Msec In Control Group Research Articles

Neuronal nitric oxide synthase inhibition exacerbates atrial electrical remodeling via small-conductance Ca2+-activated K+ channel activation

Abstract Funding Acknowledgements Type of funding sources: Public Institution(s). Main funding source(s): The Japan Society for the Promotion of Science KAKENHI Background The presence of atrial fibrillation (AF) is associated with electrical remodeling processes that promote a substrate for the maintenance of AF itself. Small conductance Ca2+-activated K+ (SK) channels; K+-selective and voltage-independent ion channels are key factors in the atrial electrical remodeling (2, 3). However, the mechanism of its activation remains unclear. A recent study showed that neuronal nitric oxide synthase (nNOS) expression and activity are reduced in AF patients and that nNOS depletion causes the abbreviation of action potential duration (APD), leading to increased AF inducibility in animal experiments (4). Decreased NO production, especially driven by nNOS inhibition, might play a key role in the atrial electrical remodeling, and the downstream alteration of SK channels might result from this process. Purpose We aimed to evaluate the potential of SK channel blocking to mitigate abnormal electrophysiological properties and the inducibility of atrial tachyarrhythmia (ATA) which was induced by nNOS depletion, and to describe the related mechanism. Methods Atrial tachyarrhythmia induction and optical mapping were performed in perfused rat hearts. nNOS was pharmacologically inhibited by S-methylthiocitrulline (SMTC, 100 nM). The influence of the SK channel was examined by a specific channel inhibitor, apamin (100 nM). APD, conduction velocity, and calcium transient (CaT) parameters (CaTD, rise time, time to 50% decay, and tau) were evaluated by voltage and calcium dual optical mapping. Dominant frequency was evaluated to analyze the wave dynamics of AF. Results SMTC increased the inducibility of ATA and apamin mitigated the nNOS inhibition-induced arrhythmogenicity (0% [0/7] vs 62% [8/13] vs 15% [2/13] in control, SMTC and SMTC + apamin). SMTC caused the abbreviation and enhanced spatial dispersion of APD, which were reversed by apamin. In contrast, conduction velocity was not affected by SMTC or apamin. Moreover, apamin reduced the dominant frequency of SMTC-induced ATA. In voltage and calcium optical mapping, STMC and apamin did not alter the parameters associated with CaT, however, SMTC caused the abbreviation of APD, which was reversed by apamin (APD80: 48.4 ± 2.7 msec in control group, 30.8 ± 1.5 msec in SMTC group, p <0.0001 vs. control, 41.8 ± 1.5 msec in SMTC + apamin, p = 0.01 vs. SMTC by One-way ANOVA and Tukey’s multiple-comparison test) (Figure A-C). Conclusion Acute nNOS inhibition abbreviated APD via activating SK channels. A specific SK channel blocker mitigated APD abbreviation without the alteration of CaT, implying an underlying mechanism of post translational modification of SK channels.

Effect of Hydroxychloroquine on Visual System in Patients with Systemic Lupus Erythematosus using Visual Evoked Potential

Aim: This study was performed to determine the effect of Hydroxychloroquine on visual system in patients with systemic lupus erythematosus.Materials and methods: In a cross -sectional study, 50 subjects (without visual problem and seizure) including 25 with and 25 without systemic lupus erythematosus under treatment with chloroquine were selected. Visual evoked potential test was performed in two groups.Results: The mean amplitude was 6.04 in case and 5.84 μ∉- ι∈1/2 χo∈1/2∉ρoΔ γρo∉..π ωηιχη σηoωσ ∈1/2o σ∉α∉ισ∉ιχαΔΔψ σιγ∈1/2ιϕιχα∈1/2∉ διϕϕeρe∈1/2χe.The mean latency was 100.50 in case and 95.35 msec in control group which is not statistically significant.Conclusion: Based on the result of present work one can conclude that hydroxychloroquine has no adverse effect on visual pathway which will be discussed in detail in full paper.

