An immunoglobulin-like receptor, Allergin-1, inhibits immunoglobulin E-mediated immediate hypersensitivity reactions.

Anaphylaxis is a life-threatening immediate hypersensitivity reaction triggered by antigen capture by immunoglobulin E (IgE) bound to the high-affinity IgE receptor (FcvarepsilonRI) on mast cells. However, the regulatory mechanism of mast cell activation is not completely understood. Here we identify an immunoglobulin-like receptor, Allergin-1, that contains an immunoreceptor tyrosine-based inhibitory motif (ITIM)-like domain, and show it was preferentially expressed on mast cells. Mouse Allergin-1 recruited the tyrosine phosphatases SHP-1 and SHP-2 and the inositol phosphatase SHIP. Coligation of Allergin-1 and FcvarepsilonRI suppressed IgE-mediated degranulation of bone marrow-derived cultured mast cells. Moreover, mice deficient in Allergin-1 developed enhanced passive systemic and cutaneous anaphylaxis. Thus, Allergin-1 suppresses IgE-mediated, mast cell-dependent anaphylaxis in mice.

Paradoxical delayed capture proved the dual-loop tachycardia mechanism of a cavotricuspid isthmus-dependent atrial flutter.

A 37-year-old man underwent catheter ablation for a cavotricuspid isthmus-dependent atrial flutter. Two 20-pole deflectable electrode catheters were placed in a parallel position on the tricuspid annulus and right atrial lateral wall. The dual-loop tachycardia mechanism of the atrial flutter was suggested by paradoxical delayed capture of the lateral wall of the right atrium during entrainment pacing from the lateral tricuspid annulus.

Evaluation of repolarization dynamics using the QT-RR regression line slope and intercept relationship during 24-h Holter ECG.

QT-RR linear regression consists of two parameters, slope and intercept, and the aim of this study was to evaluate repolarization dynamics using the QT-RR linear regression slope and intercept relationship during 24-h Holter ECG. This study included 466 healthy subjects (54.6 ± 14.6 years; 200 men and 266 women) and 17 patients with ventricular arrhythmias, consisted of 10 patients with idiopathic ventricular fibrillation (IVF) and 7 patients with torsades de pointes (TDP). QT and RR intervals were measured from ECG waves based on a 15-s averaged ECG during 24-h Holter recording using an automatic QT analyzing system. The QT interval dependence on the RR interval was analyzed using a linear regression line for each subject ([QT] = A[RR] + B; where A is the slope and B is the y-intercept). The slope of the QT-RR regression line in healthy subjects was significantly greater in women than in men (0.185 ± 0.036 vs. 0.161 ± 0.033, p < 0.001) and the intercept was significantly smaller in women than in men (0.229 ± 0.028 vs. 0.240 ± 0.027, p < 0.001). A scatter diagram of the QT-RR regression line slope and intercept among healthy subjects demonstrated a statistically significant negative correlation (B = -0.62A + 0.34, r = -0.79). Distribution of both scatter diagrams of the slope and the intercept of the QT-RR regression line in patients with IVF and TDP was different from healthy subjects (left corner for IVF and upward shift for TDP). The slope and intercept relationship of the QT-RR linear regression line based on 24-h Holter ECG may become a simple useful marker for abnormality of ventricular repolarization dynamics.

Electrophysiological and anatomical differences of the slow pathway between the fast-slow form and slow-slow form of atrioventricular nodal reentrant tachycardia.

