Biomedical subjects

M S Chang

Publications and source records attributed to M S Chang.

At least 163 records · Page 9Linked to original sources

PubMed1997

Effects of different atrial pacing modes on atrial electrophysiology: implicating the mechanism of biatrial pacing in prevention of atrial fibrillation.

BACKGROUND: Multiple-site atrial pacing has been shown to prevent recurrence of atrial fibrillation. However, information about the mechanisms of different atrial pacing modes in prevention of atrial fibrillation was not clear. METHODS AND RESULTS: Forty-two patients without structural heart disease were classified into group 1 and group 2 according to absence or presence of clinical atrial fibrillation, respectively. Atrial conduction time and electrogram width of the right posterior interatrial septum (RPS) were measured during drive-train stimulation (S1) and early extrastimulation (S2). The locations of S1 were the high right atrium (HRA), distal coronary sinus (DCS), or both sites simultaneously. Effective refractory periods (ERPs) of the HRA and DCS were also determined during S1 stimulation at each site and during biatrial pacing. The ERPs were not different between single-site atrial pacing and biatrial pacing. In contrast, early S2 stimulation at the HRA caused greater atrial conduction delay and greater increment of electrogram width of the RPS in patients with a history of atrial fibrillation. Biatrial pacing significantly reduced the conduction delay and electrogram width of the RPS caused by HRA extrastimulation. In addition, in 17 group 2 patients, atrial fibrillation was induced by an early HRA S2 coupled to HRA pacing. However, with the same coupling interval of S2 at HRA, only 6 of them had the arrhythmia induced during biatrial pacing. Furthermore, conduction delay and increase of electrogram width caused by early S2 at the HRA were reduced by biatrial pacing only in patients whose arrhythmia induction was successfully prevented by biatrial pacing. CONCLUSIONS: Biatrial pacing reduced both the atrial conduction delay and increase of electrogram width at the RPS caused by early S2 at HRA, and these effects could prevent induction of atrial fibrillation.

Adult↗

PubMed1997

Characterization of low right atrial isthmus as the slow conduction zone and pharmacological target in typical atrial flutter.

BACKGROUND: Previous electrophysiological studies in patients with typical atrial flutter suggested that the slow conduction zone might be located in the low right atrial isthmus, which is a path formed by orifice of inferior vena cava, eustachian valve/ridge, coronary sinus ostium, and tricuspid annulus. The conduction characteristics during atrial pacing and responses to antiarrhythmic drugs of this anatomic isthmus were unknown. METHODS AND RESULTS: Forty-four patients, 20 patients with paroxysmal supraventricular tachycardia (group 1) and 24 patients with clinically documented paroxysmal typical atrial flutter (group 2), were studied. A 20-pole halo catheter was situated around the tricuspid annulus. Incremental pacing from the low right atrium and coronary sinus ostium was performed to measure the conduction time and velocity along the isthmus and lateral wall in the baseline state and after intravenous infusion of procainamide or sotalol. In both groups, conduction velocity in the isthmus during incremental pacing was significantly lower than that in the lateral wall before and after infusion of antiarrhythmic drugs. Furthermore, gradual conduction delay with unidirectional block in the isthmus was relevant to initiation of typical atrial flutter. Compared with group 1, group 2 had a lower conduction velocity in the isthmus and shorter right atrial refractory period. Procainamide significantly decreased the conduction velocity, but sotalol did not change it. In contrast, sotalol significantly prolonged the atrial refractory period with a higher extent than procainamide. After infusion of procainamide, the increase of conduction time in the isthmus accounted for 52+/-19% of the increase in flutter cycle length, and 5 of 12 patients (42%) had spontaneous termination of typical flutter. After infusion of sotalol, typical flutter was induced in only 6 of 12 patients (50%) without significant prolongation of flutter cycle length. CONCLUSIONS: The low right atrial isthmus with rate-dependent slow conduction properties is critical to initiation of typical human atrial flutter. It may be the potentially pharmacological target of antiarrhythmic drugs in the future.

