Heart rate dynamics before the spontaneous onset of ventricular tachyarrhythmias in Chagas' heart disease.

A lterations in the spectral analysis of heart rate (HR) have been documented in patients with Chagas’ disease, which can be interpreted as markers of an impaired cardiac neural regulatory mechanism.1,2 The aim of this study was to determine whether cardiac autonomic regulation plays a role in the onset of life-threatening arrhythmias in patients with Chagas’ disease by analyzing the HR dynamics before the onset of ventricular tachyarrhythmia events in patients with Chagas’ heart disease who experienced spontaneous ventricular tachycardia (VT) or ventricular fibrillation (VF) events after receiving an implantable cardioverter-defibrillator. • • • The study group consisted of 17 subjects with a diagnosis of Chagas’ heart disease seen at the Fundacion Cardiovascular del Oriente Colombiano, Bucaramanga, Colombia, who experienced spontaneous episodes of sustained VT and VF during a 1-year period after receiving an implantable cardioverter-defibrillator. Chagas’ heart disease was defined by a combination of epidemiologic, serologic, and clinical criteria. These included a history of residence in an endemic area, 2 positive serologic test (enzyme-linked immunosorbent assay, hemaglutination test) for Trypanosoma cruzi, a clinical syndrome compatible with Chagas’ heart disease and no evidence of another cardiac disorder to which the findings could be attributed. Two-dimensional echocardiographic and electrophysiologic studies were performed in all patients. All patients had clinical VT or VF and fulfilled generally accepted indications for implantation of a cardiac defibrillator.3 RR intervals preceding the arrhythmic episodes, including 1,000 RR intervals before the onset of VT or VF, were stored in the defibrillator’s memory. Most episodes were interrogated within the first 48 hours after the defibrillator had delivered therapy, and a similar period of RR intervals was also recorded during the control clinical visit 48 hours to 1 month after each VT or VF event. Data were downloaded from the defibrillator memory and transferred to a computer for further analysis of HR variability. The memory-retrieved right ventricular electrograms were visually analyzed to differentiate between VT and VF according to the regularity, morphology, and rate of the RR intervals. After the data were transferred to the computer, the RR intervals were edited manually and artifacts as well as ectopic beats were deleted. The details of this analytic technique have been described previously.4 The mean cycle length of all RR intervals and the SD of all RR intervals (SDNN) were computed as time domain measures from the entire recording period. The power spectra were quantified by measuring the area in 2 frequency bands: 0.04 to 0.15 Hz (low frequency) and 0.15 to 0.4 Hz (high frequency).4,5 To quantify fractal correlation properties of HR, the detrended fluctuation analysis technique was used. The method has been validated for time series data and quantifies the presence or absence of fractal correlation properties.6,7 In this method the root-meansquare fluctuation of integrated and detrended time series is measured at each observation window and plotted against the size of the observation window on a log-log scale. The signal with 1/f spectrum results in an exponent value 1.0. White Gaussian noise (random signal) results in an exponent value of 0.5 and the Brownian noise signal (1/f signal spectrum) and an exponent value of 1.5. In this study, HR correlation properties were defined separately for short-term (,11 beats, a1) and for intermediate-term (.11 beats, a2) correlations of RR interval data (shortand intermediate-term scaling exponents).6,7 The results are expressed as means 6 SD unless otherwise indicated. Repeated measurements analysis of variance followed by post hoc comparisons between the groups were used to compare clinical control visit and arrhythmic events (SPSS for Windows release 9.0, Chicago, Illinois). A p value ,0.05 was considered significant. In the light of KolmogorovSmirnov tests (z value .1.0), a logarithmic transforFrom the Division of Cardiology, Department of Medicine, University of Miami School of Medicine, Miami, Florida; Division of Cardiology, Department of Medicine, University of Oulu, Oulu, Finland; and Department of Cardiology and Cardiovascular Sciences, Fundacion Cardiovascular del Oriente Colombiano, Bucaramanga, Colombia. This study was supported in part by Grant 6566–04–788–98 provided by COLCIENCIAS (Colombian Institute for the Advancement of Science and Technology) to Dr. Morillo, by funds provided by the Cardiovascular Research Center at the Fundacion Cardiovascular del Oriente Colombiano-Instituto del Corazon, Bucaramanga, Colombia, and by grants from the Medical Council of Academic of Finland, the Finnish Foundation for Cardiovascular Research and Finnish Medical Foundation, Helsinki, Finland. Dr. Morillo’s address is: Department of Cardiology and Cardiovascular Sciences, Fundacion Cardiovascular del Oriente Colombiano, Calle 155 A No. 23-58, Bucaramanga, Colombia. E-mail: cmorillo@fcv.org. Manuscript received August 1, 2000; revised manuscript received and accepted December 5, 2000.