Spectrophotometric, chemometric and chromatographic determination of naphazoline hydrochloride and chlorpheniramine maleate in the presence of naphazoline hydrochloride alkaline degradation product

AbstractFour accurate and sensitive methods were developed and validated for determination of naphazoline hydrochloride (NAP) and chlorpheniramine maleate (CLO) in the presence of naphazoline hydrochloride alkaline degradation product (NAP Deg). The first method is a spectrophotometric one , where NAP was determined by the fourth derivative (D4) spectrophotometric method by measuring the peak amplitude at 302nm, while CLO was determined by the second derivative of the ratio spectra (DD2) spectrophotometric method at 276.4nm. The second method is a chemometric-assisted spectrophotometric method in which partial least squares (PLS-1) and partial component regression (PCR) were used for the determination of NAP, CLO and NAP Deg using the information contained in their absorption spectra of ternary mixture. The third method is a TLC-densitometric one where NAP, CLO and NAP Deg were separated using HPTLC silica gel F254 plates using ethyl acetate:methanol:ammonia: (8:2:0.5, by volume) as the developing system followed by densitometric measurement at 245nm. The fourth method is HPLC method where NAP, CLO and NAP Deg were separated using ODS C18 column and a mobile phase consisting of 0.1M KH2PO4 (pH=7):methanol (55:45 v/v) delivered at 1.5mLmin−1 followed by UV detection at 265nm. The proposed methods have been successfully applied to the analysis of NAP and CLO in pharmaceutical formulations without interference from the dosage form additives and the results were statistically compared with a reported method

Inferolateral J-waves are inducible by regional conduction delay

International audienc

Electrocardiographic T wave and its relation with ventricular repolarization along major anatomical axes

The genesis of the electrocardiographic T wave is incompletely understood and subject to controversy. We have correlated the ventricular repolarization sequence with simultaneously recorded T waves. Nine pig hearts were Langendorff-perfused (atrial pacing, cycle length 650 ms). Local activation and repolarization times were derived from unipolar electrograms sampling the ventricular myocardium. Dispersion of repolarization time was determined along 4 anatomic axes: left ventricle (LV)-right ventricle (RV), LV:apico-basal, LV:anterior-posterior, and LV:transmural. The heart was immersed in a fluid-filled bucket containing 61 electrodes to determine Tp (Tpeak in lead of maximum integral), TpTe (Tp to Tend), and TpTe_total (first Tpeak in any lead to last Tend in any lead). Repolarization was nonlinearly distributed in time. RT25 (time at which 25% of sites were repolarized, 288±26 ms) concurred with Tp. TpTe was 38±8 ms, and TpTe_total was 75±9 ms. TpTe_total correlated with dispersion of repolarization time in the entire heart (73±18 ms), but not with dispersion of repolarization times along individual axes (LV-RV, 66±17 ms; LV:apico-basal, 51±18 ms; LV:anterior-posterior, 51±27 ms; mean LV:transmural, 14±7 ms; all n=9). We provide a correlation between local repolarization and T wave in a pseudo-ECG. Repolarization differences along all anatomic axes contribute to the T wave. TpTe_total represents total dispersion of repolarization. At Tp, ≈25% of ventricular sites have been repolarize

Electrocardiographic changes after successful recanalization of a chronic total coronary occlusion. A systematic review and meta-analysis

Background: Observational studies suggest that in patients with a CTO successful recanalization is associated with better clinical outcome. This could be related to a reduction in the occurrence of arrhythmias, which may result from modifications of the hibernating myocardium in a CTO region. Methods and results: We aimed to evaluate the effect of CTO PCI on electrophysiological parameters, and conducted a systematic review and meta-analysis according to the PRISMA guidelines. MEDLINE and EMBASE were searched. Titles and abstracts identified by the search strategy were independently screened by two investigators. Data were extracted and used for meta-analyses where possible. In total, eight studies incorporating 467 patients were included in this review, evaluating the effect of successful CTO PCI on various ECG parameters. Three studies showed a significant decrease in mean QT dispersion of 17.46 ms [95% CI 10.62–24.30] after successful CTO PCI. QTc dispersion also decreased significantly, with a mean decrease of 18.74 ms [95% CI 11.53–25.94]. In one trial a significant decrease in Tp-e interval in leads V2 and V5, and a significant decrease in Tp-e/QT ratio in leads V2 and V5 post-CTO PCI were observed. Conclusions: This first systematic review and meta-analysis suggests that successful CTO PCI is associated with an immediate decrease in ECG parameters that reflect heterogeneity in depolarization and repolarization, which could lead to a reduction in the risk for ventricular arrhythmias and sudden cardiac death. We raise the hypothesis that hibernating myocardium in a CTO region may not be as deeply “in sleep” as one would assume

Documented atrial fibrillation recurrences after pulmonary vein isolation are associated with diminished quality of life

