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Objectives: Interventional elimination of chronic persistent atrial fibrillation (AFib) remains difficult. An animal model mimicking the clinical situation is important. Methods and Results: Twenty-five adult pigs were implanted with a high-speed atrial pacemaker. After continuous pacing at 600 bpm for 6 weeks, 20 (91%) of the 22 survivals developed sustained AFib lasting for at least 24 h. Epicardial dense mapping revealed multiple coexisting reentrant wavelets in the left and the right atrium (LA and RA, respectively; 10.6 ± 2.9 vs. 7.6 ± 2.4 wavelets/cm2/s; p < 0.002). The mean local A-A intervals were 87.2 ± 14.6 ms in the LA and 103.3 ± 19.0 ms in the RA (p < 0.0002). Acute termination of sustained AFib was successful in 3 of the 5 pigs by propafenone, but in none of the 6 by dl-sotalol. Epicardial cryothermal ablation failed to terminate any AFib by compartmentalization of the RA free wall alone (4 pigs) or together with the LA appendage (4 pigs). Electron microscopic examination demonstrated diffuse perinuclear myolysis, myofibrillar fragmentation and mitochondrial crystal disruption in the atrium. Conclusions: Pacing-induced sustained AFib (≧24 h) in adult pigs is a feasible and efficient animal model with electrophysiological and histological characteristics closely similar to those seen in humans.

Introduction: Heart rate turbulence (HRT) is a powerful novel predictor for cardiovascular mortality. Chronic congestive heart failure is associated with abnormal HRT. Whether antiadrenergic beta-blocker therapy can restore control of HRT in patients with chronic congestive heart failure is unknown. Methods and Results: A 24-hour Holter ECG recording was obtained before and 1 and 3 months after titrated addition of atenolol therapy in 10 consecutive patients with advanced congestive heart failure. Two parameters derived from HRT, turbulence slope (TS) and turbulence onset (TO), and time- and frequency-domain heart rate variability (HRV) parameters (SDNN, RMSSD, VLF, LF, HF) from 24-hour ECG were compared before and after beta-blocker therapy, together with the same parameters in age-matched normal control. Results showed that TS (3.1 ± 2.2 vs 6.2 ± 3.0; P = 0.001) and all HRV parameters were increased after 3 months of atenolol treatment. No changes in TO were evident (0.6 ± 0.5 vs −0.2 ± 1.3; P = 0.13). The improvement of TS and the vagally mediated parameters of mean R-R interval, RMSSD, and the HF component of HRV were positively correlated. Conclusion: Abnormal HRT caused by chronic congestive heart failure can be restored by beta-blocker therapy. The evolution of TS was positively correlated with measures of vagal modulation of heart rate. (J Cardiovasc Electrophysiol, Vol. 15, pp. 752-756, July 2004)

Introduction: The aim of the study was to identify an alternative target for more effective radiofrequency catheter ablation (RFCA) of isthmus-dependent atrial flutter (AFL). Methods and Results: We hypothesized that a functional isthmus formed by preexisting double potential barrier at the cavotricuspid isthmus (CTI) could serve as a new target site for facilitating RFCA of AFL. Forty-three consecutive patients with recurrent isthmus-dependent AFL were studied using three-dimensional navigated magnetic mapping and ablation technique. Twenty patients (47%, group A) were shown to have a narrower functional channel at the CTI (functional isthmus). The remaining 23 patients did not have this feature (53%, group B). In group A, double potentials were clustered near the border of the inferior vena cava (IVC) of the CTI and served as a functional channel along the tricuspid annulus (TA). The interspike interval of double potentials was 87 ± 26 ms near the IVC border and 45 ± 17 ms (P < 0.0001) near the TA border of CTI. RFCA targeting at the functional isthmus in group A resulted in interruption of bidirectional transisthmus conduction with fewer radiofrequency pulses (6.7 ± 4.7 in group A vs 21.1 ± 17.1 pulses in group B, P < 0.001), shorter ablation line (11.6 ± 4.0 mm vs 37.8 ± 7.2 mm, P < 0.0001) with no arrhythmia recurrence. These functional isthmuses were found to be located at the lateral third of CTI in 12 patients, middle third in 7, and medial third in 1. This finding is different from that obtained by the conventional method in group B (lateral in 5, middle in 16, medial in 2, P < 0.038). Conclusion: In our study, a functional, rather than anatomic, isthmus formed by preexisting double-potential barrier at the CTI was identified in 47% of patients with isthmus-dependent AFL. It is a useful guide to facilitate RFCA of isthmus-dependent AFL. (J Cardiovasc Electrophysiol, Vol. 15, pp. 396-401, April 2004)