Adolescent↗

PubMed1997

Identification of nitric oxide synthase in Staphylococcus aureus.

The presence of nitric oxide synthase (NOS) in Staphylococcus aureus ATCC6538P was established by western blot analysis. The identity of citrulline formed from L-arginine by the NOS was confirmed by both TLC and HPLC and the other product, NO, by directly measuring the production of nitrogen oxides (NOx) in the reaction mixture. The activity was inhibited by typical NOS inhibitors such as N-nitro-L-arginine methylester and NG,NG-dimethyl-L-arginine with the IC50 of 4.9 x 10(-4) and 2.5 x 10(-4) M, respectively. The NOS activity was maximum at pH 6.5 and at 47.5 degrees C. These results indicate that the NOS of S. aureus ATCC6538P is an isoform distinct from mammalian NOS.

Blotting, Western↗

PubMed1997

Effects of short-term treatment of nicorandil on exercise-induced myocardial ischemia and abnormal cardiac autonomic activity in microvascular angina.

The underlying mechanisms of myocardial ischemia in microvascular angina may include endothelial dysfunction, abnormal smooth muscle tone, and abnormal autonomic control of coronary microvasculatures. This randomized, double-blind, placebo-controlled, crossover study was conducted to evaluate the effect of nicorandil (a nitrate-potassium channel opener) therapy on exercise-induced myocardial ischemia and cardiac autonomic activity in 13 patients with microvascular angina. After a 2-week placebo run-in period, patients were randomly assigned to the first 2-week treatment with nicorandil 5 mg tid or placebo, then crossed over to the second 2-week treatment after a 2-week washout period. Treadmill exercise tests and 24-hour ambulatory electrocardiogram monitoring were performed at the end of each treatment phase. The results showed that both time to 1-mm ST depression and total exercise duration were significantly prolonged with nicorandil treatment compared with placebo (p = 0.026 and 0.036, respectively). Maximum exercise ST depression also tended to be less with nicorandil treatment than with placebo (p = 0.083). Compared with 10 healthy control subjects, study patients had significantly reduced heart rate variability in both low- and high-frequency bands while receiving placebo. Nicorandil treatment did not change the altered heart rate variability in either time domain or spectral analysis. Systemic hemodynamics were also unchanged with nicorandil treatment. Thus, 2-week oral nicorandil therapy moderately improved exercise-induced myocardial ischemia without modifying the already altered cardiac autonomic activity, suggesting that nicorandil might have a direct vasodilatory effect on coronary microvasculatures in patients with microvascular angina.

Administration, Oral↗

PubMed1997

Influence of beta-adrenergic and vagal activity on the effect of exogenous adenosine on supraventricular tachycardia termination.

Adenosine, which binds to cell surface receptors and couples with guanosine triphosphate-binding inhibitory proteins (G(i)), is potent in terminating supraventricular tachycardia (SVT). However, whether the differences in autonomic tone will influence this effect remains unknown. This study was designed to investigate the role of beta-adrenergic and vagal activity on the action of adenosine. Forty patients with clinically documented SVT (22 with atrioventricular node reentrant tachycardia and 18 with atrioventricular reciprocating tachycardia) were divided into 4 groups with 10 patients in each group. In groups 1 and 2, adenosine was intravenously injected during the baseline state and during infusion of isoproterenol (2 and 4 microg/min, respectively). Group 2 patients received atropine (0.04 mg/kg) injection before isoproterenol infusion. In groups 3 and 4, intravenous injection of adenosine was given during the baseline state and after injection of atropine (0.02 and 0.04 mg/kg, respectively). Group 4 patients received propranolol (0.2 mg/kg) before atropine injection. The minimal dose of adenosine to terminate tachycardia during isoproterenol infusion of 2 microg/min was greater than that during the baseline state in both groups 1 and 2. The minimal dose of adenosine during isoproterenol infusion with 4 microg/min was higher than that with 2 microg/min in group 2, but not in group 1 patients. In both groups 3 and 4, the minimal dose of adenosine required to terminate tachycardia during atropine injection with 0.02 mg/kg was greater than that during the baseline state. The minimal effective dose of adenosine during atropine injection with 0.04 mg/kg was higher than that with 0.02 mg/kg in group 4, but not in group 3 patients. In conclusion, either limb of the autonomic nervous system may modulate the adenosine dosage required for termination of SVT. Patients taking drugs such as beta blockers or vagolytic agents may need alterations in the dose of adenosine for therapy.

