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Notes: If in Human Atrial Tissue. Introduction: The funny current (If) contributes to phase IV spontaneous depolarization in cardiac pacemaker tissue. Enhanced If activity in myocardial tissue may lead to increased automatically and therefore tachyarrhythmia. We measured the amount of If, activity in the messenger ribonucleic acid (mRNA) in human atrial tissue and correlated the mRNA amount to left atrial filling pressure and atrial fibrillation (AF). Methods and Results: A total of 34 patients undergoing open heart surgery were included (15 men and 19 women, aged 55 ± 10 years). Atrial tissue was obtained from the right atrial free wall, the right atrial appendage, the left atrial free wall, and the left atrial appendage, respectively. The mRNA amount of the If channel was measured by reverse transcription polymerase chain reaction and was normalized to the mRNA levels of glyceraldehyde 3-phosphate dehydrogenase. We found that the If channel mRNA was present at all the atrial sampling sites. A higher left atrial filling pressure, an indicator of congestive heart failure, was associated with a higher If mRNA level (r2= 0.446, P 〈 0.01 by linear regression). We also found that the mRNA amount was significantly higher in patients with AF than in patients without AF (1.68 ± 0.49 vs 1.27 ± 0.43; P 〈 0.05). Age, sex, right atrial filling pressure, left atrial dimension, and left ventricular ejection fraction had no significant effect on the mRNA level. Conclusion: The nRNA of the If, channel is present in the free-wall area and appendage area from both atria. Increased left atrial filling pressure and clinical AF are associated with increased If mRNA level.

Notes: Entrance Site in ILVT. The entrance site of the slow conduction zone was identified by entrainment study in an 18 year-old woman with verapamil-sensitive idiopathic left ventricular tachycardia. Radiofrequency catheter ablation at this site eliminated the tachycardia. The entrance site was at a mid-septal location and was more than 2 cm away from the exit site. Electrophysiologic findings suggested macroreentry in the Purkinje system as the mechanism of idiopathic left ventricular tachycardia.

Notes: 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)

Notes: Bioimpedance During Radiofrequency Catheter Ablation. Introduction: Efficiency of heating (defined as the average temperature divided by the average power) during radiofrequency (RF) catheter ablation (RFCA) can be predicted by the electrode-tissue contact pressure before RFCA. To predict the efficiency of heating during RFCA, we prospectively measured bioimpedance and correlated the bioimpedance with the efficiency of heating in patients undergoing RFCA for supraventricular tachycardias. Method and Results: Of 239 RF applications in 55 patients, bioimpedance was measured from the distal pair of the electrodes of the ablation catheter using an extremely low current (10 μ A at 45 kHz). Tip electrode temperature was measured with a closed-loop RF generator. Efficiency of heating and the difference (Δbioimpedance) between preablation bioimpedance (measured from the target ablation site) and baseline bioimpedance (measured in the right atrium without tissue contact) were calculated. There was significant positive correlation between preablation bioimpedance and efficiency of heating (regression coefficient = 0.053; P = 0.003) and between Δbioimpedance and efficiency of heating (regression coefficient = 0.067; P = 0.003). The highest degree of correlation was found during RFCA of the accessory pathways in the left free wall (regression coefficient = 0.14; P 〈 0.01). With preablation Δbioimpedance 〉 21.5 Ω, applications targeted at the left free-wall, left posteroseptal, or right septal accessory pathways had a greater likelihood of achieving effective tissue heating (defined as maximal temperature achieved 〉 55°C). Conclusion: Both preablation bioimpedance and Δ bioimpedance have positive correlation with efficiency of heating during RFCA of supraventricular tachycardia. Measuring preablation bioimpedance appears to be a useful tool for predicting the efficiency of heating during RFCA.

Notes: Introduction: Functional and structural changes of atrial tissue occur during the natural course of atrial fibrillation (AF), and these changes may contribute to further AF. We investigated the changes in AF tissue using cDNA microarray and two-dimensional protein electrophoresis techniques. Methods and Results: We established a porcine model of AF by rapid right atrial appendage pacing at a rate of 600/min. Atrial tissue was obtained after rapid atrial depolarization for 6 weeks. Microarrays containing 6,035 cDNA clones were used to evaluate the alterations of mRNA. Two-dimensional protein electrophoresis was performed to compare protein patterns. In cDNA microarray studies, we identified 387 genes with significant change in the left atrium and 81 genes in the right atrium. Among the genes, the ventricular isoform of the myosin regulatory light chain (MLC-2V) showed the greatest fold of change (9.4 and 7.3 in the left and right atrium, respectively). In protein electrophoresis, the expression levels of three protein spots spanning from 18 to 20 kDa in the acidic region (PI 4.5–5.0) were specifically elevated in the AF group. Interestingly, through tandem mass spectrometric analysis, these three spots were identified as MLC-2V. Thus, MLC-2V expression at the mRNA and protein levels corresponded well, and both indicated a significant increase in AF. Conclusion: Both cDNA microarray and two-dimensional polyacrylamide protein electrophoresis studies revealed characteristic changes in AF tissue. We demonstrated the reprogramming of myosin regulatory light chain isoform composition, with a significant increase of its ventricular isoform (MLC-2V). (J Cardiovasc Electrophysiol, Vol. 15, pp. 214-223, February 2004)

Notes: Beta-Blocker Therapy and Heart Rate Variability. Introduction: 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 β blockers is unclear. Methods and Results: 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; P 〈 0.05) and the intercept (5.11 ± 0.46 vs 5.62 ± 0.24; P 〈 0.05) 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; P 〈 0.05) 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 P 〉 0.05). 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 (P 〉 0.05). Conclusion: 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.

Notes: Heart Rate Turbulence and Baroreflex Sensitivity. Introduction: 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. Methods and Results: 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 μg/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; P 〈 0.01) and combined autonomic blockade (1.23 ± 1.02 msec/beat; P 〈 0.01) but was unchanged after esmolol (4.53 ± 3.30 msec/beat; P 〉 0.05). Turbulence onset increased after atropine (0.32% ± 0.35% vs −0.45 ± 0.94 at baseline; P 〈 0.05) and combined sympathetic and parasympathetic blockade (0.58% ± 0.86%; P 〈 0.05) but was unchanged after esmolol (−0.62% ± 1.33%; P 〉 0.05). Turbulence slope was positively correlated with baroreflex sensitivity at baseline (r = 0.78, P 〈 0.01) and after esmolol (r = 0.8, P 〈 0.01), but dissociated after atropine (r = 0.16, P 〉 0.05) and combined autonomic blockade (r = 0.31, P 〉 0.05). Turbulence onset was negatively correlated with baroreflex sensitivity at baseline (r =−0.61, P 〈 0.05), after esmolol (r =−0.80, P 〈 0.01), and after atropine (r =−0.53, P 〈 0.05). Conclusion: 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.

Notes: Isthmus-Independent Atrial Flutter. Introduction: We report the electrophysiologic study and radiofrequency catheter ablation of isthmus-independent atrial flutter in 2 patients. The isthmus-independent atrial flutter in these 2 patients had similar ECG and electrophysiologic findings. Both were reproducibly induced by rapid atrial pacing. The atrial activation sequence and entrainment study proved that these atrial flutters were not isthmus-dependent. A high-right atrial site was identified as the critical site of the slow conduction zone of the tachycardia in both. This site showed double potentials and mid-diastolic potentials. Radiofrequency catheter ablation at this site successfully eliminated the isthmus-independent atrial flutter in both patients.