Prenatal three-dimensional sonographic images associated with Treacher Collins syndrome.
Explore the source record for details and available documents.
Adult↗
Biomedical subjects
M S Chang
Publications and source records attributed to M S Chang.
Byakangelicol, isolated from Angelica dahurica, inhibits both the activity and induction of cyclooxygenase-2 in human pulmonary epithelial cells.
We examined the inhibitory mechanism of byakangelicol, isolated from Angelica dahurica, on interleukin-1beta (IL-1beta)-induced cyclooxygenase-2 (COX-2) expression and prostaglandin E2 (PGE2) release in human pulmonary epithelial cell line (A549). Byakangelicol (10-50 microM) concentration-dependently attenuated IL-1beta-induced COX-2 expression and PGE2 release. The selective COX-2 inhibitor, NS-398 (0.01-1 microM), and byakangelicol (10-50 microM) both concentration-dependently inhibited the activity of the COX-2 enzyme. Byakangelicol, at a concentration up to 200 microM, did not affect the activity and expression of COX-1 enzyme. IL-1beta-induced p44/42 mitogen-activated protein kinase (MAPK) activation was inhibited by the MAPK/extracellular signal-regulated protein kinase (MEK) inhibitor, PD 98059 (30 microM), while byakangelicol (50 microM) had no effect. Treatment of cells with byakangelicol (50 microM) or pyrrolidine dithiocarbamate (PDTC; 50 microM) partially inhibited IL-1beta-induced degradation of IkappaB-alpha in the cytosol, translocation of p65 NF-kappaB from the cytosol to the nucleus and the NF-kappaB-specific DNA-protein complex formation. Taken together, we have demonstrated that byakangelicol inhibits IL-1beta-induced PGE2 release in A549 cells; this inhibition may be mediated by suppression of COX-2 expression and the activity of COX-2 enzyme. The inhibitory mechanism of byakangelicol on IL-1beta-induced COX-2 expression may be, at least in part, through suppression of NF-kappaB activity. Therefore, byakangelicol may have therapeutic potential as an anti-inflammatory drug on airway inflammation.
Cell Survival↗
Metabotropic glutamate receptor 5-induced phosphorylation of extracellular signal-regulated kinase in astrocytes depends on transactivation of the epidermal growth factor receptor.
G-protein-coupled receptors (GPCRs) induce the phosphorylation of mitogen-activated protein (MAP) kinase by actions on any of a number of signal transduction systems. Previous studies have revealed that activation of the G(q)-coupled metabotropic glutamate receptor 5 (mGluR5) induces phosphorylation of the MAP kinase extracellular signal-regulated kinase 2 (ERK2) in cultured rat cortical astrocytes. We performed a series of studies to determine the mechanisms underlying mGluR5-induced phosphorylation of MAP kinase in these cells. Interestingly, our studies suggest that mGluR5-mediated ERK2 phosphorylation is dependent on the activation of G(alphaq) but is not mediated by the activation of phospholipase Cbeta1, activation of protein kinase C, or increases in intracellular calcium. Studies with peptide inhibitors suggest that this response is not dependent on G(betagamma) subunits. However, the activation of ERK2 was dependent on activation of the epidermal growth factor (EGF) receptor and activation of a Src family tyrosine kinase. Furthermore, activation of mGluR5 induced an association of this receptor and the EGF receptor, suggesting the formation of a signaling complex involved in the activation of ERK2. These data suggest that mGluR5 increases ERK2 phosphorylation in astrocytes by a novel mechanism involving the activation of G(alphaq) and both receptor and nonreceptor tyrosine kinases but that is independent of the activation of phospholipase Cbeta1.
Animals↗
Effects of rapid atrial pacing on the arrhythmogenic activity of single cardiomyocytes from pulmonary veins: implication in initiation of atrial fibrillation.
