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Notes: The δ- and κ-receptor subtypes are both abundantly expressed in the human heart and participate in age- and stress-related alterations of cardiac function. Opioid receptor agonists mediate cardioprotection in response to ischemic preconditioning via increased intracellular Ca2+ levels, opening mitochondrial KATP channels, and PKC activation. We studied the expression of opioid receptor subtypes κ and δ, and of their ligand precursors, proopiomelanocortin (POMC) and preproenkephalin A (PENKA), in human atrial tissue of patients in sinus rhythm (SR), or persistent atrial fibrillation (AF). The mitochondrial size was also compared between the two groups. The atrial mRNA expression of opioid peptide precursors and receptors was assessed by competitive and real-time RT-PCR in 16 patients in AF and 16 patients in SR. Mitochondria were analyzed in the atrial tissue by electron microscopy in four patients in AF and four patients in SR. Both PENKA (SR: 100 ± 33% vs AF: 33 ± 21%; P 〈 0.05) and κ-receptor mRNA amounts (AF: 78 ± 20% vs SR: 100 ± 11%; P 〈 0.05) were both decreased in AF in comparison to SR. In addition, POMC mRNA levels were decreased in AF (SR: 100 ± 54% vs AF: 37 ± 26%; P 〈 0.05), whereas the expression of the corresponding δ-opioid receptor was unchanged (AF: 102 ± 34% vs 100 ± 44%). Mitochondrial size was increased during persistent AF. Persistent AF is associated with the down-regulation of the opioid receptor/ligand expression. This suggests a loss of protective capacity in the fibrillating atrial tissue, resulting in an ultrastructural remodeling of atrial myocytes.

Notes: GOETTE, A., et al.: Pacing of Bachmann's Bundle After Coronary Artery Bypass Grafting. The purpose of this randomized, prospective trial was to determine if Bachmann's bundle pacing reduces the incidence of AF after CABG. The study included 161 patients with no history of AF who were randomized to three groups. Group 1 included 50 patients as controls. Group 2 included 60 patients who had an epicardial wire placed at the lateral wall of the right atrium. In the 51 patients of group 3, the wire was placed at the Bachmann's bundle. In groups 2 and 3, atrial pacing (AAI 96 beats/min) was initiated immediately after CABG and continued for 5 days. The study endpoint was AF lasting ≥ 1 minute. Baseline clinical parameters were similar in all three groups. The incidence of AF was not reduced by pacing (group 1: 42%; group 2: 48%; group 3: 37%; P = NS). The paced P wave duration was increased in group 2 (129 ± 14 ms vs group 3: 96 ± 21 ms; P 〈 0.05). Paced P wave duration was a risk factor for postoperative AF (odds ratio 1.015; 95% CI 1.0021–1.028; P 〈 0.05). Analysis comparing the pacing groups revealed a reduction in AF during Bachmann's bundle pacing (50 vs 29%; P 〈 0.01). Pacing thresholds were significantly better at Bachmann's bundle compared to group 2. In conclusion, an anatomically guided pacing at the Bachmann's bundle does not reduce the overall incidence of postoperative AF compared to controls. However, the Bachmann's bundle offers favorable capabilities for postoperative atrial pacing, and thus it is a preferable site for electrode placement if postoperative atrial pacing is required.

Notes: BOLLMANN, A., et al.: Electrocardiographic Characteristics in Patients with Nonrheumatic Atrial Fibrillation and their Relation to Echocardiographic Parameters. The aim of this study was to determine the relation between (1) ECG fibrillatory wave amplitude and left atrial diameter and left atrial appendage (LAA) flow velocity using different ECG recording techniques, and (2) ECG fibrillatory frequency and frequency of LAA contractions in patients with nonrheumatic AF. In 36 patients (22 men, 14 women, mean age 61 ± 11 years) with persistent AF, ECG recordings were performed using a standard 12-lead ECG and an orthogonal ECG lead system using a high gain, high resolution ECG. AF was classified as coarse (fibrillatory amplitude ≥ 1 mm) or fine (fibrillatory amplitude 〈 1 mm) in leads I, aVF, V1 and corresponding leads X, Y, and Z. Fibrillatory frequency from the ECG was determined by subtracting averaged QRST complexes and applying a Fourier analysis to the resulting signal. Doppler flow was obtained from LAA during transesophageal echocardiography and LAA emptying velocity was determined. Fourier analysis was also applied to the Doppler signal generating the frequency of LAA contractions. Coarse AF was observed in 0, 9, and 18 patients in leads I, aVF, and V, respectively. It was more often (P 〈 0.05) detected in corresponding leads X (n = 13), Y (n = 31), and Z (n = 23). Fine AF in lead X was associated with a reduced LAA velocity (33 ± 16 cm/s in coarse AF vs 22 ± 13 cm/s in fine AF, P = 0.05). There was neither a relation between AF coarseness in any other ECG lead and LAA flow velocity, left atrial diameter, or echo contrast. In 25 patients with an active LAA flow, the mean frequency of LAA contractions was 6.8 ± 0.8 Hz. The corresponding mean frequency obtained from the ECG was 6.7 ± 0.7 Hz (r = 0.85, P 〈 0.001). The mean difference between these two measures was 0.04 Hz, and the 95% confidence limits were 0.90 and – 0.82 Hz using the Bland-Altman method. In conclusion, AF coarseness and its relation to LAA flow velocity depend on the ECG recording technique used. LAA contractions represent one mechanical correlate of the electrical fibrillatory activity in AF.