A smooth pseudo Wigner-Ville distribution was employed to investigate both time and frequency characteristics in a very low-frequency component (less than 0.04 Hz) of 24-hour heart rate fluctuation. In some cases of heart failure the authors could see remarkable and very low-frequency oscillations of the Wigner-Ville distribution, which are related to Cheyne-Stokes respiration. However the Wigner-Ville distribution of normal subjects did not have such oscillations, but more random spectral characteristics instead. Furthermore, the authors calculated 1/f/sup /spl alpha// regression slopes of average spectrum to be a crude estimate of fractal dimensions. The slopes are more negative in heart failure patients than normals (-1.866/spl plusmn/0.888 vs. -0.957/spl plusmn/0.180 p

Heart rate turbulence is a powerful de novo risk predictor for patients surviving acute myocardial infarction. However, little is known about its underlying physiologic mechanism.Hypothesizing that heart rate turbulence is barorceptor reflex related, we studied heart rate and blood pressure fluctuations at rest and after systematically introduced ventricular premature beats in 16 patients without structural heart disease (10 men and 6 women; mean age 45 +/- 17 years) before and after sequential sympathetic (esmolol 4-mg bolus followed by 120 microg/kg/min intravenously), parasympathetic (atropine 0.04 mg/kg intravenously), and combined autonomic blockade (esmolol plus atropine). Turbulence onset (%) and turbulence slope (msec/beat) were averaged from 10 respective ventricular premature beats. Spontaneous baroreflex sensitivity (msec/mmHg) was calculated from 5 minutes of sinus rhythm recording. The results showed that turbulence slope decreased after atropine (0.71 +/- 0.50 msec/beat vs 5.17 +/- 3.96 msec/beat at baseline; P0.01) and combined autonomic blockade (1.23 +/- 1.02 msec/beat; P0.01) but was unchanged after esmolol (4.53 +/- 3.30 msec/beat; P0.05). Turbulence onset increased after atropine (0.32% +/- 0.35% vs -0.45 +/- 0.94 at baseline; P0.05) and combined sympathetic and parasympathetic blockade (0.58% +/- 0.86%; P0.05) but was unchanged after esmolol (-0.62% +/- 1.33%; P0.05). Turbulence slope was positively correlated with baroreflex sensitivity at baseline (r = 0.78, P0.01) and after esmolol (r = 0.8, P0.01), but dissociated after atropine (r = 0.16, P0.05) and combined autonomic blockade (r = 0.31, P0.05). Turbulence onset was negatively correlated with baroreflex sensitivity at baseline (r = -0.61, P0.05), after esmolol (r = -0.80, P0.01), and after atropine (r = -0.53, P0.05).Heart rate turbulence of turbulence onset and turbulence slope is critically vagal dependent and highly correlated with spontaneous baroreflex sensitivity, which underscores its clinical importance in cardiovascular risk stratification.

The slope of the power spectrum in heart rate variability (HRV) reflects the fractal or scaling behavior in HR dynamics and recently was confirmed as an independent predictor of postmyocardial infarction survival. Whether or not the new measurement in HRV foresees the functional evolution in patients with advanced congestive heart failure treated by beta blockers is unclear.Sequential 24-hour Holter ECG recordings were obtained at baseline, and 1 and 3 months after addition of atenolol therapy for advanced congestive heart failure in 10 patients. The slope and intercept of the regression line of power-law behavior, the short- and intermediate-term of detrended fluctuated analysis (DFA), the approximate entropy (ApEn), and the standard frequency spectra of the 24-hour HRV were compared sequentially as well as with those in 12 age-matched normal controls. The results showed that the slope (-1.70 +/- 0.45 vs -1.22 +/- 0.21; P0.05) and the intercept (5.11 +/- 0.46 vs 5.62 +/- 0.24; P0.05) of the regression line of power-law behavior and the short-term DFA (for 4 to 11 beats) (0.78 +/- 0.18 vs 1.13 +/- 0.21; P0.05) increased after 3 months of atenolol treatment. However, the change in intermediate-term DFA (11 beats) and ApEn was not apparent (1.24 +/- 0.21 vs 1.22 +/- 0.15 and 1.34 +/- 0.14 vs 1.36 +/- 0.11; both P0.05). The evolution of the slope or intercept of the regression line of the HRV power spectrum did not correlate with the echocardiographic or clinical cardiac function, or with the frequency spectral components of the HRV (P0.05).Additional beta-blocker therapy upregulated the fractal behavior control of the HRV in patients with advanced congestive heart failure. The improvement was independent of subjective and objective global cardiac performance.