Bibliothek

Notizen: 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.

Notizen: 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)

Notizen: 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)

Notizen: 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.

Notizen: 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.

Notizen: 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)

Notizen: Surgically induced abnormalities in atrial conduction could result in unusual P wave changes. A 31-year-old woman underwent concomitant mitral valve surgery and atrial compartment operation for mitral stenosis and atrial fibrillation (AF). After operation, the AF was successfully converted to sinus rhythm, whereas an unusual electrocardiogram (ECG) with a discrete negative deflection before the T wave in V1 was noted. Electrophysiological study showed a marked conduction delay from the high right atrium (HRA) to the right atrial appendage (RAA) compartment, which resulted in a separation of P waves. The P wave preceding the QRS complex represented the activation of sinus node and the left atrial compartments, and the P at the vicinity of T wave represented the activation of RAA compartment. The conduction from HRA to RAA was worsened on HRA pacing at a faster rate, and improved after isoproterenol infusion. This report demonstrated that conduction across a surgically created isthmus in the atrium could be severely impaired and result in unusual P wave separation. (PACE 2004; 27:547–550)

Notizen: The P wave in the surface ECG represents atrial electrical activation and may be altered in certain pathological conditions. Atrial compartment operation has been used to convert chronic AF to sinus rhythm. However, this procedure may result in changes of impulse conduction in various atrial compartments and alters the P wave morphology. This study sought to elucidate the P wave changes after the atrial compartment operation for AF. Fifteen patients undergoing the atrial compartment operation for chronic AF were studied. In the operation, the atrium was divided into three compartments, namely the left atrium, the atrial septum including sinus and AV nodes, and the right atrial compartment. The anatomic connection between adjacent compartments were preserved at the posterior lower margin of incisions. The surface lead P waves were correlated with intracardiac recording and stimulation in various atrial compartments. Fifteen age- and sex-matched control patients without structural heart diseases were compared. The results showed that patients undergoing the atrial compartment operation had a prolonged P wave duration ( 190 ± 27 vs 95 ± 14  ms, P 〈 0.001 ), a prolonged PR interval ( 207 ± 23 vs 155 ± 20  ms, P 〈 0.001 ), and a shortened PR segment ( 17 ± 19 vs 60 ± 17  ms, P 〈 0.001 ). The increase in P wave duration was primarily due to a conduction delay from the sinus node to the other atrial compartments as the conduction time from the high right atrium to the right atrial appendage was 132 ± 57  ms (vs 21 ± 6  ms for control, P 〈 0.001 ), and the conduction time from the high right atrium to the distal coronary sinus was 140 ± 55  ms (vs 70 ± 15  ms, P 〈 0.001 ). However, the conduction from the high right atrium to the low septal right atrium, which were located in the same compartment, was not impaired. Also, the conduction in the AV node and His-Purkinje system were not impaired. The mean axis of P waves varied greatly, but was not statistically different from that of the control group ( 60 ± 48° vs 52 ± 18° , P 〉 0.05 ). Although the patients undergoing atrial compartment operation had a larger left atrial size, their P wave amplitude was smaller ( 1.0 ± 0.3 vs 1.3 ± 0.3 mm, P 〈 0.01 ), and an increased negative terminal force in V1 was not seen ( 0.02 ± 0.02 vs 0.02 ± 0.01 mm/s, P 〉 0.05 ). Alteration in P wave morphology was seen in 14 patients. All the P waves showed a biphasic configuration with an initial positive and a terminal slurred negative deflection in leads II, III, and aVF. The terminal components represented the activation of right atrial appendage in 5 patients, the left atrium in 1, and the combined activation of right atrial appendage and the left atrium in 8 patients. The P wave morphology suggested that activation of both the right atrial appendage and the left atrial compartments proceeded in a caudocranial direction as a result of the atrial incisions. In conclusion, atrial compartment operation altered the conduction time and direction in the atria and resulted in characteristic P wave changes. (PACE 2003; 26:1864–1872)

Notizen: The purpose of this study was to investigate the atrioventricular AV nodal physiology and the inducibility of AV nodal reentrant tachycardia (AVNRT) under pharmacological autonomic blockade (AB). Seventeen consecutive patients (6 men and 11 women, mean age 39 ± 17 years) with clinical recurrent slow-fast AVNRT received electrophysiological study before and after pharmacological AB with atropine (0.04 mg/kg) and propranolol (0.2 mg/kg). In baseline, all 17 patients could be induced with AVNRT, 5 were isoproterenol-dependent. After pharmacological AB, 12 (71 %) of 17 patients still demonstrated AV nodal duality. AVNRT became noninducible in 7 of 12 nonisoproterenol dependent patients and remained noninducible in all 5 isoproterenol dependent patients. The sinus cycle length (801 ± 105 ms vs 630 ± 80 ms, P 〈 0.005) and AV blocking cycle length (365 ± 64 ms vs 338 ± 61 ms, P 〈 0.005) became shorter after AB. The antegrade effective refractory period and functional refractory period of the fast pathway (369 ± 67 ms vs 305 ± 73 ms, P 〈 0.005; 408 ± 56 ms vs 350 ± 62 ms, P 〈 0.005) and the slow pathway (271 ± 30 ms vs 258 ± 27 ms, P 〈 0.01; 344 ± 60 ms vs 295 ± 50 ms, P 〈 0.005) likewise became significantly shortened. However, the ventriculoatrial blocking cycle length (349 ± 94 ms vs 326 ± 89 ms, NS) and effective refractory period of retrograde fast pathway (228 ± 38 ms vs 240 ± 80 ms, NS) remained unchanged after autonomic blockade. Pharmacological AB unveiling the intrinsic AV nodal physiology could result in the masking of AV nodal duality and the decreased inducibility of clinical AVNRT.

Notizen: General anesthesia is sometimes required during radiofrequency catheter ablation (RFCA) of various tachyarrhythmias because of an anticipated prolonged procedure and the need to ensure stability during critical ablation. In this study, we examine the feasibility of using propofol anesthesia for RFCA procedure. There were 150 patients (78 male, 72 female; mean age 30 years, range 4–96 years) in the study. Electro physiologic study was performed before and during propofol infusion in the initial 20 patients and was performed only during propofol infusion in the remaining 130 patients. In the initial 20 patients, propofol infusion increased the sinus rate and facilitated AV nodal conduction. The accessory pathway effective refractory period, as well as the sinus node recovery time, atrial effective refractory period, and ventricular effective refractory period were not significantly changed. There were 152 tachyarrhythmias in 150 patients (24 atrial flutter, 31 AV nodal reentrant tachycardia, 68 AV reciprocating tachycardia, 12 ventricular tachycardia, and 17 atrial tachycardia). Most (148/152) tachycardias remained inducible after anesthesia and RFCA was performed uneventfully. However, in four of the seven pediatric patients with ectopic atrial tachycardia, the tachycardia terminated after propofol infusion and could not be induced by isoproterenol infusion. Consequently, RFCA could not be performed. Intravenous propofol anesthesia is feasible during RFCA for most tachyarrhythmias except for ectopic atrial tachycardia in children