Adenosine↗

PubMed1997

Discovery of a second 15S-lipoxygenase in humans.

The lipoxygenase metabolism of arachidonic acid occurs in specific blood cell types and epithelial tissues and is activated in inflammation and tissue injury. In the course of studying lipoxygenase expression in human skin, we detected and characterized a previously unrecognized enzyme that at least partly accounts for the 15S-lipoxygenase metabolism of arachidonic acid in certain epithelial tissues. The cDNA was cloned from human hair roots, and expression of the mRNA was detected also in prostate, lung, and cornea; an additional 16 human tissues, including peripheral blood leukocytes, were negative for the mRNA. The cDNA encodes a protein of 676 amino acids with a calculated molecular mass of 76 kDa. The amino acid sequence has approximately 40% identity to the known human 5S-, 12S-, and 15S-lipoxygenases. When expressed in HEK 293 cells, the newly discovered enzyme converts arachidonic acid exclusively to 15S-hydroperoxyeicosatetraenoic acid, while linoleic acid is less well metabolized. These features contrast with the previously reported 15S-lipoxygenase, which oxygenates arachidonic acid mainly at C-15, but also partly at C-12, and for which linoleic acid is an excellent substrate. The different catalytic activities and tissue distribution suggest a distinct function for the new enzyme compared with the previously reported human 15S-lipoxygenase.

Amino Acid Sequence↗

PubMed1997

Genistein directly induces cardiac CFTR chloride current by a tyrosine kinase-independent and protein kinase A-independent pathway in guinea pig ventricular myocytes.

With one-suction electrode voltage-clamp technique, we demonstrated that genistein, a tyrosine kinase (TK) inhibitor, could directly activate cystic fibrosis transmembrane regulator (CFTR) chloride current in guinea pig ventricular myocytes. The activation showed concentration-dependent effect with the estimated IC50 of 39.7 microM. Tyrphostin 51, another TK inhibitor, had no effect, suggesting that genistein's effect might be unrelated to TK inhibition. After the chloride current had been activated by the maximally elevated intracellular cAMP content by saturating concentration of isoproterenol, forskolin and IBMX, genistein could further enhance the current. Pre-treatment with saturating concentration of a specific protein kinase A (PKA) inhibitor, H-89, or other protein kinase inhibitors H-8 and H-9 in the perfusate or intracellularly could not prevent the activation of the current by genistein, suggesting a PKA-independent activity. Furthermore, saturating concentration of calyculin A, a specific inhibitor of phosphotase 1 and 2A, in the perfusate or intracellularly could not block genistein's action. It is possible that genistein opens the channels directly or inhibits the dephosphorylation process of CFTR, which is not sensitive calyculin A.

Adrenergic beta-Agonists↗

PubMed1997

Complex electrophysiological characteristics in atrioventricular nodal reentrant tachycardia with continuous atrioventricular node function curves.