Cardiac findings in Behçet’s patients

Behçet's disease is a chronic multi-system inflammatory disorder and the severity and clinical manifestations of Behçet's patients may show geographic variation. We aimed to detect the cardiac findings in 30 Behçet's patients and compare them with the normal population (n = 29). We used color-doppler echocardiography and transesophageal echocardiography in combination. We calculated manually QT intervals and QT dispersion (QTd) from twelve-lead ECG recordings. There was no E/A inversion and coronary ischemia in all patients or control group. The E velocity difference between groups was not significant. The mean A velocity was significantly lower in Behçet's patients than normal group. The mean DT was 154.4 +/- 5.8 msec in Behçet's patients and 122.59 +/- 0.96 msec in control group (P < 0.0001). The mean IVRT was 75.66 +/- 1.36 msec in Behçet's patients and 69.1 +/- 0.55 msec in control group (P < 0.0001). There was no QTc time difference between the Behçet's patients and the control group. The mean QT dispersion (QTd) interval was 45.46 +/- 2.65 msec in Behçet's patients and 31.83 +/- 1.23 msec in control group (P < 0.0001). Atrial septal aneurysm, mitral valve prolapse and insufficiency, tricuspid valve insufficieny, and pulmonary hypertension frequencies in Behçet's patients were significantly higher than in the control group. We concluded that Behçet's cardiac involvement may effect cardiac structure and cause diastolic dysfunction, electrical instability and structural abnormalities. We also concluded that cardiac involvement in Behçet's disease may be specific for this geographic area.

Baroreflex sensitivity, but not heart rate variability, is reduced in patients with life-threatening ventricular arrhythmias long after myocardial infarction

Low values of heart rate variability (HRV, a marker of vagal tone) and baroreflex sensitivity (BRS, a marker of vagal reflexes) identify patients at higher risk soon after myocardial infarction (MI). However, it is still unknown whether HRV and BRS correlate with malignant arrhythmias after the recovery from the transient post-MI autonomic disturbance. This study assessed whether HRV and BRS would differ in patients with malignant ventricular arrhythmias occurring long after MI compared with those in a control population. Twenty-eight patients entered the study: 14 patients with episodes of sustained ventricular tachycardia or ventricular fibrillation occurring more than 1 year after MI, age (mean ± SEM) 64 ± 2 years, and left ventricular ejection fraction 34% ± 3% ( VT VF group) were compared with 14 similar patients with no ventricular tachycardia (control group). Mean RR interval was not different in the two groups (844 ± 37 msec in VT VF and 892 ± 24 msec in control group). Also, no difference was found in any time- or frequency-domain measure of heart rate variability. However, patients in the VT VF group had a significantly lower baroreflex sensitivity compared with patients in the control group (4.2 ± 0.5 vs 8.0 ± 1.1 msec/mm Hg, p = 0.008). Thus BRS but not HRV was reduced in patients with life-threatening ventricular arrhythmias occurring long after MI. A persistent depression of vagal reflexes may play a role in the occurrence of malignant arrhythmias, and analysis of BRS may potentially be helpful in the identification of patients at high risk long after myocardial infarction.

Clinical significance of the pre-atrial electrical activity recorded by the catheter electrode in high right atrium.

1) In canine experiment, the averaging of high right atrial electrical activity revealed the pre-A preceding the atrial deflection, which was proven to be a part of the electrical activity of sinus nodal region. 2) The pre-A was obtained in 114 (75%) of 153 clinical cases. 3) The mean pre-A interval was 18 +/- 4 msec in control group, and was prolonged in cases with sick sinus syndrome, ischemic heart disease and myocarditis. 4) The significant correlation existed between the pre-A interval and the SACT by Strauss' method (r = 0.80, p < 0.01). 5) The pre-A obtained by averaging technique is relatively simple, safe and reliable method, and is useful for evaluating the sino-atrial function.