BACKGROUND: Pulmonary veins (PVs) are important sources of paroxysmal atrial fibrillation. Long-term rapid atrial pacing (RAP) changes atrial electrophysiology and facilitates the maintenance of atrial fibrillation. It is not clear whether RAP alters the arrhythmogenic activity of PVs. The purpose of this study was to isolate single PV cardiomyocytes from control and RAP dogs and evaluate their electrophysiological characteristics. METHODS AND RESULTS: The action potential and ionic currents were investigated in PV cardiomyocytes from control and long-term (6 to 8 weeks) RAP (780 bpm) dogs by use of the whole-cell clamp technique. Dissociation of PVs yielded rod-shaped single cardiomyocytes without (n=91, 60%) or with (n=60, 40%) pacemaker activity. Compared with the control group, the RAP dog PV cardiomyocytes had faster beating rates (0.86+/-0.28 versus 0.45+/-0.07 Hz, P<0.05) and shorter action potential duration. The RAP dog PV cardiomyocytes with pacemaker activity have a higher incidence of delayed (59% versus 7%, P<0.001) or early (24% versus 0%, P<0.005) after depolarization. The RAP dog PV cardiomyocytes with pacemaker activity had smaller slow inward and transient outward but larger transient inward (0.017+/-0.004 versus 0.009+/-0.002 pA/pF, P<0.05) and pacemaker (0.111+/-0.019 versus 0.028+/-0.008 pA/pF, P<0.001) currents. The RAP dog PV cardiomyocytes without pacemaker activity had only smaller slow inward and transient outward and larger pacemaker currents. CONCLUSIONS: PVs contain multiple cardiomyocytes with distinct electrophysiological characteristics. RAP changes the electrophysiological characteristics and arrhythmogenic activity of PVs.
Action Potentials↗
Pulsatility of ascending aorta and restenosis after coronary angioplasty in patients >60 years of age with stable angina pectoris.
A recent study has demonstrated that the pulsatility of the ascending aorta is a strong predictive factor for restenosis after coronary angioplasty. However, whether the pulsatility of the ascending aorta is still a significant predictor for restenosis in elderly patients with a stiffer aorta is unknown. We investigated the relation between arterial pulsatility in the ascending aorta and restenosis after coronary angioplasty in patients aged > 60 years. Eighty-seven consecutive patients (80 men, aged 72.5 +/- 5.1 years) with stable angina were included. Before angioplasty, the arterial systolic, diastolic, and mean pressure waveforms of the ascending aorta were measured. We used fractional pulse pressure (PPf, the ratio of pulse pressure to mean pressure) and pulsatility index (PI, the ratio of pulse pressure to diastolic pressure) to estimate the pulsatility of the ascending aorta. Angiographic restenosis occurred in 39 patients. Pulse pressure, PPf, and PI were significantly higher in patients with restenosis after coronary angioplasty (restenosis vs without restenosis: pulse pressure, 77.6 +/- 12.2 vs 66.1 +/- 15.4 mm Hg [p < 0.001]; PPf, 0.80 +/- 0.09 vs 0.69 +/- 0.11 [p < 0.001]; PI, 1.19 +/- 0.20 vs 0.98 +/- 0.21 [p < 0.001]). After multivariate stepwise adjustment of risk factors of restenosis and using receiver-operating characteristic analysis, the odds ratio (OR) of restenosis was: pulse pressure > 66 mm Hg, OR 5.88 (95% confidence interval [CI] 2.17 to 15.93); PPf > 0.72, OR 13.71 (95% CI 4.81 to 39.05); PI > 1.06, OR 13.56 (95% CI 4.67 to 39.38). Moreover, among patients aged > 70 years (n = 60), the predictive values of PPf and PI were even higher than those in patients aged < or = 70 years (n = 27). Thus, in elderly patients with stable angina, the pulsatility of the ascending aorta is a powerful predictor of restenosis after coronary angioplasty.
Aged↗
RNA editing of the human serotonin 5-HT2C receptor alters receptor-mediated activation of G13 protein.
The recent completion of the human genome predicted the presence of only 30,000 genes, stressing the importance of mechanisms that increase molecular diversity at the post-transcriptional level. One such post-transcriptional event is RNA editing, which generates multiple protein isoforms from a single gene, often with profound functional consequences. The human serotonin 5-HT(2C) receptor undergoes RNA editing that creates multiple receptor isoforms. One consequence of RNA editing of cell surface receptors may be to alter the pattern of activation of heterotrimeric G-proteins and thereby shift preferred intracellular signaling pathways. We examined the ability of the nonedited 5-HT(2C) receptor isoform (INI) and two extensively edited isoforms, VSV and VGV, to interact with various G-protein alpha subunits. Two functional assays were utilized: the cell-based functional assay, Receptor Selection/Amplification Technology(TM), in which the pharmacological consequences of co-expression of 5HT(2C) receptor isoforms with G-protein alpha subunits in fibroblasts were studied, and 5HT(2C) receptor-mediated rearrangements of the actin cytoskeleton in stable cell lines. These studies revealed that the nonedited 5-HT(2C) receptor functionally couples to G(q) and G(13). In contrast, coupling to G(13) was not detected for the extensively edited 5-HT(2C) receptors. Thus, RNA editing represents a novel mechanism for regulating the pattern of activation of heterotrimeric G-proteins, molecular switches that control an enormous variety of biological processes.