BACKGROUND: Although typical atrioventricular nodal reentrant tachycardia (AVNRT) with discontinuous AV node function curves has been well studied, there has been a lack of any significant information about AVNRT without evidence of dual AV nodal pathway physiology during atrial extrastimulus testing or atrial pacing. METHODS AND RESULTS: Group 1 included 9 patients with continuous curves during atrial extrastimulus testing but without a jump (> or = 50 ms) of the atrial-His bundle (AH) interval during incremental atrial pacing. The maximal AH interval during atrial pacing (266 +/- 61 versus 168 +/- 27 ms, P = .007) or extrastimulus testing (290 +/- 60 versus 176 +/- 18 ms, P = .005) shortened significantly after ablation. Antegrade and retrograde AV node properties were similar before and after ablation. Group 2 included 14 patients with continuous curves and a jump of the AH interval during incremental atrial pacing. The atrial pacing cycle length with 1:1 AV conduction and effective refractory period (ERP) of the antegrade AV node increased significantly, whereas the maximal AH interval during atrial pacing (358 +/- 70 versus 203 +/- 28 ms, P = .001) or extrastimulus testing (338 +/- 75 versus 196 +/- 34 ms, P = .002) shortened significantly after ablation. Group 3 included 24 patients with discontinuous curves. The maximal AH interval during atrial pacing or extrastimulus testing and the ERP of the antegrade fast AV node shortened, whereas the ERP of the antegrade AV node increased significantly after ablation. The maximal AH interval before ablation, extent of decrease in maximal AH interval after ablation, ERP of the retrograde AV node before ablation, and tachycardia cycle length were significantly shorter in group 1 than groups 2 and 3. CONCLUSIONS: In AVNRT with continuous AV node function curves, dual AV nodal pathway physiology may or may not be demonstrated during atrial pacing. Significant shortening of the maximal AH interval during atrial pacing after radiofrequency ablation suggests successful elimination of AVNRT.

Catheter Ablation↗

PubMed1997

Osteoprotegerin: a novel secreted protein involved in the regulation of bone density.

A novel secreted glycoprotein that regulates bone resorption has been identified. The protein, termed Osteoprotegerin (OPG), is a novel member of the TNF receptor superfamily. In vivo, hepatic expression of OPG in transgenic mice results in a profound yet nonlethal osteopetrosis, coincident with a decrease in later stages of osteoclast differentiation. These same effects are observed upon administration of recombinant OPG into normal mice. In vitro, osteoclast differentiation from precursor cells is blocked in a dose-dependent manner by recombinant OPG. Furthermore, OPG blocks ovariectomy-associated bone loss in rats. These data show that OPG can act as a soluble factor in the regulation of bone mass and imply a utility for OPG in the treatment of osteoporosis associated with increased osteoclast activity.

Amino Acid Sequence↗

PubMed1997

Comparisons of oral propafenone and sotalol as an initial treatment in patients with symptomatic paroxysmal atrial fibrillation.

The main goal of this study is to evaluate the safety and efficacy of propafenone versus sotalol as an initial choice of treatment in patients with symptomatic paroxysmal atrial fibrillation (AF), according to a double-blind randomized system. In the oral propafenone group (n = 41), 2 patients (5%) discontinued therapy because of gastrointestinal discomfort in 1 and dizziness in the other. Thirty-one (79%) of the 39 patients who continued the treatment had effective response to oral propafenone (>75% reduction of symptomatic arrhythmic attacks) on a mean dose of 663 +/- 99 mg/day with a decrease in attack frequency from 10 +/- 3 to 2 +/- 1 times per week. In the oral sotalol group (n = 38), 4 patients (11%) discontinued treatment because of dizziness in 2 and symptomatic bradycardia in 2. Twenty-six of the 34 patients (76%) who continued the treatment had effective response to oral sotalol on a mean dose of 200 +/- 57 mg/day with a decrease in attack frequency from 11 +/- 3 to 2 +/- 1 times per week. Comparisons of the results between propafenone and sotalol groups showed a similar incidence of intolerable (2 of 41 vs 4 of 38, p = 0.42) and tolerable side effects (10 of 39 vs 8 of 34, p = 1.0). The attack frequency at baseline (11 +/- 3 vs 10 +/- 4 times per week, p = 0.23) and after treatment (3 +/- 1 vs 3 +/- 2 times per week, p = 0.85) did not differ significantly between the 2 groups. The incidence of effective response to drugs was also similar (31 of 39 vs 26 of 34, p = 0.78). Furthermore, the decrease of symptom scores (-32 +/- 8% vs -29 +/- 7%, p = 0.18) and percentage decrease of ventricular rate (-15 +/- 4% vs -18 +/- 4%, p = 0.10) during AF were also similar between the 2 groups. In conclusion, oral propafenone and sotalol are equally effective and safe in preventing attacks and alleviating symptoms of paroxysmal AF.

