Browsing by Author "George, Alfred L."

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    Low-Pass filtering approach via empirical mode decomposition improves short-scale entropy-based complexity estimation of QT interval variability in long QT syndrome type 1 patients
    (MDPI, 2014-09-05) Bari, Vlasta; Marchi, Andrea; De Maria, Beatrice; Girardengo, Giulia; George, Alfred L.; Brink, Paul A.; Cerutti, Sergio; Crotti, Lia; Schwartz, Peter J.; Porta, Alberto
    Entropy-based complexity of cardiovascular variability at short time scales is largely dependent on the noise and/or action of neural circuits operating at high frequencies. This study proposes a technique for canceling fast variations from cardiovascular variability, thus limiting the effect of these overwhelming influences on entropy-based complexity. The low-pass filtering approach is based on the computation of the fastest intrinsic mode function via empirical mode decomposition (EMD) and its subtraction from the original variability. Sample entropy was exploited to estimate complexity. The procedure was applied to heart period (HP) and QT (interval from Q-wave onset to T-wave end) variability derived from 24-hour Holter recordings in 14 non-mutation carriers (NMCs) and 34 mutation carriers (MCs) subdivided into 11 asymptomatic MCs (AMCs) and 23 symptomatic MCs (SMCs). All individuals belonged to the same family developing long QT syndrome type 1 (LQT1) via KCNQ1-A341V mutation. We found that complexity indexes computed over EMD-filtered QT variability differentiated AMCs from NMCs and detected the effect of beta-blocker therapy, while complexity indexes calculated over EMD-filtered HP variability separated AMCs from SMCs. The EMD-based filtering method enhanced features of the cardiovascular control that otherwise would have remained hidden by the dominant presence of noise and/or fast physiological variations, thus improving classification in LQT1.
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    Multiscale complexity analysis of the cardiac control identifies asymptomatic and symptomatic patients in long QT syndrome type 1
    (PLoS, 2014-04-04) Bari, Vlasta; Valencia, Jose F.; Vallverdu, Montserrat; Girardengo, Giulia; Marchi, Andrea; Bassani, Tito; Caminal, Pere; Cerutti, Sergio; George, Alfred L.; Brink, Paul A.; Crotti, Lia; Schwartz, Peter J.; Porta, Alberto
    The study assesses complexity of the cardiac control directed to the sinus node and to ventricles in long QT syndrome type 1 (LQT1) patients with KCNQ1-A341V mutation. Complexity was assessed via refined multiscale entropy (RMSE) computed over the beat-to-beat variability series of heart period (HP) and QT interval. HP and QT interval were approximated respectively as the temporal distance between two consecutive R-wave peaks and between the R-wave apex and T-wave end. Both measures were automatically taken from 24-hour electrocardiographic Holter traces recorded during daily activities in non mutation carriers (NMCs, n = 14) and mutation carriers (MCs, n = 34) belonging to a South African LQT1 founder population. The MC group was divided into asymptomatic (ASYMP, n = 11) and symptomatic (SYMP, n = 23) patients according to the symptom severity. Analyses were carried out during daytime (DAY, from 2PM to 6PM) and nighttime (NIGHT, from 12PM to 4AM) off and on beta-adrenergic blockade (BBoff and BBon). We found that the complexity of the HP variability at short time scale was under vagal control, being significantly increased during NIGHT and BBon both in ASYMP and SYMP groups, while the complexity of both HP and QT variability at long time scales was under sympathetic control, being smaller during NIGHT and BBon in SYMP subjects. Complexity indexes at long time scales in ASYMP individuals were smaller than those in SYMP ones regardless of therapy (i.e. BBoff or BBon), thus suggesting that a reduced complexity of the sympathetic regulation is protective in ASYMP individuals. RMSE analysis of HP and QT interval variability derived from routine 24-hour electrocardiographic Holter recordings might provide additional insights into the physiology of the cardiac control and might be fruitfully exploited to improve risk stratification in LQT1 population.