3T3 Cells↗
Effects of cavotricuspid isthmus ablation on atrioventricular node electrophysiology in patients with typical atrial flutter.
BACKGROUND: The atrial musculature in the cavotricuspid isthmus is a part of posterior inputs to the AV node. In patients with typical atrial flutter, effects of radiofrequency ablation of this isthmus on AV node conduction are still unknown. METHODS AND RESULTS: This study included 16 patients with clinically documented typical atrial flutter. Group 1 had 8 patients without and group 2 had 8 patients with dual AV nodal pathway physiology. Electrical pacing from the interatrial septum and low right atrium was performed to evaluate antegrade AV node function before and after ablation of the cavotricuspid isthmus. In group 1, the AV node conduction properties were similar before and after ablation. In group 2, the AV node Wenckebach cycle length and maximal AH interval during low right atrium (356+/-58 versus 399+/-49 ms, P=0.008; 303+/-57 versus 376+/-50 ms, P=0.008) and interatrial septum (365+/-62 versus 393+/-59 ms, P=0.008; 324+/-52 versus 390+/-60 ms, P=0.008) pacing were significantly longer after ablation. Elimination of the slow pathway after ablation was noted in 2 patients, including 1 with AV nodal reentrant echo beats. CONCLUSIONS: Radiofrequency ablation of the cavotricuspid isthmus was effective in eliminating typical atrial flutter without injury of antegrade fast AV node conduction. The atrial musculature in the cavotricuspid isthmus significantly contributed to the slow AV node conduction.
Aged↗
Cloning and characterization of hMAP126, a new member of mitotic spindle-associated proteins.
One novel gene product, hMAP126, was demonstrated to interact with p29 in the yeast two-hybrid assay. The full-length cDNA of hMAP126 has been obtained and encodes a protein of 1120 amino acids. Multiple tissue Northern blot analysis showed that hMAP126 was abundantly expressed in the testis. Polyclonal antiserum against hMAP126 was raised and affinity-purification of anti-hMAP126 antibodies was performed. The subcellular distribution of hMAP126 was localized to the mitotic spindle. Furthermore, hMAP126 was identified to be post-translationally modified and phosphorylated by p34(cdc2) kinase in vitro. Taken together, we have isolated a novel protein, hMAP126, which may be involved in the functional and dynamic regulation of mitotic spindles.
Amino Acid Sequence↗
Evidence for inhibition of low density lipoprotein oxidation and cholesterol accumulation by apolipoprotein H (beta2-glycoprotein I).
Low density lipoprotein (LDL) oxidation and lipid accumulation are thought to enhance the progression of atherosclerosis. Apolipoprotein H (apoH) has been implicated in the development of human atherosclerosis. However, the roles of apoH in the oxidative modification of LDL and cellular accumulation of lipid constituents remained uncharacterized. In this study, the level of plasma apoH was found to be significantly associated with the oxidative susceptibility of LDL in human subjects. Plasma levels of apoH were positively correlated with the lag time but negatively correlated with LDL oxidation rate in conjugated diene formation. By using a J774 A.1 macrophage culture system, we found that apoH could not only inhibit the formation of conjugated diene and thiobarbituric acid-reactive substances, but also reduce the electrophoretic mobility of oxidized LDL. Furthermore, apoH decreased cellular accumulation of cholesterol via a reduction in cholesterol influx and an increase in cholesterol efflux. This is the first demonstration that apoH appears to have "antioxidant"-like effects on LDL oxidation. The results also suggest that apoH can inhibit the translocation of cholesterol from extracellular pools to macrophages, suggesting that apoH may play an important role in the prevention of atherosclerosis.
Arteriosclerosis↗
Association of p53 and BCL-2 expression with Epstein-Barr virus infection in the cancers of head and neck.