AIMS: This study aimed to clarify whether electrophysiological and anatomical properties of the slow pathway (SP) could be different between the fast-slow form (F/S) and the slow-slow form (S/S) atrioventricular nodal reentrant tachycardia (AVNRT). METHODS AND RESULTS: Nine patients with F/S and 15 patients with S/S of atypical AVNRT were studied. The patients with S/S were divided into two groups; those with the anterograde SP being eliminated (S/S aSP-E) or preserved (S/S aSP-P) during catheter ablation. HA (CS-His) was determined as the difference of the shortest HA interval between the His bundle region and the coronary sinus (CS) region. The ratio of the amplitudes of atrial and ventricular potential (A/V ratio) of the successful ablation site of the SP was also evaluated. Effective refractory period of the retrograde SP was shorter and HA intervals during both tachycardia and ventricular pacing were longer in F/S than in S/S. HA (CS-His) did not differ between F/S and S/S (-4.3 ± 20.2 vs.-4.4 ± 18.4 ms, NS). The A/V ratio was significantly greater in the S/S aSP-P group compared with the both groups of F/S and S/S aSP-E (0.83 ± 0.29 vs. 0.38 ± 0.09 and 0.26 ± 0.15 ms, P < 0.01). CONCLUSION: Properties of the retrograde SP differ between F/S and S/S of AVNRT. Fast-slow form may utilize the same pathway for the retrograde conduction as the anterograde SP in S/S.

Xanthine oxidase inhibition prevents atrial fibrillation in a canine model of atrial pacing-induced left ventricular dysfunction.

AIMS: Oxidative stress could be a possible mechanism and a therapeutic target of atrial fibrillation (AF). Xanthine oxidase (XO) inhibition reduces oxidative stress, but the effects of XO inhibitor on AF have not been evaluated. Hence, we assessed the effects of XO inhibitor, allopurinol, on progression of atrial vulnerability in dogs associated with tachycardia-induced cardiomyopathy. METHODS AND RESULTS: The dogs were subjected to atrial tachypacing (ATP, 400 bpm) without atrioventricular block for 4 weeks. The dynamics of atrial-tachycardia remodeling were evaluated in allopurinol-treated dogs (ALO, n = 5), placebo-treated controls (CTL, n = 6), and sham-operated dogs (n = 6). In CTL dogs, 4 weeks of ATP significantly increased AF duration (DAF; from 0.2 ± 0.2 seconds to 173 ± 67 seconds, P < 0.05) and decreased atrial effective refractory period (ERP; from 152 ± 9 milliseconds to 80 ± 4 milliseconds at a cycle length of 350 milliseconds, P < 0.01). Allopurinol attenuated the ATP effects on ERP (118 ± 6 milliseconds, P < 0.01) or DAF (0.6 ± 0.3 seconds, P < 0.05). In CTL dogs, ATP-induced rapid ventricular responses decreased left ventricular ejection fraction (LVEF; from 58.6 ± 0.1 to 23.5 ± 2.4%, P < 0.01), and increased left atrial diameter (LAD; from 17 ± 1 mm to 24 ± 1 mm, P < 0.01). ATP increased atrial fibrosis when compared with sham-operated dogs (CTL 10.7 ± 0.8% vs Sham 1.1 ± 0.3%, P < 0.01). Allopurinol suppressed atrial fibrosis (2.3 ± 0.6%, P < 0.01 vs CTL) and eNOS reduction without affecting LVEF (20.6 ± 2.2%, ns) and LAD (23 ± 1 mm, ns). CONCLUSION: Allopurinol suppresses AF promotion by preventing both electrical and structural remodeling. These results suggest that XO may play an important role in enhancement of atrial vulnerability, and might be a novel target of AF therapy.

Anticoagulation control quality affects the D-dimer levels of atrial fibrillation patients.

BACKGROUND: Anticoagulation control quality affects the incidence of thromboembolic events in atrial fibrillation (AF) patients. However, the effects of anticoagulation control quality on the prothrombotic state of AF patients are unclear. METHODS AND RESULTS: Ninety-five AF patients who had been treated with warfarin were prospectively followed-up for 449 ± 92 days. We analyzed whether time in the therapeutic range (TTR) of the international normalized ratio (INR) of prothrombin time, percentage of INR values in the range (%INR), and coefficient of variation of INR values (CV-INR) were related to D-dimer levels. The mean values of TTR, %INR, and CV-INR were 62%, 59%, and 0.19, respectively, and their median values were 67%, 63%, and 0.19, respectively. TTR was significantly correlated with %INR (R(2) = 0.917, P<0.01), but not with CV-INR (R(2) = 0.050, P = 0.26). The mean and median D-dimer levels were 0.79 and 0.60 µg/ml, respectively. Low TTR, low %INR, and high CV-INR were found to contribute to high D-dimer levels (P = 0.02, 0.03, and 0.02, respectively). CONCLUSIONS: In AF patients treated with warfarin, not only the duration outside the target INR range, but also the fluctuation in INR level may influence the prothrombotic state.

