21 research outputs found

    A Large-Scale, Energetic Model of Cardiovascular Homeostasis Predicts Dynamics of Arterial Pressure in Humans

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    Orthonormal-basis partitioning and time-frequency representation of cardiac rhythm dynamics

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    Although a number of time-frequency representations have been proposed for the estimation of time-dependent spectra, the time-frequency analysis of multicomponent physiological signals, such as beat-to-beat variations of cardiac rhythm or heart rate variability (HRV), is difficult. We thus propose a simple method for 1) detecting both abrupt and slow changes in the structure of the HRV signal, 2) segmenting the nonstationary signal into the less nonstationary portions, and 3) exposing characteristic patterns of the changes in the time-frequency plane. The method, referred to as orthonormal-basis partitioning and time-frequency representation (OPTR), is validated using simulated signals and actual HRV data. Here we show that OPTR can be applied to long multicomponent ambulatory signals to obtain the signal representation along with its time-varying spectrum. © 2005 IEEE

    Adrenergic stimulation promotes T-wave alternans and arrhythmia inducibility in a TNF-α genetic mouse model of congestive heart failure

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    T-wave alternans (TWA) is a proarrhythmic repolarization instability that is common in congestive heart failure (CHF). Although transgenic mice are commonly used to study the mechanisms of arrhythmogenesis in CHF, little is known about the dynamics of TWA in these species. We hypothesized that TWA is present in a TNF-α model of CHF and can be further promoted by adrenergic stimulation. We studied 16 TNF-α mice and 12 FVB controls using 1) in vivo intracardiac electrophysiological testing and 2) ambulatory telemetry during 30 min before and after an intraperitoneal injection of isoproterenol. TWA was examined using both linear and nonlinear filtering applied in the time domain. In addition, changes in the mean amplitude of the T wave and area under the T wave were computed. During intracardiac electrophysiological testing, none of the animals had TWA or inducible arrhythmias before the injection of isoproterenol. After the injection, sustained TWA and inducible ventricular tachyarrhythmias were observed in TNF-α mice but not in FVB mice. In ambulatory telemetry, before the isoproterenol injection, the cardiac cycle length (CL) was longer in TNF-α mice than in FVB mice (98 ± 9 and 88 ± 3 ms, P = 0.04). After the injection of isoproterenol, the CL became 8% and 6% shorter in TNF-α and FVB mice (P < 10−4); however, the 2% difference between the groups in the magnitude of CL changes was not significant. In TNF-α mice, the magnitude of TWA was 1.5–2 times greater than in FVB mice both before and after the isoproterenol injection. The magnitude of TWA increased significantly after the isoproterenol injection compared with the baseline in TNF-α mice (P = 0.003) but not in FVB mice. The mean amplitude of the T wave and area under the T wave increased 60% and 80% in FVB mice (P = 0.006 and 0.009) but not in TNF-α mice. In conclusion, TWA is present in a TNF-α model of CHF and can be further promoted by adrenergic stimulation, along with the enhanced susceptibility for ventricular arrhythmias
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