a graph-theoretic approach for calculating the Control Coefficients of metabolic pathways. It is shown that a directed graph representing the control structure of a metabolic pathway can be constructed in a heuristic manner directly from the reaction diagram of the pathway, without the necessity of writing down the governing equations for the Control Coefficients. The Control Coefficients are derived from an analysis of the topology of the directed graph. The graph-theoretic approach also provides a visual framework for analysing the functional relationships of the individual enzymes. The control structures of the following pathways are examined here: (a) a simple unbranched pathway with four enzymes, (b) a simple branched pathway with three enzymes, and (c) a branched pathway with both carbon and energy (ATP) fluxes.

Metabolism↗
PubMed1995

Oxidation of cis-5-unsaturated fatty acids in intact rat liver mitochondria: the operation of reduction pathways.

The metabolism of cis-5 unsaturated fatty acids was studied in intact rat liver mitochondria to assess the operation of a reduction pathway. By using direct quantification of metabolites with a capillary-column gas chromatography, 3-hydroxydodecanoate was identified among other metabolites when cis-5-dodecenoate was metabolized in intact rat liver mitochondria. The formation of 3-hydroxydodecanoate supports the existence of a reduction pathway in the metabolism of cis-5-unsaturated fatty acids. This metabolite cannot be produced from the conventional isomerase-mediated pathway. However, the data also indicated the possible operation of the conventional isomerase-mediated pathway in intact rat liver mitochondria. The reduction pathway appears to account for at least 61% of the pathway for cis-5-dodecenoate. This reduction pathway was likely to proceed from the dehydrogenation to trans-2,cis-5-dodecadienoyl-CoA, which was isomerized to delta 3, delta 5-dodecadienoyl-CoA, then to trans-2,trans-4-dodecadienoate. The reduction was mediated by 2,4-dienoyl-CoA reductase by the conversion of trans-2,trans-4-dodecadienoyl-CoA into trans-3-dodecenoyl-CoA. However, direct reduction of the cis-5 double bond was also shown to be operating, although to a lesser extent.

Animals↗
PubMed2000

Modulation of signal-transduction pathways by chemopreventive agents.

For a disease such as cancer, where a number of alterations to normal cell function accumulate over time, there are several opportunities to inhibit, slow down or even reverse the process. Many of the changes which drive the disease process occur in cell-signalling pathways that regulate proliferation and apoptosis. As our knowledge of these complicated signalling networks improves, it is becoming clear that many molecules, both drugs and naturally occurring dietary constituents, can interact beneficially with deregulated pathways. Aspirin and other non-steroidal anti-inflammatory drugs, as well as natural compounds present in plants such as green vegetables and tea, can modulate signalling by affecting kinase activity and therefore phosphorylation of key molecules. Examples of pathways which can be modulated by these agents include activation of the transcription factor nuclear factor kappaB by tumour promoters or cytokines, signalling by growth factors through the growth-factor receptor/extracellular-regulated protein kinase pathways and by a number of other molecules through the stress-activated c-Jun N-terminal kinase and p38 pathways. These mitogen-activated protein kinase pathways regulate a number of transcription factors including c-Fos and c-Jun. Evidence exists, at least from in vitro experiments, that by targeting such pathways, certain dietary compounds may be able to restore abnormal rates of apoptosis and proliferation to more normal levels.

Animals↗
PubMed2002

FLC, a repressor of flowering, is regulated by genes in different inductive pathways.

The MADS-box protein encoded by FLOWERING LOCUS C (FLC) is a repressor of flowering. Loci in the autonomous flowering pathway control FLC levels. We show the epistatic groupings of autonomous pathway mutants fca/fy and fve/fpa, based on their effects on flowering time, are consistent with their effects on FLC transcript and protein levels. We demonstrate that synergistic increases in FLC mRNA and protein expression occur in response to interactions between the autonomous pathway mutants fca and fpa and mutants in other pathways (fe, ft, fha) that do not regulate FLC when present as single mutants. These changes in FLC levels provide the molecular basis of the interactions previously shown in genetic analyses. The interactions between genes of multiple pathways emphasize the central position of FLC in the control of floral initiation. FLC protein levels match those of its mRNA for a range of genetic, developmental and environmental variables, indicating that control of FLC is at the level of transcription or transcript stability. The autonomous and photoperiod pathways also interact at the level of SOC1. FLC acts as a repressor of SOC1, and SOC1 levels are low when FLC levels are high. In C24 plants which have moderately high FLC levels, flowering occurs without a decrease in FLC level, but the SOC1 level does increase. Thus SOC1 levels can be upregulated through the activities of other pathways, despite the repression by FLC.