BACKGROUND: Reports that have both evaluated the site-specific Epstein-Barr virus (EBV) infection and compared it with the expression of the EBV-related proto-oncogenes and tumor suppressor genes in the various cancers of head and neck are scarce. METHODS: Thirty-eight nasopharyngeal carcinoma (NPC) cases, 32 oropharyngeal or hypopharyngeal carcinoma (OPC/HPC) cases, and 93 laryngeal carcinoma (LC) cases were evaluated with in situ hybridization on EBV-encoded small RNA (EBER) and immunohistochemical assessments of the p53, bcl-2, and epidermal growth factor receptor (EGFR) by use of formalin-fixed paraffin-embedded tissue array slides. RESULTS: The expression of viral EBERs was observed in more than two thirds (71.1%) of the NPC cases. In contrast, only 1 case of OPC and none of the HPC or LC cases exhibited EBV positivity. In the nonkeratinizing NPC, the EBV positivity was significantly associated with both frequent p53 overexpression (p =.033) and bcl-2 expression (p =.001). In the EBV-positive nonkeratinizing NPC, a correlation between p53 overexpression and the tumor infiltration lymphocyte (TIL) density was noted (p =.012). CONCLUSIONS: A site-specific expression of viral EBER was demonstrated in the head and neck cancers, which suggests an important role for both p53 and bcl-2 in the carcinogenesis of an EBV-infected NPC. The correlation between p53 overexpression and the TIL density in the EBV-infected NPC suggests that the product of a lymphoepithelial interaction, such as A20, can induce a dysfunctional p53 protein.
Adolescent↗
Transcriptional activation of the human Cu/Zn superoxide dismutase gene by 2,3,7,8-tetrachlorodibenzo-p-dioxin through the xenobiotic-responsive element.
Cu/Zn superoxide dismutase (SOD1) catalyzes the dismutation of superoxide radicals produced during biological oxidations and environmental stress. Here we have investigated the effect of the most toxic dioxin, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), on the promoter of the Cu/Zn superoxide dismutase (SOD1) gene in HepG2 and HeLa cells using the chloramphenicol acetyltransferase gene as a reporter. The SOD1 promoter was activated 4- to 5-fold by TCDD treatment, in a concentration-dependent manner. In addition, the level of SOD1 mRNA and the enzymatic activity of the SOD1 protein were also enhanced on exposure of the cells to TCDD. Functional analysis of the regulatory region of the SOD1 gene by deletion and point mutation, and the use of a heterologous promoter system, showed that the SOD1 gene was transactivated by TCDD via the xenobiotic-responsive element (XRE). Gel mobility shift assays also confirmed the induction and the inducible binding of a receptor-ligand complex to XRE. Yeast cells that overexpress hSOD1 appeared to be more resistant to TCDD than the wild type. These results demonstrate that SOD1 is induced by TCDD via the XRE. The induced SOD1 may accelerate the neutralization of the superoxide anion and thus reduce the oxidative damage associated with dioxin toxicity.
Animals↗
Frequent gain of copy number on the long arm of chromosome 3 in human cervical adenocarcinoma.
We analyzed genomic aberrations in 20 cervical adenocarcinomas by comparative genomic hybridization (CGH). Most tissue samples (85%) showed DNA copy number changes; gains were more common than losses. The most consistent region of chromosomal gain was mapped to chromosome arm 3q, found in 70% of the cases, with a minimal common region of 3q28-ter. Other recurrent amplifications of genetic material were detected on 17q (45%), 1p (30%), 1q (25%), and 11q (20%). High-level copy number increases were found in chromosomal regions 3q27-ter and 9pter-13. DNA losses were seldom observed, occurring primarily in underrepresented regions of chromosome arms 4q, 13q, and 18q. The presence of high-risk human papilloma virus genomes in the cervical adenocarcinoma samples was detected in 90% of the cases. However, there was no correlation between human papilloma virus type and the pattern of genomic changes. This study is the first report of CGH analysis in human cervical adenocarcinoma. Among the major genomic alterations, our results demonstrate the importance of DNA copy increases of chromosome arm 3q in the development of cervical adenocarcinoma and identify other amplified chromosomal regions that are also associated with cervical carcinogenesis.