Administration, Oral↗

PubMed1997

Results of radiofrequency ablation in patients with clinically documented, but noninducible, atrioventricular node reentrant tachycardia and orthodromic atrioventricular reciprocating tachycardia.

Among 1,281 patients with symptomatic supraventricular tachycardia, 34 patients (2.7%) with presumed diagnosis of atrioventricular node reentrant tachycardia and orthodromic atrioventricular reciprocating tachycardia did not have inducible tachycardia in the electrophysiologic laboratory. Application of radiofrequency energy to the presumed arrhythmogenic sites could achieve a high success rate, with a low recurrence rate in these patients.

Adult↗

PubMed1997

Electron microscopic studies of phenotypic modulation of smooth muscle cells in coronary arteries of patients with unstable angina pectoris and postangioplasty restenosis.

BACKGROUND: Proliferation and matrix protein secretion of coronary smooth muscle cells (SMCs) have been suggested as one of the mechanisms responsible for the development of postangioplasty restenosis and an alternative cause of unstable angina. Phenotypic modulation of SMCs may produce a pool of cells potentially responsive to growth stimulation that can synthesize abundant extracellular matrix. This study tested the hypothesis that phenotypic modulation of SMCs occurred during the evolution of postangioplasty restenosis and unstable angina. METHODS AND RESULTS: The SMCs of coronary atherectomy specimens from 24 patients were identified under electron microscope. Volume fractions of synthetic organelles (VFSOs) and other features related to phenotypic modulation of SMCs were measured. The results showed that the VFSO in SMCs from 5 patients with unstable angina (group 2) resembled those from 9 patients with postangioplasty restenosis (group 3; 0.42 +/- 0.13 versus 0.36 +/- 0.10; P = NS), and both were significantly higher than those from 6 patients with stable angina (group 1; 0.21 +/- 0.11). Four patients with restenosis lesions who underwent angioplasty > 6 months ago (group 4) also had a low VFSO in SMCs (0.19 +/- 0.05). This value was significantly less than those in groups 2 and 3 (P < .05) but similar to that in group 1. CONCLUSIONS: The coronary lesions from patients with unstable angina resembled those from patients with postangioplasty restenosis in terms of the phenotypic modulation and VFSO in SMCs. Our findings therefore suggest that after phenotypic modulation, the SMCs may become responsive to growth stimulation, with an ability to massively proliferate and synthesize abundant extracellular matrix. These processes may lead to plaque expansion and eventually to the development of unstable angina and restenosis.

Aged↗

PubMed1997

Electrophysiologic characteristics and radiofrequency catheter ablation of fast-slow form atrioventricular nodal reentrant tachycardia.

This study demonstrates that the fast-slow form of atrioventricular nodal reentrant tachycardia is usually catecholamine-sensitive and its electrophysiologic characteristics are significantly different from those of the slow-fast form. However, radiofrequency catheter ablation is a safe and effective treatment for patients with the fast-slow form of atrioventricular nodal reentrant tachycardia.

Adrenergic beta-Agonists↗

PubMed1997

C/EBP alpha is a major activator for the transcription of rat Cu/Zn superoxide dismutase gene in liver cell.

The rat Cu/Zn superoxide dismutase (SOD1) is expressed in all tissues. Sequence analysis of the SOD1 promoter region showed that none of the cis-elements of hepatocyte-specific nuclear factors (HNF) were observed. The cis-element of C/EBP alpha in the proximal region of the SOD1 promoter and the high level of C/EBP alpha in the liver tissue led us to focus on the transcriptional regulation of the SOD1 gene by C/EBP alpha. Cotransfection assays with the plasmid expressing transcription factor C/EBP alpha showed that C/EBP alpha transactivated SOD1 gene by 27 fold. The marked transactivation and direct binding of C/EBP alpha to the SOD1 promoter were confirmed by deletion analyses and mobility shift assays. These results suggested that C/EBP alpha plays a major role in the tissue distribution of SOD1.