Conversion to partial isthmus-dependent flutter during cavotricuspid isthmus ablation: The utility of Advisor HD grid in identifying local fragment electrograms.

Complete block creation by radiofrequency (RF) ablation at the cavotricuspid isthmus (CTI) is a highly successful procedure for the treatment of typical atrial flutter (AFL). Occasionally, a rare type of AFL, such as lower or upper loop reentry, or partial isthmus-dependent flutter, can coexist with typical right AFL. A 73-year-old man underwent CTI ablation for a clockwise CTI-dependent typical atrial flutter. During the ablation procedure, the morphology of the flutter wave changed in the surface electrocardiogram and endocardial atrial activation sequence, suggesting that the typical AFL had converted to another AFL (AFL2). High-density mapping using the HD grid catheter could not reveal the reentrant circuit of AFL2 but detected a critical conduction gap at the boundary between the inferior vena cava and CTI. There was also an impulse collision in the remaining CTI. The RF application at the gap terminated the AFL2 and completed the block line of the CTI. Based on these findings, AFL2 was comparable with partial isthmus-dependent flutter. The present case demonstrates the utility of high-density mapping with a HD grid for the identification of small amplitude high-frequency electrograms at critical sites of the arrhythmia. Learning objective: A rare type of atrial flutter (AFL) can coexist with typical AFL. In such cases, a high-density mapping is useful to identify the critical portion of the reentrant circuit. The Advisor HD grid multipolar catheter (Abbott, St Paul, MN, USA) is unique in that it allows bipolar recording perpendicular and parallel to the splines via 16 electrodes. In this case report, high density mapping using HD grid catheter identified small amplitude high-frequency electrograms at critical sites of the arrhythmia.

Identification of a novel TPM1 mutation in a family with left ventricular noncompaction and sudden death.

Left ventricular noncompaction (LVNC) is a cardiomyopathy morphologically characterized by 2-layered myocardium, numerous prominent trabeculations, and deep intertrabecular recesses communicating with the left ventricular cavity. The purpose of this study was to investigate patients with LVNC for possible disease causing mutations. We screened 4 genes (TAZ, LDB3, DTNA and TPM1) in 51 patients with LVNC for mutations by polymerase chain reaction and direct DNA sequencing. A novel missense substitution in exon 1 of TPM1 (c.109A>G: p.Lys37Glu) was identified in three affected members of a family with isolated LVNC. The substitution brings about a change in amino acid charge at a highly conserved residue and could result in aberrant mRNA splicing. This variant was not identified in 200 normal control samples. Pathologic analysis of a right ventricular myocardial specimen from the proband's maternal aunt revealed endocardial and subendocardial fibrosis with prominent elastin deposition, as well as the presence of adipose tissue between muscle layers, pathologic changes that are distinct from those seen in patients with HCM or DCM. Screening of the proband and her mother for variants in other sarcomeric protein-encoding candidate genes, MYH7, MYBPC3, TNNT2, TNNI3, ACTC, MYL2, and MYL3, did not identify any other non-synonymous variants or variants in splice donor-acceptor sequences that were potentially disease causing. We conclude TPM1 is a potential candidate disease-causing gene for isolated LVNC, especially in patients experiencing sudden death.

Early repolarization in Wolff-Parkinson-White syndrome: prevalence and clinical significance.