Adenocarcinoma↗
First trimester diagnosis of holoprosencephaly and cyclopia with triploidy by transvaginal three-dimensional ultrasonography.
We present the prenatal three-dimensional (3D) ultrasound findings in a case of holoprosencephaly and cyclopia at 11 weeks gestation. Only holoprosencephaly with missing cyclopia were initially diagnosed because suboptimal views of the fetal face were obtained with transvaginal two-dimensional (2D) ultrasonography due to fetal position. Chromosomes identified by analysis of a fluid sample from early amniocentesis demonstrated a triploidy (69, XXX), spontaneous fetal demise occurred at 12 weeks and the pregnancy was terminated. This case demonstrated the usefulness of transvaginal 3D ultrasonography in establishing the final diagnosis.
Adult↗
Electrophysiologic characteristics in initiation of paroxysmal atrial fibrillation from a focal area.
OBJECTIVES: We investigated the electrophysiologic characteristics in the initiation of paroxysmal atrial fibrillation (PAF) from a focal area. BACKGROUND: The electrophysiologic characteristics in the initiation of PAF are still not clear. METHODS: The study group consisted of 77 patients (M/F = 65/12, age 66 +/- 12 years) with frequent episodes of PAF; we analyzed: 1) 15 cycle lengths of electrical activity before the onset of atrial fibrillation (AF); 2) coupling interval (CI) of the first ectopic beat just before the initiation of AF; and 3) the prematurity of an ectopic beat (prematurity index [PI] = CI/mean of preceding 15 cycle lengths). RESULTS: A total of 111 episodes of sustained AF were identified. Two patterns of AF initiation were observed: group I (59/111, 53%) included the episodes preceded by cycle length oscillation, and group II (52/111, 47%) included the episodes initiated by a single ectopic beat with preceding cycle length relatively constant. The PI of group I episodes was significantly greater than that of group II (0.41 +/- 0.12 vs. 0.34 +/- 0.10, p < 0.01). The CI (267 +/- 54 ms vs. 217 +/- 55 ms, p < 0.05), AF1 (194 +/- 36 ms vs. 153 +/- 37 ms, p < 0.05) and PI (0.49 +/- 0.13 vs. 0.37 +/- 0.11, p < 0.01) of the AF episodes from the superior vena cava (SVC) were significantly longer and greater than those of AF episodes from pulmonary veins (PVs). CONCLUSIONS: In patients with PAF originating from PVs or the SVC, two major initiating patterns were found. Moreover, the electrophysiologic characteristics in the initiation of AF originating from the SVC were also different from those of AF initiating from the PVs.
Adult↗
Prolonged fractionation of paced right atrial electrograms in patients with atrial flutter and fibrillation.
OBJECTIVES: This study investigated the extent of fractionation of paced right atrial electrograms in patients with and without paroxysmal atrial flutter (AFL) or atrial fibrillation (AF). BACKGROUND: Slow conduction through nonuniform anisotropic atrial muscles, represented by fractionated electrograms, may favor the generation of atrial tachyarrhythmias. METHODS: This study included 10 control patients (Group 1), 8 patients with documented paroxysmal AFL (Group 2) and 10 patients with documented paroxysmal AF (Group 3). Five electrode catheters were placed in the different sites of the right atrium and one catheter was positioned at the coronary sinus ostium. Atrial pacing from one site was done by a constant drive train with an extrastimulus inserted every fourth beat while recording at the other five sites was performed. The delay of each fractionated potential in the high-pass filtered atrial electrogram in response to extrastimulation was determined and used to construct conduction curves of delay versus the S1S2 interval. RESULTS: The mean increase in electrogram duration between a coupling interval of 350 ms and 10 ms above atrial refractoriness was significantly greater in Groups 2 and 3 compared with that in Group 1 (8.5 +/- 2.5 vs. 11.0 +/- 2.7 vs. 5.9 +/- 2.3 ms, respectively, p < 0.001). The mean S1S2 interval at which delay increased suddenly was also longer in Groups 2 and 3 compared with Group 1 (326 +/- 9 vs. 343 +/- 12 vs. 307 +/- 17 ms, respectively, p < 0.001). CONCLUSIONS: Increased delays in the individual potential of the fractionated atrial electrograms may be related to the development of AFL and AF.
Action Potentials↗
Mechanism of spontaneous transition from typical atrial flutter to atrial fibrillation: role of ectopic atrial fibrillation foci.