Notes: An increase in sinus rate has been previously described in patients with AV node reentry (AVNRT) following successful A V node modification. This increase could either be a specific sign of elimination of slow pathway conduction or it could be a consequence of energy application in the posteroseptal area. Thus, we compared the changes in sinus cycle length following successful slow pathway ablation (defined as complete elimination of dual AV node physiology) in patients having AVNRT with those in patients undergoing successful ablation of a posteroseptal atriovetriricular accessory connection. Twenty five patients (16 women and 9 men, mean age 41 ± 4 years) with typical AVNRT (cycle length 378 ± 12 ms and 29 patients (16 women and 13 men, age 34 ± 5 years) with an accessory connection (17 manifest and 12 concealed) were studied. The electrophysiology study was performed during sedation with Fentanyl and Midazolam. The mean number of energy applications was 3 ± 1 for successful slow pathway ablation and 4 ± 1 for successful ablation of the accessory connection (p:NS). Following the successful energy application, the sinus cycle length decreased significantly 776 ms at baseline to 691 ms in patients with AVNRT. Following successful ablation of the posteroseptal AC, sinus cycle length decreased from 755 ms at baseline to 664 ms (p 〈 0.05 in both groups [difference between groups not significant]). The decrease in sinus cycle length did not correlate with the number ofRF energy applications required for successful ablation or the total energy delivered. In conclusion, ablation of the AV node slow pathway and a posteroseptal accessory connection results in similar increases in the sinus rate. Thus, the increase in sinus rate is probably due to energy application in the posteroseptal space, possibly due to concomitant destruction of vagal inputs, and it is not specific for elimination of slow pathway conduction.

Notes: Ventricular tachyarrhythmias are the most common cause for sudden cardiac death. The success of catheter ablation for supraventricular tachycardias led to the supposition that ablation could also be used in the treatment of ventricular tachycardias. Despite the promising results in bundle branch reentry and some forms of idiopathic ventricular tachycardia, the success rate in patients with coronary artery disease is still low. There is hope that new approaches to reliably localize the critical region of the tachycardia and new ablation techniques to create larger areas of injury may lead to a wider application of ablation therapy in the treatment of ventricular tachycardia. Survivors of cardiac arrest typically have more rapid and unstable arrhythmias than patients with sustained ventricular tachycardia, and these rapid arrhythmias frequently degenerate into ventricular fibrillation. The instability of the arrhythmia makes it impossible to localize the arrhythmia origin with current mapping techniques. Experimental and clinical data, however, suggest that these arrhythmias also frequently start from a localized area of electrical activation. With developments in mapping techniques and energy delivery, catheter ablation may soon become a feasible therapeutic approach in some patients with unstable arrhythmias. The article discusses the prerequisites for this approach and suggests the patients who may be appropriate candidates for this technique.

Notes: The Wearable Cardioverter Defibrillator (WCD) automatically detects and treats ventricular tachyarrhythmias without the need for assistance from a bystander, while at the same time allowing the patient to ambulate freely. It represents an alternative to emergency medical services for outpatient populations with a temporary risk of sudden cardiac death. While the original devices used a monophasic truncated exponential waveform for cardioversion/defibrillation shocks, a new, biphasic shock was developed for the next device generation. In 12 patients undergoing electrophysiological testing for ventricular tachyarrhythmias, termination of electrically induced ventricular fibrillation (VF) was attempted via the WCD. In 22 episodes, induced VF was promptly terminated by the first 70 J (n = 12) or 100 J (n = 10) biphasic shocks. Time between arrhythmia initiation and shock delivery was 22 ± 6 seconds (70 J) and 21 ± 6 seconds (100 J) (P = NS). The measured transthoracic impedance was 71 ± 5 Ω (64–79 Ω) for the 70 J shock and 64 ± 8 Ω (47–72 Ω) for the 100 J shock. The present study demonstrates that a single low energy biphasic shock delivered by the WCD, reliably terminates electrically induced VF (100% of episodes). The results of this study suggest that there is an acceptable safety margin to the maximum output of the device (150 J). Despite our promising data, we recommend that programming all shocks for maximum energy output should be done when using the WCD in ambulatory patients. (PACE 2003; 26:2016–2022)

Notes: Although novel cryoablation systems have recently been introduced into clinical practice for catheter ablation of supraventricular tachycardia, the feasibility of catheter cryoablation of VT is unknown. Thus, the present study evaluates catheter cryoablation of the ventricular myocardium (1) in healthy sheep and (2) of VT in chronic myocardial infarction (MI). In three healthy sheep, 21 ventricular lesions (12 left and 9 right ventricle) were created with a catheter cryoablation system. Different freeze/thaw characteristics were used for lesion creation. The mean nadir temperature was -84.1°C ± 0.9°C, mean lesion volume was 175.8 ± 170.3 mm3, and 5 of 21 lesions were transmural. Lesion dimensions were 7.5 ± 3.1 mm (width) and 4.2 ± 2.5 mm (depth). Left ventricular lesions were significantly larger than right ventricular lesions (262 ± 166 vs 60.5 ± 91.6 mm3, P = 0.0025). There was no difference in lesion volume with respect to different freeze/thaw characteristics. Anatomically (n = 3) or electrophysiologically (n = 3) guided catheter cryoablation was attempted in six sheep 105 ± 56 days after MI, three of six animals had reproducibly inducible VT with a mean cycle length of 215 ± 34 ms prior to ablation. In these animals, five VTs were targeted for ablation. A mean of 6 ± 3 applications for nine left ventricular lesions were applied, six of nine lesions were transmural. The mean lesion volume was 501 ± 424 mm3. No VT was inducible in two of three animals after cryoablation using an identical stimulation protocol. Therefore, catheter cryoablation of VT in healed MI is feasible, and no acute complications were observed.