AIMS: Idiopathic ventricular fibrillation (IVF) with early repolarization (ER) has recently been reported; however, ER is a common finding in healthy subjects and is also found sporadically in patients with Wolff-Parkinson-White (WPW) syndrome. The present study was designed to evaluate the prevalence and clinical significance of ER in patients with WPW syndrome. METHODS AND RESULTS: One hundred and eleven patients with WPW syndrome were studied retrospectively. Early repolarization was defined as QRS slurring or notching with J-point elevation ≥ 1 mm. The prevalence of ER was determined before and after successful catheter ablation. Before ablation, ER was found in 35 of 75 patients with a left free wall, 6 of 23 with a right free wall, and 7 of 13 with a septal accessory pathway (48 of 111, 43% as a whole). Early repolarization was always observed in leads with positive deflection of the initial part of the delta wave. After successful ablation of accessory pathways, ER was preserved in 28 (25%), disappeared in 20 (18%), and newly developed in 8 (7%) patients. In the remaining 55 (50%) patients, ER was not observed either before or after ablation. In patients with persistent ER, the amplitude and width of ER were significantly decreased 3-7 days after the ablation (1.7 ± 0.7 vs. 1.4 ± 0.6 mm, P < 0.005 and 42 ± 11 vs. 34 ± 9 ms, P < 0.001, respectively). CONCLUSION: In patients with WPW syndrome, ER could be partly related to early depolarization through the accessory pathway. However, persistent ER and new ER appearing after the ablation were frequently found. Therefore, in these patients, mechanisms other than early depolarization may be involved in the genesis of ER.

Comparison of QT/RR relation based on a 15-s averaged ECG and a single beat ECG during atrial fibrillation.

BACKGROUND: The aim of this study was to compare QT/RR relation based on a 15-s averaged beat ECG with a single beat ECG during atrial fibrillation (AF) and to determine which was better to estimate the QT interval after sinus restoration. METHODS AND RESULTS: QT and RR intervals were measured using an automatic QT analyzing system in 33 patients who had both AF and sinus rhythm on the same 24-h Holter ECG recording. In 14 patients, antiarrhythmic drugs (AAD) were administered. QT/RR relations were analyzed from ECG waves obtained by the summation of consecutive QRS-T complexes during each 15-s period (QT/RR-average) and a single beat QRS-T (QT/RR-single). During sinus rhythm, the slope of QT/RR-average did not differ from that of QT/RR-single in patients with and without AAD. On the other hand, during AF, the slope of QT/RR-average was significantly greater than that of QT/RR-single (without AAD: 0.12±0.06 vs. 0.06±0.03, P<0.001; with AAD: 0.15±0.05 vs. 0.08±0.04, P<0.001). During AF, the QT interval at an RR interval of 1.2-s (QT-1.2) determined from QT/RR-average was significantly greater than QT-1.2 from QT/RR-single in patients with and without AAD. QT-1.2 in QT/RR-single during AF was significantly smaller than that during sinus rhythm but QT-1.2 in QT/RR-average during AF was not. CONCLUSIONS: The QT interval after sinus restoration could be estimated better using QT/RR-average than using QT/RR-single during AF.

Narrow QRS ventricular tachycardia from the posterior mitral annulus without involvement of the His-Purkinje system in a patient with prior inferior myocardial infarction.

A 54-year-old man with prior inferior myocardial infarction suffered from monomorphic ventricular tachycardia (VT) with narrow QRS complex of 120 ms. During VT, a fragmented prepotential preceding QRS onset by 30 ms at the right ventricular posterior septum and a late diastolic potential preceding QRS onset by 70 ms at the infarcted posterior mitral annulus were recorded. Radiofrequency energy delivered to the late diastolic potential at the posterior mitral annulus eliminated VT. During sinus rhythm, the late diastolic potential shifted to the end of QRS complex and no Purkinje potentials were observed. Synchronized excitation of both ventricles from the posterior infarcted mitral annulus in this patient may make the QRS width during VT narrow, without involvement of the His-Purkinje system.

Deficiency of testosterone associates with the substrate of atrial fibrillation in the rat model.