Pulmonary vein isolation (PVI) aims at eliminating symptomatic atrial fibrillation. In this regard, the most relevant indication for this procedure is the reduction of symptoms and improvement of quality of life (QoL) in patients who remain symptomatic despite antiarrhythmic drug treatment. We investigated the relation between documented atrial fibrillation recurrences and QoL in patients after PVI. One hundred and six PVIs were performed in 99 patients. Follow-up was mainly performed at referring hospitals. Short Form 36 (SF-36) QoL questionnaires were completed before and 1 year after PVI. Electrocardiographic recordings from the first postprocedural year were retrospectively collected, 3 months blanking excluded. Atrial fibrillation recurrence was defined as any recurrence of atrial arrhythmia documented on ECG or 24-h-Holter. Before PVI, patients had lower QoL than the general Dutch population in 7/8 SF-36 questionnaire subscales (sumQoL 419.4 ± 161 vs. 617.9, P  < 0.001). Atrial fibrillation recurred in 52 (49%) patients. In these patients, four subscales increased following PVI (physical functioning P  < 0.001, role physical P = 0.006, bodily pain P = 0.011 and social functioning P = 0.047). SumQoL remained lower than the general Dutch population (546.7 ± 157, P = 0.003). In patients without documented recurrences, QoL improved to a level similar to that of the general Dutch population (602.9 ± 148; P = 0.46). The number of electrocardiographic recordings was lower in the group without documented recurrences (2.5 ± 1.8 vs. 3.8 ± 1.7, P = 0.002). In patients without documentation of atrial fibrillation, QoL increased up to the level of the general population after PVI, but it remained lower in patients with recurrences. In the latter group more ECGs were done, suggesting that QoL relates particularly to symptomatic episodes. Improvement of QoL is therefore an important attribute of PV

ST-Segment Elevation and Fractionated Electrograms in Brugada Syndrome Patients Arise From the Same Structurally Abnormal Subepicardial RVOT Area but Have a Different Mechanism

Brugada syndrome (BrS) is characterized by a typical ECG pattern. We aimed to determine the pathophysiologic basis of the ST-segment in the BrS-ECG with data from various epicardial and endocardial right ventricular activation mapping procedures in 6 BrS patients and in 5 non-BrS controls. In 7 patients (2 BrS and 5 controls) with atrial fibrillation, an epicardial 8×6 electrode grid (interelectrode distance 1 mm) was placed epicardially on the right ventricular outflow tract (RVOT) before video-assisted thoracoscopic surgical pulmonary vein isolation. In 2 other BrS patients, endocardial, epicardial RV (CARTO), and body surface mapping was performed. In 2 additional BrS patients, we performed decremental preexcitation of the RVOT before endocardial RV mapping. During video-assisted thoracoscopic surgical pulmonary vein isolation and CARTO mapping, BrS patients (n=4) showed greater activation delay and more fractionated electrograms in the RVOT region than controls. Ajmaline administration increased the region with fractionated electrograms, as well as ST-segment elevation. Preexcitation of the RVOT (n=2) resulted in ECGs that supported the current-to-load mismatch hypothesis for ST-segment elevation. Body surface mapping showed that the area with ST-segment elevation anatomically correlated with the area of fractionated electrograms and activation delay at the RVOT epicardium. ST-segment elevation and epicardial fractionation/conduction delay in BrS patients are most likely related to the same structural subepicardial abnormalities, but the mechanism is different. ST-segment elevation may be caused by current-to-load mismatch, whereas fractionated electrograms and conduction delay are expected to be caused by discontinuous conduction in the same area with abnormal myocardiu

Reduced sodium current in the lateral ventricular wall induces inferolateral J-waves

Background: J-waves in inferolateral leads are associated with a higher risk for idiopathic ventricular fibrillation. We aimed to test potential mechanisms (depolarization or repolarization dependent) responsible for inferolateral J-waves. We hypothesized that inferolateral J-waves can be caused by regional delayed activation of myocardium that is activated late during normal conditions. Methods: Computer simulations were performed to evaluate how J-point elevation is influenced by reducing sodium current conductivity (GNa), increasing transient outward current conductivity (Gto) or cellular uncoupling in three predefined ventricular regions (lateral, anterior or septal). Two pig hearts were Langendorff-perfused with selective perfusion with a sodium channel blocker of lateral or anterior/septal regions. Volume-conducted pseudo-electrocardiograms (ECG) were recorded to detect the presence of J-waves. Epicardial unipolar electrograms were simultaneously recorded to obtain activation times (AT).Results: Simulation data showed that conduction slowing, caused by reduced sodium current, in lateral, but not in other regions induced inferolateral J-waves. An increase in transient outward potassium current or cellular uncoupling in the lateral zone elicited slight J-point elevations which did not meet J-wave criteria. Additional conduction slowing in the entire heart attenuated J-waves and J-point elevations on the ECG, because of masking by the QRS. Experimental data confirmed that conduction slowing attributed to sodium channel blockade in the left lateral but not in the anterior/septal ventricular region induced inferolateral J-waves. J-waves coincided with the delayed activation.Conclusion: Reduced sodium current in the left lateral ventricular myocardium can cause inferolateral J-waves on the ECG