Arabidopsis↗
PubMed2002

Metastatic pathways and time courses in the orderly progression of cutaneous melanoma.

BACKGROUND: It is known that two-thirds of patients who develop clinical metastases following treatment of a primary cutaneous melanoma initially present with locoregional metastases and one-third initially present with distant metastases. However, few reports in the literature give detailed figures on different metastatic pathways in cutaneous melanoma. OBJECTIVES: The aim of the present study was to perform a detailed analysis of the different metastatic pathways, the time course of the development of metastases and the factors influencing them. METHODS: In a series of 3001 patients with primary cutaneous melanoma at first presentation, 466 subsequently developed metastasis and were followed-up over the long term at the University of Tuebingen, Germany between 1976 and 1996. Different pathways of metastatic spread were traced. Associated risk factors for the different pathways were assessed. Differences in survival probabilities were calculated by the Kaplan-Meier method and evaluated by the log-rank test. RESULTS: In 50.2% of the patients the first metastasis after treatment of the primary tumour developed in the regional lymph nodes. In the remaining half of the patient sample the first metastasis developed in the lymphatic drainage area in front of the regional lymph nodes, as satellite or in-transit metastases (21.7%) or as direct distant metastases (28.1%). Anatomical location, sex and tumour thickness were significant risk factors for the development of metastasis by different pathways. The most important risk factor appeared to be the location of the primary tumour. The median intervals elapsing before the first metastasis differed significantly between the different metastatic pathways. The direct distant metastases became manifest after a median period of 25 months, thus later than the direct regional lymph node metastases (median latency period, 16 months) and the direct satellite and in-transit metastases (median latency period, 17 months). In patients who developed distant metastases the period of development was independent of the metastatic route. The time at which the distant metastases developed was roughly the same (between 24 and 30 months after the detection of the primary tumour), irrespective of whether satellite or in-transit metastases, lymph node metastases or distant metastases were the first to occur. CONCLUSIONS: The time course of the development of distant metastasis was more or less the same irrespective of the metastatic pathway; this suggests that in patients with in-transit or satellite metastasis or regional lymph node metastasis, haematogenic metastatic spread had already taken place. Thus, the diagnostic value of sentinel lymph node biopsy and the therapeutic benefit of elective lymph node dissection may be limited, as satellite and in-transit metastases or direct distant metastases will not be detected and haematogenous spread may already have taken place when the intervention is performed.

Adolescent↗
PubMedDate not supplied

Cytoplasmic signalling pathways in alveolar macrophages involved in the production of nitric oxide after stimulation with excretory/secretory antigens of Toxocara canis.

We studied the cytoplasmic signalling pathways involved in the generation of nitric oxide (NO) after stimulation with adult excretory/secretory antigens (ESA) of Toxocara canis. The pathways of phospholipase A2 (PLA2) and phospholipase C (PLC) were considered as potentially involved in the synthesis of nitric oxide. We used inhibitors of these pathways at different levels. Several concentrations of lithium chloride, verapamil, TMB-8 and staurosporine were used to inhibit the PLC pathway. Inhibition of the PLA2 pathway was attempted with mepacrine, diethylcarbamazine or meloxicam. Lithium chloride, verapamil and TMB-8 reduced the production of NO induced by ESA in a concentration-dependent manner. Regarding the PLA2 pathway, a range of concentrations of mepacrine greatly reduced the production of NO induced by ESA. Meloxicam inhibition was always higher than 50%. Diethylcarbamazine showed a dose-dependent effect on the production of NO induced by the ESA. Our results suggest that both the PLC and the PLA2 pathways play an essential role in activating the production of macrophage NO triggered by the ESA of T. canis. This could indicate that NO production in our experimental conditions is due to both an increase of intracellular calcium and to the participation of the arachidonic acid cascade. The implications of these activations on the host-parasite relationship are discussed and compared with LPS-stimulated macrophages.

Animals↗
PubMed1998

Reversible protein phosphorylation regulates jasmonic acid-dependent and -independent wound signal transduction pathways in Arabidopsis thaliana.