BACKGROUND: Since the prevalence of atrial fibrillation (AF) increases progressively with aging, especially in men, we hypothesized that testosterone might affect the occurrence of AF. METHODS AND RESULTS: We examined the electrophysiological properties of the atria in isolated-perfused hearts of sham-operated male (SM), female (SF), orchiectomized male with and without administration of testosterone (ORCH-T and ORCH), and ovariectomized female (OVX) Sprague-Dawley rats. An electrophysiological study revealed that repetitive atrial responses induced by electrical stimuli significantly increased in ORCH rats without changes in other electrophysiological properties and were abolished by administration of testosterone. To investigate the underlying mechanisms, we evaluated the expression level of calcium-handling proteins. In ORCH rats, the immunoreactive protein level of ryanodine receptor type 2 (RyR2) and sodium-calcium exchanger significantly increased as compared with SM and ORCH-T rats without alterations in the level of FK506-binding protein (FKBP12.6), sarcoendoplasmic reticulum Ca-ATPase, and phospholamban. Immunoprecipitation analysis demonstrated decreased binding of FKBP12.6 to RyR2 in ORCH rats, which was prevented by testosterone. In contrast, the expression levels of these proteins showed no significant differences between SF and OVX rats. CONCLUSION: Deficiency of testosterone was arrhythmogenic in rat atria possibly through less binding of FKBP12.6 to RyR2, which could induce feasible calcium leakage from the sarcoendoplasmic reticulum. These results would explain, at least in part, the increase in the prevalence of AF in accordance with the decline of testosterone particularly in elderly men.

d,l-Sotalol reverses abbreviated atrial refractoriness and prevents promotion of atrial fibrillation in a canine model with left ventricular dysfunction induced by atrial tachypacing.

BACKGROUND: This study evaluated antiarrhythmic effects of d,l-sotalol in a canine atrial fibrillation (AF) model with left ventricular dysfunction. METHODS AND RESULTS: Thirteen beagles (Sotalol group n=7 and Control group n=6) were subjected to atrial tachypacing (ATP) (400 beats/min) with intact atrioventricular conduction for 4 weeks. Oral d,l-sotalol (2 mg/kg) was administered 1 week after starting ATP and continued throughout the experiment. One week after starting ATP, atrial effective refractory periods (AERPs) were shortened in both groups. However, d,l-sotalol treatment gradually prolonged AERP, resulting in a significant prolongation of AERP compared with the Control group at 4 weeks (Control 76 +/-4 and Sotalol 126 +/-5 ms, p<0.01). d,l-Sotalol treatment showed lower AF inducibility and shorter AF duration at 4 weeks. In the control group, expressions of L-type Ca(2+) channel alpha1c and Kv4.3 mRNA were downregulated by 46.2% and 43.0%, respectively, after 4 weeks of ATP; d,l-sotalol treatment did not affect these changes. CONCLUSIONS: d,l-Sotalol treatment prolonged AERP, even after atrial electrical remodeling had developed, and prevented AF perpetuation without affecting downregulated expression of L-type Ca(2+) channel alpha1c and Kv4.3 mRNA in an ATP-induced canine AF model.

Effects of a heat shock protein inducer on the atrial fibrillation substrate caused by acute atrial ischaemia.