Animals↗

PubMed1997

Atrioventricular node reentrant tachycardia in patients with a long fast pathway effective refractory period: clinical features, electrophysiologic characteristics, and results of radiofrequency ablation.

Twenty-two patients (group 1) with AV node reentrant tachycardia and a baseline fast pathway effective refractory period (ERP) > or = 500 msec were compared with 30 consecutive patients (group 2) with AV node reentrant tachycardia and a fast pathway ERP < 500 msec. Both groups underwent slow pathway ablation. In the patients with complete elimination of slow pathway, the fast pathway ERP and shortest 1:1 conduction cycle length shortened significantly after ablation but was greater in group 1 (n = 14) than in group 2 (n = 21) (125 +/- 78 msec vs 48 +/- 29 msec, p < 0.001 and 103 +/- 72 msec vs 52 +/- 30 msec, p < 0.001, respectively). In group 1, the shortening of fast pathway ERP was correlated to baseline difference between anterograde fast and anterograde slow ERP (r = 0.806, p < 0.001, slope = 1.08), and the shortening of fast pathway shortest 1:1 conduction cycle length was correlated to baseline difference between anterograde fast and anterograde slow shortest 1:1 conduction cycle length (r = 0.885, p < 0.001, slope = 1.47). During follow-up bradycardia did not develop in any patient and no one required pacing. This shortening of the fast pathway ERP and shortest 1:1 conduction cycle length after complete elimination of slow pathway reduced the concern of subsequent impairment of AV node conduction.

Adrenergic beta-Agonists↗

PubMed1997

Role of the surface electrocardiogram in the diagnosis of patients with supraventricular tachycardia.

In this era of interventional electrophysiology, the accuracy of the electrocardiogram in diagnosis of supraventricular tachycardia could be improved by detailed endocardial mapping and confirmed by results of radiofrequency catheter ablation. This article describes the electrocardiographic characteristics for different types of supraventricular tachycardia: atrial fibrillation, atrial flutter, atrial tachycardia, atrioventricular reciprocating tachycardia using an accessory pathway, and atrioventricular node reentrant tachycardia. Several limitations, including the identification of P wave morphologies and polarities and separation between the terminal part of T wave and P wave during tachycardia, should be resolved before an accurate algorithm of the 12-lead surface electrocardiogram is developed for the diagnosis of supraventricular tachycardia.

Atrial Fibrillation↗

PubMed1997

A new electrocardiographic algorithm using retrograde P waves for differentiating atrioventricular node reentrant tachycardia from atrioventricular reciprocating tachycardia mediated by concealed accessory pathway.