Plants responses to mechanical injury are complex and include the induced expression of defence-related genes. The phytohormone JA has been reported to mediate some of these responses. To elucidate further the signal transduction processes involved, the action of specific agonists and antagonists of known signalling effectors on the response of Arabidopsis thaliana plantlets to JA and wounding was investigated. The identification and characterization of a reversible protein phosphorylation step in a transduction pathway leading to JA-induced gene transcription is reported. This phosphorylation event involved the opposing activities of a staurosporine-sensitive protein kinase, negatively regulating the pathway, and a protein phosphatase, most probably of type 2 A, which activated JA-responsive gene expression. JA activation via this pathway was blocked in the A. thaliana JA-insensitive mutants jin1, jin4 and coi1, and by exogenous application of cycloheximide or auxins. Wound-induced activation of JA-responsive genes was also regulated by this protein phosphorylation step. An alternative wound signalling pathway, independent of JA, was also identified, leading to the transcriptional activation of a different set of genes. This JA-independent pathway was also regulated by a protein phosphorylation switch, in which the protein kinase positively regulated the pathway while the protein phosphatase negatively regulated it. Moreover, a labile protein apparently repressed the expression of these genes. One of the genes analysed, JR3, had a complex pattern of expression, possibly because it was regulated via both of the wound signalling pathways identified. According to the function of an homologous gene, JR3 may be involved in feedback inhibition of the JA response.

Arabidopsis↗
PubMed2003

The ERK/MAP kinase pathway couples light to immediate-early gene expression in the suprachiasmatic nucleus.

Signalling via the p42/44 mitogen-activated protein kinase (MAPK) pathway has been identified as an intermediate event coupling light to entrainment of the mammalian circadian clock located in the suprachiasmatic nucleus (SCN). Given this observation, it was of interest to determine where within the entrainment process the MAPK pathway was functioning. In this study, we examined the role of the MAPK pathway as a regulator of light-induced gene expression in the SCN. Towards this end, we characterized the effect pharmacological disruption of the MAPK cascade has on the expression of the immediate-early genes c-Fos, JunB and EGR-1. We report that uncoupling light from MAPK pathway activation attenuated the expression of all three gene products. In the absence of photic stimulation, inhibition of the MAPK pathway did not alter basal gene product expression levels. Light-induced activation of cAMP response element (CRE)-dependent transcription, as assessed using a CRE-LacZ transgenic mouse strain, was also disrupted by blocking MAPK pathway activation. These results reveal that the MAPK cascade functions as one of the first transduction steps leading from light to rapid transcriptional activation, an essential event in the entrainment process. MAPK pathway-dependent gene expression in the SCN may result, in part, from stimulation of CRE-dependent transcription.

Animals↗
PubMed2003

The effect of 6-hydroxydopamine lesions on the release of amino acids in the direct and indirect pathways of the basal ganglia: a dual microdialysis probe analysis.

The loss of dopaminergic neurons of the substantia nigra in Parkinson's disease and in animal models of Parkinson's disease is associated with an imbalance in the activity of the so-called 'direct' and 'indirect' pathways of information flow through the basal ganglia. The aim of the present study was to determine whether the imbalance is reflected in changes in the release of GABA, aspartate and glutamate in the pathways using dual probe microdialysis in freely moving rats. Control and 6-hydroxydopamine-(6-OHDA)-lesioned rats were implanted with microdialysis probes in the neostriatum and substantia nigra or globus pallidus and the release of amino acids was analysed in the dialysates. Basal levels of amino acids were largely unaltered by the 6-OHDA lesion; however, the levels of GABA in the globus pallidus dialysates were significantly elevated in the lesioned rats, indicating an imbalance in favour of the indirect pathway. Administration of kainic acid to the neostriatum enhanced the release of GABA locally and in the distal probes in the substantia nigra and globus pallidus. In 6-OHDA-lesioned rats, stimulated release of GABA in the substantia nigra was abolished, indicating a reduction in transmission along the direct pathway. Thus, consistent with the direct-indirect pathway model of the basal ganglia, the 6-OHDA lesion results in an elevation of the basal release of GABA in the striatopallidal (indirect) pathway and a reduction in the evoked release of GABA in the striatonigral (direct) pathway. These imbalances may underlie, at least in part, the motor abnormalities of Parkinson's disease and in animal models of Parkinson's disease.

Adrenergic Agents↗
PubMed2003

Effects of a blocked atrial beat on the atrioventricular nodal recovery property in patients with dual nodal pathways.