AIMS: Heat shock proteins (HSPs) are a set of endogenous cytoprotective factors activated by various pathological conditions. This study addressed the effects of geranylgeranylacetone (GGA), an orally active HSP inducer, on the atrial fibrillation (AF) substrate associated with acute atrial ischaemia (AI). METHODS AND RESULTS: Four groups of mongrel dogs were studied: (1) a group subjected to AI without GGA (AI-CTL, n = 13 dogs); (2) dogs that underwent AI after GGA pretreatment (120 mg/kg/day; AI-GGA, n = 12); (3) dogs receiving GGA pretreatment without AI (n = 5); (4) control dogs for tissue sampling (n = 5). Isolated right AI was produced by occluding a right atrial (RA) coronary-artery branch. AI reduced ischaemic-zone conduction velocity (CV, from 94 +/- 3 to 46 +/- 5 cm/s; P < 0.01) and increased maximum local phase delays (P95, from 1.6 +/- 0.1 to 4.6 +/- 0.6 ms/mm; P < 0.01), conduction heterogeneity index (CHI, from 0.7 +/- 0.1 to 2.9 +/- 0.5; P < 0.01), and the mean duration of burst pacing-induced AF (DAF, from 44 +/- 18 to 890 +/- 323 s; P < 0.01) in AI-CTL dogs. GGA pretreatment attenuated ischaemia-induced conduction abnormalities (CV, 77 +/- 8 cm/s; P95, 2.1 +/- 0.4 ms/mm; CHI, 1.1 +/- 0.2; all P < 0.01 vs. AI-CTL) and DAF (328 +/- 249 s; P < 0.01) in AI-GGA dogs. GGA treatment alone, without ischaemia, did not alter DAF or conduction indices. AI slightly prolonged atrial refractory period, an effect also prevented by GGA. GGA significantly increased HSP70 protein expression in RA tissues of ischaemic hearts. CONCLUSIONS: GGA prevents ischaemia-induced atrial conduction abnormalities and suppresses ischaemia-related AF. These results suggest that HSP induction might be a useful new anti-AF intervention for patients with coronary artery disease.

Junctional rhythm associated with ventriculoatrial block during slow pathway ablation in atypical atrioventricular nodal re-entrant tachycardia.

AIMS: We assessed responses to slow pathway ablation with respect to the appearance of ventriculoatrial (VA) block during junctional rhythm in both typical and atypical types of atrioventricular nodal re-entrant tachycardia (AVNRT). METHODS AND RESULTS: The 31 subjects included 16 patients with slow-fast type of typical AVNRT and 15 patients with atypical AVNRT (9 patients with fast-slow type and 6 patients with slow-slow type). During atypical AVNRT, the HA interval was prolonged (>70 ms) and the earliest atrial activation was located around the coronary sinus (CS) ostium. The difference in atrial activation times at the CS ostium and His-bundle area [A(CS-His)] during AVNRT was measured. Slow pathway ablation was performed using a classical electro-anatomical approach. In typical AVNRT, A(CS-His) was -21.3 +/- 3.4 ms, and the HA interval was 34 +/- 14 ms. During slow pathway ablation, all patients with typical AVNRT had junctional rhythm with retrograde atrial conduction. In contrast, in patients with atypical AVNRT, A(CS-His) was 12 +/- 19.3 ms and the HA interval was 189 +/- 77 ms. In 13 of the 15 patients with atypical AVNRT, slow pathway ablation induced junctional rhythm, which was not associated with retrograde atrial conduction. After ablation, AVNRT became non-inducible and antegrade atrioventricular (AV) conduction was preserved in all patients. CONCLUSION: In patients with atypical AVNRT, junctional rhythm with VA block during slow pathway ablation is commonly observed and indicates the success of the ablation of retrograde slow pathway conduction, but has no relation to the risk of subsequent AV block. During junctional rhythm, occasional appearance of the sinus beats with intact antegrade AV conduction is essential for safety of ablation.

Bepridil reverses atrial electrical remodeling and L-type calcium channel downregulation in a canine model of persistent atrial tachycardia.

INTRODUCTION: This study tested whether bepridil, a multichannel blocker, would reverse electrical remodeling induced by persistent atrial tachycardia. METHODS AND RESULTS: Fourteen dogs were subjected to rapid atrial pacing at 400 bpm for 6 weeks after atrioventricular block was created to control the ventricular rate. During the study period, seven dogs were given placebo for 6 weeks (Control group), and seven were given placebo for 3 weeks, followed by 3 weeks of bepridil (10 mg/kg/day, Bepridil group). The atrial effective refractory period (ERP) and the inducibility and duration of atrial fibrillation (AF) were determined on a weekly basis. After 6 weeks, expression of L-type calcium channel alpha1C messenger ribonucleic acid (mRNA) was quantified by real-time reverse transcription-polymerase chain reaction. In the Control group, ERP was shortened and the inducibility and duration of AF increased through the 6-week period. In the Bepridil group, the same changes occurred during the first 3 weeks, but were gradually reversed with bepridil. After 6 weeks, ERP was longer, AF inducibility was lower, and AF duration was shorter in Bepridil group than in the Control group. Expression of alpha1C mRNA was decreased by 64% in the Control group (P < 0.05 vs sham), but in the Bepridil group, it was not different compared with the sham dogs. As a whole group of dogs, ERP was positively correlated with alpha1C mRNA expression. CONCLUSION: Bepridil reverses the electrophysiological consequences of atrial remodeling to some extent and L-type calcium channel downregulation in a canine model of atrial tachycardia.

