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Notes: Age-dependent changes in the expression of neuropeptide Y (NPY) peptides and prepro-NPY mRNA (NPY mRNA) were studied in rat adrenal gland and brain areas by means of radioimmunoassay, immunohistochemistry, and northern blot analysis. In the adrenal gland, NPY immunoreactívity (NPY-I) increased by 80-fold, mainly in the chromaffin cells, during aging (from 7 to 33 weeks old). The increase in NPY-I was accompanied by a concomitant increase in the content of NPY mRNA (800 bases in size, by 16-fold) and putative NPY pre-mRNA, a result suggesting that this increase results from that in NPY gene expression, probably at the level of transcription. In contrast, in some brain areas, such as striatum and medulla oblongata plus pons, NPY-I decreased in an age-dependent manner, whereas NPY mRNA abundances in these areas increased by twofold with age (from 7 to 33 weeks old). The opposite changes between NPY and NPY mRNA content in specific brain areas suggested the accelerated turnover/degradation of NPY peptide in the brain areas. Furthermore, β-actin mRNA abundance did not change in rat adrenal gland and brain areas during aging. Thus, the characteristic age-related increase in NPY gene expression in rat adrenal gland and some brain areas seems to be important for physiological regulation of some neuronal functions, such as blood pressure, in aged animals.

Notes: Background: During ventricular extrastimulation, His bundle potential (H) following ventricular (V) and followed by atrial potentials (A), i.e., V-H-A, is observed in the His bundle electrogram when ventriculo-atrial (VA) conduction occurs via the normal conduction system. We examined the diagnostic value of V-H-A for atypical form of atrioventricular nodal reentrant tachycardia (AVNRT), which showed the earliest atrial activation site at the posterior paraseptal region during the tachycardia. Methods: We prospectively examined the response of VA conduction to ventricular extrastimulation during basic drive pacing performed during sinus rhythm in 16 patients with atypical AVNRT masquerading atrioventricular reciprocating tachycardia (AVRT) utilizing a posterior paraseptal accessory pathway and 21 with AVRT utilizing a posterior paraseptal accessory pathway. Long RP' tachycardia with RP'/RR 〉 0.5 was excluded. The incidences of V-H-A and dual AV nodal physiology (DP) were compared between atypical AVNRT and AVRT. Results: V-H-A was demonstrated in all the 16 patients (100%) in atypical AVNRT and in only 1 of the 21 (5%) in AVRT (P 〈 0.001). DP was demonstrated in 10 patients (63%) in atypical AVNRT and in 4 (19%) in AVRT (P 〈 0.05). The sensitivity of V-H-A for atypical AVNRT was higher than that of DP (P 〈 0.05). Positive and negative predictive values were 94% and 100%, respectively, for V-H-A and 71% and 74%, respectively, for DP. Conclusions: The appearance of V-H-A during ventricular extrastimulation is a simple criterion for differentiating atypical AVNRT masquerading AVRT from AVRT utilizing a posterior paraseptal accessory pathway.

Notes: Sustained atrial flutter (AFL) can be induced by creating a lesion between the vena cava in dogs. In previous studies on this model, the crista terminalis (CT) was often injured, and thus, role of CT in sustained reentry was not well understood. We hypothesized that impaired longitudinal conduction in CT is necessary for sustained AFL. In 16 anesthetized, open-chest dogs, linear radiofrequency ablation of the intercaval region was performed without interrupting CT. Intra-atrial conduction times (IAT) along CT were measured using a plaque electrode (25 × 35 mm) containing 30 bipolar electrodes before and after additional ablation of CT (group A, n = 10) or the pectinate muscle (PM) region (group B, n = 6). In group A, IAT along CT was 27 ± 5 ms at baseline and was increased to 43 ± 3 ms after ablation of CT (P 〈 0.001). In group B, IAT along CT was 28 ± 4 ms at baseline and 27 ± 3 ms after ablation of PM (P = NS). Sustained AFL lasting 〉20 minutes was induced in 10/10 dogs in group A only after additional ablation of CT, and in 0/6 dogs in group B (P 〈 0.001). The cycle lengths of AFL after ablation of the intercaval region and additional ablation of CT were 119 ± 14 and 140 ± 14 ms, respectively (P 〈 0.01). There was a significant positive correlation between the cycle length of AFL and IAT along CT (r2= 0.63, P 〈 0.001). These results indicate that longitudinal conduction property in CT and not in PM strongly affects sustenance of AFL in this model. (PACE 2003; 26:2008–2015)