OBJECTIVES: The purpose of this study was to use an electrocardiographic (ECG) algorithm, derived from the results of radiofrequency ablation, to discriminate atrioventricular node reentrant tachycardia (AVNRT) from atrioventricular reciprocating tachycardia (AVRT) and to localize a concealed accessory pathway, prospectively. BACKGROUND: Information about ECG criteria for differentiating AVNRT from AVRT is limited and has not been confirmed by surgical or catheter ablation. METHODS: Four hundred six ECGs (obtained from 406 different patients) that demonstrated narrow QRS complex (< 0.12 s) supraventricular tachycardia with an RP' interval less than the P'R interval or pseudo r' wave in lead V1 or pseudo S wave in inferior leads, or both, were examined, and the results were confirmed by radiofrequency catheter ablation. The initial 226 ECGs were analyzed to develop a stepwise algorithm, and the subsequent 180 ECGs were prospectively evaluated by the new algorithm. RESULTS: The presence of a pseudo r' wave in lead V1 or a pseudo S wave in leads II, III, aVF indicated anterior-type AVNRT with an accuracy of 100%. With the difference of RP' intervals in leads V1 and III > 20 ms, posterior-type AVNRT could be differentiated from AVRT utilizing a posteroseptal pathway with a sensitivity of 71% (95% confidence interval [CI] 55% to 89%), a specificity of 87% (95% CI 67% to 97%) and a positive predictive value of 75% (95% CI 56% to 91%). According to the polarity of retrograde P waves in leads V1, II, III, aVF and I during AVRT, the concealed accessory pathway could be localized to one of the nine regions on the atrioventricular annuli with an accuracy of 75% (for a right midseptal pathway) to 93.8% (for a left posterior pathway). Overall, the new algorithm had an accuracy of 97.8% in discriminating AVNRT from AVRT and 88.1% in localizing a concealed accessory pathway, prospectively. Prediction was incorrect in only 15 patients (9.1%). CONCLUSIONS: The new ECG algorithm derived from the analysis of retrograde P waves during tachycardia could provide a criterion for differential diagnosis between AVNRT and AVRT and for predicting the location of concealed accessory pathways.

Adolescent↗

PubMed1997

Effect of high intensity drive train stimulation on dispersion of atrial refractoriness: role of autonomic nervous system.

OBJECTIVES: This study evaluated the effect of high intensity drive train (S1) stimulation on the atrial effective refractory period (ERP) and its relation to the autonomic nervous system. BACKGROUND: High intensity S1 stimulation was demonstrated to shorten the ventricular ERP and to increase dispersion of refractoriness. These effects may be due to local release of neurotransmitters. The response of the atrium and ventricle to neurotransmitters was different. The effects of high intensity S1 stimulation at the atrial tissue were evaluated. METHODS: Forty patients without structural heart disease were studied. In group 1, 20 patients, the atrial ERP was measured at 0, 7, 14, 21 and 28 mm away from the S1 site under both twice diastolic threshold and high intensity (10 mA) S1 stimulation. The same protocol was repeated after sequential administration of propranolol (0.2 mg/kg body weight) and atropine (0.04 mg/kg). In group 2, the other 20 patients, the atrial ERP was studied at three atrial sites (high lateral right atrium [HLRA], right posterior interatrial septum [RPS] and distal coronary sinus [DCS] with twice diastolic threshold and high intensity S1 stimulation at baseline and after sequential autonomic blockade. The three atrial sites were randomly assigned as the S1 location. RESULTS: In group 1, high intensity S1 stimulation shortened the atrial effective refractory period most prominently at the site of S1: (mean +/- SD) 13.3 +/- 6.4% (p < 0.001), 8.1 +/- 3.8% (p < 0.001), 4.8 +/- 4.3% (p < 0.001), 3.7 +/- 4.7% (p < 0.001) and 0.5 +/- 2.6% at 0, 7, 14, 21 and 28 mm from the S1 site, respectively. The effect of high intensity S1 stimulation was blunted with propranolol and autonomic blockade but persisted after atropine alone. High intensity S1 stimulation also increased dispersion of refractoriness (from 23 +/- 11 ms to 31 +/- 12 ms, p = 0.01), which was eliminated with autonomic blockade. In group 2, high intensity S1 stimulation had similar effects at different locations (ERP shortening of 10.8 +/- 2.7%, 10.8 +/- 2.2% and 12.2 +/- 4.6% at the HLRA, RPS and DCS, respectively). The responses to sequential autonomic blockade were similar to those in group 1. However, high intensity S1 stimulation at HLRA increased dispersion of refractoriness, but at DCS it reduced dispersion of refractoriness. CONCLUSIONS: High intensity S1 stimulation led to local shortening of the atrial ERP and increased dispersion of refractoriness. These effects were blunted with propranolol and autonomic blockade. High intensity S1 stimulation at the HLRA increased dispersion of atrial refractoriness, whereas the same stimulation at the DCS decreased dispersion of atrial refractoriness.

Adolescent↗