Postprandial augmentation of bradycardia-dependent ST elevation in patients with Brugada syndrome.

INTRODUCTION: In patients with Brugada syndrome, the circadian variation of ST elevation could be modulated by the autonomic nervous activity and RR interval. Recently, glucose-induced insulin secretion was also reported to contribute to fluctuation of ST elevation. Therefore, we assessed the effects of taking meals on the ST-RR relationship in the daily life of patients with Brugada syndrome. METHODS AND RESULTS: Twenty-eight patients with Brugada syndrome, who had the type I ST elevation, were categorized into 12 symptomatic and 16 asymptomatic patients. Unipolar lead (V2) Holter ECG was recorded and ST-RR relationships for a 2-hour period were compared before and after each meal. From ST-RR linear regression lines, ST-RR slope (mm/sec) and ST(mm) at RR intervals of both 0.6 seconds and 1.2 seconds (ST(0.6) and ST(1.2)) were determined. The ST-RR slope increased significantly after lunch (2.6 +/- 0.4 vs 4.4 +/- 1.2, P < 0.05) and dinner (2.1 +/- 1.0 vs 5.2 +/- 1.9, P < 0.01) in symptomatic patients, but not in asymptomatic patients. In both groups, ST(0.6) was not different before or after each meal. However, ST(1.2) increased after each meal in symptomatic patients. After dinner, ST(1.2) was significantly higher in symptomatic patients than in asymptomatic patients (5.0 +/- 2.7 vs 3.6 +/- 0.8, P < 0.05). Postprandial increase in both ST-RR slope and ST(1.2) was greatest at dinner in symptomatic patients; however, this tendency was not seen in asymptomatic patients. CONCLUSIONS: In symptomatic patients with Brugada syndrome, bradycardia-dependent augmentation of ST elevation was enhanced for the postprandial period, especially after dinner. This could be related to occurrence of ventricular fibrillation in the late evening.

Effect of oral L-type calcium channel blocker on repetitive paroxysmal atrial fibrillation: spectral analysis of fibrillation waves in the Holter monitoring.

AIMS: The electrical remodelling is considered to play a role in promoting arrhythmogenic substrate of atrial fibrillation (AF), and intracellular calcium overload may play a key role, especially in its early phase. The effect of oral verapamil on repetitive paroxysmal AF (PAF) was evaluated in clinical cases. METHODS AND RESULTS: Thirty-five patients with repetitive PAF (total PAF duration >2/24 h) were divided into two groups with and without verapamil administration (240 mg/day) and they were followed-up for 12 months. Before and after the follow-up period, 24 h Holter ECG was recorded. In each Holter recording, total PAF duration and the longest PAF duration was evaluated and spectral analysis was performed for fibrillation waves in PAF episodes to evaluate the fibrillatory frequency. Total PAF duration was prolonged by 45 +/- 79 min in the control group (n = 18) whereas shortened by 25 +/- 55 min in the verapamil group (n = 17, P = 0.005). The fibrillatory frequency was increased from 5.66 +/- 1.05 to 6.73 +/- 1.02 Hz in the control group and was unchanged in the verapamil group. There was inverse relationship between Deltatotal PAF duration and Deltafibrillatory frequency (P = 0.0002). CONCLUSION: Verapamil prevented the increase in fibrillatory frequency in PAF patients in relatively long-term observation. Verapamil might be effective for prevention of the electrophysiological change and increase in PAF episodes at least in specific type of PAF cases.