Notes: Background: Abnormal heart rate turbulence (HRT) reflects autonomic derangements predicting all-cause mortality, yet has not been shown to predict ventricular arrhythmias in at-risk patients. We hypothesized that HRT at programmed ventricular stimulation (PVS) would predict arrhythmia initiation in patients with left ventricular dysfunction. Methods: We studied 27 patients with coronary disease, left ventricular ejection fraction (LVEF) 26.7 ± 9.1%, and plasma B-type natriuretic peptide (BNP) 461 ± 561 pg/mL. Prior to arrhythmia induction at PVS, we measured sinus cycles after spontaneous or paced premature ventricular contractions (PVCs) for turbulence onset (TO; % cycle length change following PVC) and slope (TS; greatest slope of return to baseline cycle). T-wave alternans (TWA) was also measured during atrial pacing. Results: At PVS, abnormal TO (≥0%) predicted inducible ventricular tachycardia (VT; n = 10 patients; P 〈 0.05). TO was greater in inducible than in noninducible patients (2.3 ± 3.1% vs –0.02 ± 2.8%, P 〈 0.05) and correlated with LVEF (P 〈 0.05) but not with BNP. TS did not differ between groups. Conversely, ambulatory HRT differed significantly from HRT at PVS (TO –0.55 ± 1.08% vs 0.85 ± 3.02%, P 〈 0.05; TS 2.63 ± 2.09 ms/RR vs 8.70 ± 6.56 ms/RR, P 〈 0.01), and did not predict inducible VT but trended (P = 0.05) to predict sustained VT on 739 ± 179 days follow-up. TWA predicted inducible (P 〈 0.05) and spontaneous (P = 0.0001) VT but did not co-migrate with HRT. Conclusions: Abnormal HRT measured at PVS predicted the induction of sustained ventricular arrhythmias in patients with ischemic cardiomyopathy. However, HRT at PVS did not correlate with ambulatory HRT, nor with TWA, both of which predicted spontaneous ventricular arrhythmias. Thus, HRT may reflect the influence of autonomic milieu on arrhythmic susceptibility and is likely complementary to traditional arrhythmic indices.

Notes: To examine the characteristics of Haïssaguerre's slow potential (SP) specific to effective catheter ablation of the slow pathway in AV nodal reentrant tachycardia, the properties of SP and its recording site ware analyzed in 52 patients who underwent successful SP-guided ablation. The properties of SP included the ratio of the amplitude of SP to that of atrial potential (A)(SP/A), the SP duration, the interval between His-bundle potential (HP) and SP (HP-SP), the interval between A and SP (A-SP), the interval between SP and ventricular potential (V) (SP-V), and the ratio of A-SP to the interval between A and the V (A-SP/A-V). The SP recording site was determined by the ratio of the amplitude of A to that of V (A/V) and by the relative position of the ablation catheter on X ray (right anterior oblique projection), expressed as the ratio of the distance between the coronary sinus ostium and SP site to that between the coronary sinus ostium and HP recording site (relative SP position). Twenty-eight slow pathways were ablated with a single energy application, while the other 24 required applications ≥ 2. In all successful applications, SP/A, SP duration, HP-SP, A-SP. SP-V, A-SP/A-V, A/V, and relative SP position were 51 %± 25%, 28 ± 5 ms, -11 ± 9 ms, 57 ± 25 ms, 68 ± 13 ms, 46%± 9%, 15%± 13%, and 51%± 13%, respectively. A significant correlation was observed between the relative SP position and A-SP, and between the relative SP position and A-SP/A-V (r = 0.60 and 0.37, respectively), while it was not between the relative SP position and HP-SP, nor between the relative SP position and SP-V. When the characteristics of SP were comparatively analyzed between the effective and ineffective applications in 24 patients in whom applications ≥ 2 were required, there was no difference observed in HP-SP, A-SP, SP-V, A-SP/A-V, and A/V. However, SP/A, SP duration, and the relative SP position in the effective applications were all greater than those in the ineffective ones (56%± 20% vs 35%± 18%, P 〈 0.001; 29 ± 4 vs 26 ± 5 ms, P 〈 0.01; and 52%± 15% vs 33%± 11%, P 〈 0.001, respectively). These results indicate that SP with an amplitude over a half of A amplitude and recorded at the mid-septum of the tricuspid annulus can be a marker for successful slow pathway ablation. Although the local atrial electrogram appears late as the SP recording site shifts to the lower position, the timing of SP relative to HP and V remained unchanged, suggesting that SP is independent of the local atrial activation.

