RESUMO
Background: Brugada syndrome (BrS) is a cardiac ion channelopathy that predisposes affected individuals to sudden cardiac death (SCD). Type 1 BrS is thought to take a more malignant clinical course than non-type 1 BrS. We hypothesized that the degrees of abnormal repolarization and conduction are greater in type 1 subjects and these differences can be detected by electrocardiography (ECG). Methods: Electrocardiographic data from spontaneous type 1 and non-type 1 BrS patients were analyzed. ECG parameters were measured from leads V1 to V3. Values were expressed as median [lower quartile-upper quartile] and compared using Kruskal-Wallis ANOVA. Results: Compared to non-type 1 BrS patients (n = 29), patients with spontaneous type 1 patterns (n = 22) showed similar (P > 0.05) heart rate (73 [64-77] vs. 68 [62-80] bpm), QRS duration (136 [124-161] vs. 127 [117-144] ms), uncorrected QT (418 [393-443] vs. 402 [386-424] ms) and corrected QT intervals (457 [414-474] vs. 430 [417-457] ms), JTpeak intervals (174 [144-183] vs. 174 [150-188] ms), Tpeak- Tend intervals (101 [93-120] vs. 99 [90-105] ms), Tpeak- Tend/QT ratios (0.25 [0.23-0.27] vs. 0.24 [0.22-0.27]), Tpeak- Tend/QRS (0.77 [0.62-0.87] vs. 0.77 [0.69-0.86]), Tpeak- Tend/(QRS × QT) (0.00074 [0.00034-0.00096] vs. 0.00073 [0.00048-0.00012] ms-1), index of Cardiac Electrophysiological Balance (iCEB, QT/QRS, marker of wavelength: 3.14 [2.56-3.35] vs. 3.21 [2.85-3.46]) and corrected iCEB (QTc/QRS: 3.25 [2.91-3.73] vs. 3.49 [2.99-3.78]). Higher QRS dispersion was seen in type 1 subjects (QRSd: 34 [24-66] vs. 24 [12-34] ms) but QT dispersion (QTd: 48 [39-71] vs. 43 [22-94] ms), QTc dispersion (QTcd: 52 [41-79] vs. 46 [23-104] ms), JTpeak dispersion (44 [23-62] vs. 45 [30-62] ms), Tpeak- Tend dispersion (28 [15-34] vs. 29 [22-53] ms) or Tpeak- Tend/QT dispersion (0.06 [0.03-0.08] vs. 0.08 [0.04-0.12]) did not differ between the two groups. Type 1 subjects showed higher (QRSd × Tpeak- Tend)/QRS (25 [19-44] vs. 19 [9-30] ms) but similar iCEB dispersion (0.83 [0.49-1.14] vs. 0.61 [0.34-0.92]) and iCEBc dispersion (0.93 [0.51-1.15] vs. 0.65 [0.39-0.96]). Conclusion: Higher levels of dispersion in conduction and repolarization are found in type 1 than non-type 1 BrS patients, potentially explaining the higher incidence of ventricular arrhythmias in the former group.
RESUMO
AIMS: The aim of this study was to assess the contribution of left ventricular (LV) systolic dyssynchrony to functional mitral regurgitation (MR). METHODS AND RESULTS: Patients (n = 136) with LV systolic dysfunction (ejection fraction <50%) and at least mild MR were prospectively recruited. The effective regurgitant orifice area (EROA) was assessed by the proximal isovelocity surface area method. Left ventricular global systolic dyssynchrony [the maximal difference in time to peak systolic velocity among the 12 LV segments (Ts-Dif)] and regional systolic dyssynchrony (the delay between the anterolateral and posteromedial papillary muscle attaching sites) were assessed by tissue Doppler imaging. Left ventricular global and regional remodelling, systolic function, indices of mitral valvular and annular deformation were also measured. The size of the EROA correlated with the degrees of mitral deformation, LV remodelling, systolic function, and systolic dyssynchrony. By multivariate logistic regression analysis, the mitral valve tenting area (OR = 1.020, P < 0.001) and the Ts-Dif (OR = 1.011, P = 0.034) were independent determinants of significant functional MR (defined by EROA ≥20 mm(2)). From the receiver-operating characteristic curve, the tenting area of 2.7 cm(2) (sensitivity 83%, specificity 82%, AUC 0.86, P < 0.001) and the Ts-Dif of 85 ms (sensitivity 66%, specificity 72%, AUC 0.74, P < 0.001) were associated with significant functional MR. The assessment of Ts-Dif showed an incremental value over the mitral valve tenting area for determining functional MR (χ(2) = 53.92 vs.49.11, P = 0.028). CONCLUSION: This cross-sectional study showed that LV global, but not regional systolic dyssynchrony, is a determinant of significant functional MR in patients with LV systolic dysfunction, and is incremental to the tenting area that is otherwise the strongest factor for mitral valve deformation.