Dual AVN physiology can be demonstrated by a variety of maneuvers. To determine whether AVN recovery times following a blocked extrastimulus facilitate or obscure detection of dual AVN physiology, 11 patients (9-17 years) were studied with dual AVN pathways by using single and double atrial extrastimuli. With a single atrial extrastimuli, the premature atrial stimulus (A2) was coupled to basic atrial beats (A1). The fast and slow AVN recovery curves were constructed with plots of the nodal conduction time against the recovery time (A1A2,A2H2). With double atrial extrastimuli, a fixed blocked A2 beat (A2B) was followed by a scanning atrial beat (A3). The nodal recovery property post-A2B was studied by plots of A2BA3,A3H3. In all patients the recovery curve of the fast pathway post-A2B had a leftward shift when compared to that of the pre-A2B curve (i.e., the AH was shortened at the same recovery time). The window of slow pathway conduction post-A2B disappeared totally in five patients and decreased significantly in six patients (post-A2B: 26 +/- 42 ms; pre-A2B: 80 +/- 65 ms, P < 0.05). In the six patients that still had slow pathway conduction post-A2B, the slow pathway effective refractory period post-A2B was significantly less than that of pre-A2B (215 +/- 38 vs 268 +/- 16 ms, P < 0.05). The fast pathway effective refractory period post-A2B was also diminished significantly (235 +/- 62 vs 357 +/- 76 ms, P < 0.0001). The authors conclude that blocked atrial beats decrease the visibility of the slow pathway conduction.

Adolescent↗
PubMed2002

Genomic analysis of the aromatic catabolic pathways from Pseudomonas putida KT2440.

Analysis of the catabolic potential of Pseudomonas putida KT2440 against a wide range of natural aromatic compounds and sequence comparisons with the entire genome of this microorganism predicted the existence of at least four main pathways for the catabolism of central aromatic intermediates, that is, the protocatechuate (pca genes) and catechol (cat genes) branches of the beta-ketoadipate pathway, the homogentisate pathway (hmg/fah/mai genes) and the phenylacetate pathway (pha genes). Two additional gene clusters that might be involved in the catabolism of N-heterocyclic aromatic compounds (nic cluster) and in a central meta-cleavage pathway (pcm genes) were also identified. Furthermore, the genes encoding the peripheral pathways for the catabolism of p-hydroxybenzoate (pob), benzoate (ben), quinate (qui), phenylpropenoid compounds (fcs, ech, vdh, cal, van, acd and acs), phenylalanine and tyrosine (phh, hpd) and n-phenylalkanoic acids (fad) were mapped in the chromosome of P. putida KT2440. Although a repetitive extragenic palindromic (REP) element is usually associated with the gene clusters, a supraoperonic clustering of catabolic genes that channel different aromatic compounds into a common central pathway (catabolic island) was not observed in P. putida KT2440. The global view on the mineralization of aromatic compounds by P. putida KT2440 will facilitate the rational manipulation of this strain for improving biodegradation/biotransformation processes, and reveals this bacterium as a useful model system for studying biochemical, genetic, evolutionary and ecological aspects of the catabolism of aromatic compounds.

Adipates↗
PubMed2001

The Ras-ERK pathway is required for the induction of neuronal nitric oxide synthase in differentiating PC12 cells.

We have studied the role of MAP kinase pathways in neuronal nitric oxide synthase (nNOS) induction during the differentiation of PC12 cells. In nerve growth factor (NGF)-treated PC12 cells, we find nNOS induced at RNA and protein levels, resulting in increased NOS activity. We note that neither nNOS mRNA, nNOS protein nor NOS activity is induced by NGF treatment in cells that have been infected with a dominant negative Ras adenovirus. We have also used drugs that block MAP kinase pathways and assessed their ability to inhibit nNOS induction. Even though U0126 and PD98059 are both MEK inhibitors, we find that U0126, but not PD98059, blocks induction of nNOS protein and NOS activity in NGF-treated PC12 cells. Also, the p38 kinase inhibitor, SB203580, does not block nNOS induction in our clone of PC12 cells. Since the JNK pathway is not activated in NGF-treated PC12 cells, we conclude that the Ras-ERK pathway and not the p38 or JNK pathway is required for nNOS induction in NGF-treated PC12 cells. We find that U0126 is much more effective than PD98059 in blocking the Ras-ERK pathway, thereby explaining the discrepancy in nNOS inhibition. We conclude that the Ras-ERK pathway is required for nNOS induction.