Notes: IWASA, A., et al.: Atrial Activation Sequence During Junctional Tachycardia Induced by Thermal Stimulation of Koch's Triangle in Canine Blood-Perfused Atrioventricular Node Preparation. Junctional tachycardia is observed during radiofrequency ablation of the slow pathway. The authors investigated the atrial activation sequence during junctional tachycardia induced with thermal stimulation in canine blood-perfused atrioventricular node (AVN) preparation. The canine heart was isolated (n = 7) and cross-circulated with heparinized arterial blood of the support dog. The activation sequence in the region of Koch's triangle (15 × 21 mm) was determined by recording 48 unipolar electrograms. Atrial sites anterior to the coronary sinus ostium (site AN), close to the His-potential recording site (site N) and superior to site N (site F), were subjected to a continuous temperature rise from 38°C to 50°C with a heating probe. The temperature of the tissue adjacent to the heating site was monitored simultaneously. Junctional tachycardia at a rate of 92 ± 12 beats/min with the His potential preceding the atrial one in the His-bundle electrogram was induced during thermal stimulation at site AN (temperature 42.1°C ± 0.9°C) in all seven preparations, whereas junctional tachycardia was induced during stimulation at site N in one and at site F in none. In each case, the temperature rose only at the site of stimulation. The earliest activation site during junctional tachycardia induced by site AN stimulation was at the His-potential recording site in five preparations and the middle of Koch's triangle in the other two. After creating an obstacle between sites AN and N, atrial tachycardia at a rate of 85 ± 11 beats/min was induced during site AN stimulation. The earliest activation site during this tachycardia was site AN. Thus, junctional tachycardia induced by thermal stimulation was suggested to originate from the AN thermal stimulation site. The impulse from the stimulation site appeared to conduct via the posterior input to the compact AVN and junctional tachycardia was generated. When the posterior input was interrupted, atrial tachycardia was generated.

Notes: Atrial ectopy sometimes appears during RF ablation of the slow pathway in patients with atrioventricular nodal reentrant tachycardia (AVNRT). However, its origin, characteristics, and significance are still unclear. To examine these issues, we analyzed 67 consecutive patients with AVNRT (60 with slow-fast AVNRT and 7 with fast-slow AVNRT), which was successfully eliminated by RF ablation to the sites with a slow potential in 63 patients and with the earliest activations of retrograde slow pathway conduction in 4 patients. During successful RF ablation, junctional ectopy with the activation sequence showing H-A-V at the His-bundle region appeared in 52 patients (group A) and atrial ectopy with negative P waves in the inferior leads preceding the QRS and the activation sequence showing A-H-V at the His-bundle region appeared in 15 patients (group B). Atrial ectopy was associated with (10 patients) or without junctional ectopy (5 patients). Before BF ablation, retrograde slow pathway conduction induced during ventricular burst and/or extrastimulus pacing was more frequently demonstrated in group B than in group A (9/15 [60%] vs 1/52 [2%], P 〈 0.001). Successful ablation site in group A was distributed between the His-bundle region and coronary sinus ostium, while that in group B was confined mostly to the site anterior to the coronary sinus ostium. In group B, atrial ectopy also appeared in 21 % of the unsuccessful RF ablations. In conclusion, atrial ectopy is relatively common during slow pathway ablation and observed in 8% of RF applications overall and 22% of RF applications that successfully eliminated inducible AVNRT. Atrial ectopy appears to be closely related to successful slow pathway ablation among patients with manifest retrograde slow pathway function.

Notes: Purpose: We report a case of prolonged nocturnal penile tumescence (NPT) caused by the antiallergic agent epinastine.Methods/Results: We measured NPT using Rigiscan-PlusTM (DacoMed, Minneapolis, MN, USA) with or without the patient having taken epinastine.Conclusions: Considering its pharmacological effects on cyclic nucleotides, epinastine may have an effect on erectile function.

Notes: 1. Neuropeptide Y (NPY) gene expression in human phaeochromocytomas was investigated by measuring the levels of NPY mRNA and NPY-immunoreactivity (NPY-IR) in human phaeochromocytoma tissues in comparison with those in normal human adrenal tissues.2. The amounts of NPY mRNA and NPY-IR in human phaeochromocytomas were 18 and 93 times higher, respectively, than those in normal adrenal glands. In contrast, beta-actin gene expression was similar in human phaeochromocytomas to that in normal adrenal glands.3. The amount of NPY mRNA relative to total cellular RNA was 6-fold higher in phaeochromocytoma tissues than in normal human adrenal medulla, suggesting increased NPY gene expression in the tumour cells.4. Induction of differentiation of PC12 rat phaeochromocytoma cells by compounds, such as dexamethasone and nerve growth factor, resulted in a marked increase in the NPY mRNA level.5. These findings suggest that NPY gene expression is increased in well-differentiated human phaeochromocytoma cells. Its high level of expression could be responsible for the marked overproduction of NPY by this tumour.

Notes: Left Ventricular Outflow Tract Tachycardia. Idiopathic left ventricular outflow tract (LVOT) tachycardia has been shown to originate from a supravalvular site in some patients. Considerable attention recently has focused on identifying this variant of LVOT tachycardia on 12-lead ECG. We report the case of 15-year-old boy in whom a noncontact three-dimensional mapping electrode deployed in the right ventricular outflow tract (RVOT) assisted in identifying a supravalvular LVOT tachycardia. Observation of two early breakthrough sites in the RVOT and right ventricular septum suggested a right aortic cusp origin of the tachycardia. Pace mapping in the right aortic cusp identified a successful ablation site.