Paroxysmal AF has been known to be initiated by ectopic beats, especially in the pulmonary veins (PVs), and radiofrequency catheter ablation could cure it. We considered that the spontaneous transition from typical atrial flutter to AF also could be initiated by ectopic beats. Twenty patients (18 men, mean age 66 +/- 14 years) with episodes of spontaneous transition from typical atrial flutter to AF were included in this study. They underwent detailed mapping of both atria. All the patients had spontaneous AF initiated by ectopic beats, and all of them had typical atrial flutter and spontaneous transition from typical atrial flutter (12 patients with counterclockwise atrial flutter and 8 patients with clockwise atrial flutter) to AF. The transition was initiated by ectopic beats from the PVs (17 foci, 85%), crista terminalis (2 foci, 10%), and superior vena cava (1 focus, 5%). After successful ablation of AF foci, typical atrial flutter was induced again, but no spontaneous transition was found after at least 10 minutes of observation. We concluded that paroxysmal AF and spontaneous transition from typical atrial flutter to AF were initiated by ectopic beats, and successful catheter ablation of the ectopic foci can eliminate paroxysmal AF and spontaneous transition from typical atrial flutter to AF.
Aged↗
Pulmonary vein dilation in patients with atrial fibrillation: detection by magnetic resonance imaging.
INTRODUCTION: The positive relationship between left atrial (LA) size and atrial fibrillation (AF) is well recognized; however, there is little information on the association of pulmonary vein (PV) diameter and AF. The purpose of this study was to investigate by magnetic resonance angiography the change of PV and LA size in patients with no history of AF, patients with paroxysmal AF (PAF), and patients with chronic AF (CAF). METHODS AND RESULTS: The study included 47 patients. Group I included 15 patients with normal sinus rhythm and no history of documented AF. Group II included 24 patients with drug-refractory PAF who underwent electrophysiologic study and radiofrequency ablation of PV foci. Group III included 8 patients with CAF who were converted to sinus rhythm by external electrical cardioversion. Age and concomitant heart diseases were similar among the three groups. We measured the diameter of each PV at its junction with the LA in addition to LA dimensions by gadolinium-enhanced magnetic resonance angiography with three-dimensional reconstruction. Significant dilation of both superior PVs (P < 0.01) and transverse diameter of LA (P < 0.01) was seen in the three groups. There were no significant changes of both inferior PVs, corrected PV (PV/LA) diameter, or longitudinal diameter of LA among the three groups. Only 28% patients showed arrhythmogenic foci from the largest PV. CONCLUSION: Significant dilation of both superior PVs with simultaneous LA enlargement was demonstrated i
Aged↗
Acquired pulmonary vein stenosis after radiofrequency catheter ablation of paroxysmal atrial fibrillation.
INTRODUCTION: Elimination of the initiating focus within the pulmonary vein (PV) using radiofrequency (RF) catheter ablation is a new treatment modality for treatment of drug-refractory atrial fibrillation. However, information on the long-term safety of RF ablation within the PV is limited. METHODS AND RESULTS: In 102 patients with drug-refractory atrial fibrillation and at least one initiating focus from the PV, series transesophageal echocardiography was performed to monitor the effect of RF ablation on the PV. There were 66 foci in the right upper PV and 65 foci in the left upper PV. Within 3 days of ablation, 26 of the ablated right upper PVs (39%) had increased peak Doppler flow velocity (mean 130+/-28 cm/sec, range 106 to 220), and 15 of the ablated left upper PVs (23%) had increased peak Doppler flow velocity (mean 140+/-39 cm/sec, range 105 to 219). Seven patients had increased peak Doppler flow velocity in both upper PVs. No factor (including age, sex, site of ablation, number of RF pulses, pulse duration, and temperature) could predict PV stenosis after RF ablation. Three patients with stenosis of both upper PVs experienced mild dyspnea on exertion, but only one had mild increase of pulmonary pressure. There was no significant change of peak and mean flow velocity and of PV diameter in sequential follow-up studies up to 16 (209+/-94 days) months. CONCLUSION: Focal PV stenosis is observed frequently after RF catheter ablation applied within the vein, but usually is without clinical significance. However, ablation within multiple PVs might cause pulmonary hypertension and should be considered a limiting factor in this procedure.
Adult↗