Animals↗
PubMed2003

Activation and cellular localization of the p38 and JNK MAPK pathways in rat crescentic glomerulonephritis.

BACKGROUND: The p38 and c-Jun N-terminal kinase (JNK) mitogen-activated protein kinase (MAPK) are intracellular signal transduction pathways involved in the production of inflammatory mediators. Little, however, is known about the contribution of these pathways to renal inflammation, nor the cell types in which these pathways are activated within normal and inflamed kidneys. The aim of this study was therefore to delineate the pattern and cellular localization of p38 and JNK activation in normal rat kidney and rat acute and chronic inflammatory renal disease. METHODS: Normal male Sprague-Dawley rats and groups of rats given accelerated anti-glomerular basement membrane (GBM) disease were killed at 3 hours, day 1, day 7, or day 28 and examined for p38 and JNK pathway activation by Western blotting and immunolocalization of the phosphorylated p38 (p-p38) and JNK (p-JNK) kinases. RESULTS: In terms of glomerular MAPK activation, Western blotting identified the presence of both p-p38 and p-JNK in normal glomeruli, localized by immunohistochemistry to podocytes and epithelial cells of Bowman's capsule. In anti-GBM disease, Western blotting showed that p38 activation peaked at 3 hours and remained elevated above normal throughout the disease time course. JNK activation (via the 54 kD isoform) likewise increased at 3 hours of anti-GBM disease and remained elevated throughout disease. At 3 hours, p-p38, but not p-JNK, was localized to neutrophils and glomerular endothelial cells. p-JNK was localized to glomerular endothelial cells at day 7. Macrophages, lymphocytes, activated podocytes, and myofibroblasts were positive for both p-p38 and p-JNK. In terms of tubular MAPK activation, Western blotting identified p38 and JNK activation in tubules of normal kidney. Immunostaining showed that most cortical tubules contained some p-p38 and p-JNK stained cells. There was a significant increase in tubular p38 activation at 3 hours of anti-GBM disease, followed by increased JNK activation of the 54 kD isoform from day 7 onward, and the 46 kD isoform at day 28. Immunostaining of diseased tissue localized p-p38 and p-JNK to virtually all cortical tubular cells. CONCLUSION: The p38 and JNK MAPK pathways are activated in glomeruli and tubules of normal kidney. In acute anti-GBM disease, there was an increase in p38 activation within glomerular endothelial cells and within infiltrating neutrophils, suggesting an important role for p38 MAPK in acute inflammation. In progressive anti-GBM disease, p38 and JNK activation in podocytes, glomerular endothelial cells, infiltrating macrophages, T cells, and myofibroblasts suggests that both the p38 and JNK MAPK pathways are important in chronic inflammation and fibrosis. Blockade of these pathways may therefore be potentially therapeutic in the treatment of acute and chronic renal inflammation.

Animals↗
PubMed2002

Accessory pathway localization by QRS polarity in children with Wolff-Parkinson-White syndrome.

INTRODUCTIONS: Location of the accessory pathway (AP) in Wolff-Parkinson-White (WPW) syndrome can be determined accurately by the QRS polarity on resting ECG. These ECG characteristics may be different in children, and no algorithm has yet been tested. METHODS AND RESULTS: A total of 153 resting ECGs of symptomatic children with WPW syndrome were retrospectively analyzed. The anatomic AP location had been established fluoroscopically at eight possible sites during radiofrequency catheter ablation. Two independent observers predicted AP location on blinded ECGs with a QRS polarity algorithm for adults using leads II, III, aVL, V1, and V2. Subsequently, the QRS polarity for all individual ECG leads was evaluated and a new algorithm for children was devised. With the adult algorithm, the observers correctly predicted only 55% to 58% of AP locations. The septal and right-sided pathways often were inseparable, and mid-septal and parahisian pathways were missed. In the new children's algorithm, left lateral, left posteroseptal, and posteroseptal pathways shared a positive or intermediate QRS polarity on V1, with the left lateral pathway separated by a positive QRS polarity on lead III. Negative QRS polarity on lead V1 and positive QRS polarity on lead V3 were shared by right posteroseptal, mid-septal, parahisian, and anteroseptal pathways, with the latter two having a positive QRS polarity on lead aVF. Right lateral pathways had negative QRS polarity on lead V1 and negative or intermediate QRS polarity on lead V3. Overall accuracy for these five regions was 90%. CONCLUSION: AP characterization by QRS polarity in children with WPW syndrome is more diverse than in adults and requires other ECG leads to establish five AP regions.

Adolescent↗
PubMed2002

Assessment of accessory atrioventricular pathways by Doppler myocardial imaging.

PURPOSE: The use of electrophysiologic studies (EPS) for the localization of accessory atrioventricular connections in Wolff-Parkinson-White syndrome (WPW) requires accurate evaluation of the site of bypass tract insertion. Doppler myocardial imaging (DMI) is a new ultrasound technique that allows the detection of abnormal and early regional myocardial depolarization. The purpose of this study was to identify an abnormal pathway site in WPW patients. METHODS: Twenty-one patients with ventricular preexcitation were studied by DMI. Two-dimensional color DMI, velocity maps, acceleration maps, and pulsed-wave applications were used. A subsequent diagnostic EPS was performed. The results of EPS were taken as the gold standard diagnostic procedure. Radiofrequency catheter ablation therapy was then performed on all patients. RESULTS: The anomalous pathway was detected by DMI in 16 (76%) of 21 patients (9 [90%] of 10 with left pathways and 7 [64%] of 11 with right pathways), with respect to results of the EPS. Pathway detection was better with pulsed-wave DMI (76%) with its higher temporal resolution as compared with M-mode velocity map (57%) and acceleration map (47%). In most of the patients with successful radiofrequency ablation, an immediate resolution of the abnormal ventricular depolarization occurred and was detectable by DMI. CONCLUSIONS: Our findings demonstrate the feasibility of DMI to assess the early ventricular contraction associated with atrioventricular accessory pathways. Therefore, DMI appears to be a clinically useful adjunct to noninvasive evaluation of abnormal myocardial depolarization in WPW and to evaluate the results after radiofrequency ablation, even though its accuracy is considerably better for left-sided accessory pathways than for right-sided ones.

Adult↗
PubMed2002

Arrhythmia recurrences are rare when the site of radiofrequency ablation of the slow pathway is medial or anterior to the coronary sinus os.

AIMS: The site of successful ablation of the slow atrioventricular (AV) nodal pathway may be located in the posteroseptal or midseptal area. We have previously shown that the site of successful radiofrequency (RF) ablation of the slow pathway, rather than residual slow pathway conduction correlates with AV nodal re-entrant tachycardia (AVNRT) recurrences, with more recurrences noted in inferoposterior (to the coronary sinus os) locations. Accordingly, we have since modified our approach, and in a consecutive series of 105 patients we have performed slow pathway RF ablation exclusively at medial or anterior locations, with the objective of prospectively examining the recurrence rate of AVNRT incurred with this approach. METHODS AND RESULTS: The study included 40 men and 65 women, aged 42 +/- 18 years, having RF ablation for symptomatic AVNRT exclusively in anterior to the coronary sinus os locations. A combined anatomical and electrophysiological approach to slow pathway ablation was employed. This series of patients was compared with the previous series of 55 patients (historical group) with AVNRT undergoing RF ablation at both inferoposterior and anteromedial locations. The mean cycle length of the induced AVNRT was 329 +/- 48 ms. RF ablation was successful in all patients (100%). A mean of 7 +/- 6 lesions were applied. Persistent jump or echo beats were noted in 48 patients (46%). The procedure lasted for 2.1 +/- 1.0 h. Fluoroscopy time was 23 +/- 14 min. Procedures were complicated by heart block in two patients (1.9%). Over 26 +/- 19 months, there has been only one recurrence of AVNRT (1%). The historical group had similar age (37 +/- 18 years), gender (17 men/38 women), AVNRT cycle length (340 +/- 60 ms), number of RF lesions (9 +/- 6), or residual slow pathway conduction (42%), but longer fluoroscopy time (41 +/- 25 min) and procedure duration (4 +/- 1 h), and a significantly higher recurrence rate (seven patients/13%) (P=0.004) at a much shorter follow-up period of 12 +/- 8 months. CONCLUSION: AVNRT recurrences are rare (1%) when slow pathway RF ablation is performed in medial or anterior locations at the tricuspid annulus, rather than in inferoposterior sites, whereby a higher (13%) recurrence rate has been previously noted.

Adult↗