[TEE-guided cardioversion in patients with atrial fibrillation without previous anticoagulation]. / TEE-geführte Kardioversion bei Patienten mit Vorhofflimmern ohne vorherige Antikoagulation.

A total of 332 patients (mean age 65+/-10 years, 86 female) with nonvalvular atrial fibrillation (AF) of more than 48 hours duration and lack of a sufficient anticoagulation were included. After exclusion of thrombotic material in the left atrium using transesophageal echocardiography (TEE) cardioversion (CV) was performed within 24 hours. At the same time oral anticoagulation (AC) (overlapping with PTT-affecting heparinisation) was started. If thrombi were found by TEE, the examination was repeated after at least four weeks of anticoagulation. If thrombi were absent at this time, CV was performed. Periprocedural embolism was defined as primary endpoint, whereas the detection of atrial thrombi before CV was defined as secondary endpoint. In 33 of the 332 Patients (9.9%) the TEE showed a thrombus in the left atrium respectively the left atrial appendage (n=22) or thrombi could not be excluded (n=11). 383 TEEs were performed without complications in an overall of 332 patients.A total of 305 CV were performed (electrical n=300, pharmacological n=5) and during periprocedural monitoring and in the time of four weeks after CV no thromboembolic complications were observed.TEE-guided CV in patients with AF persisting for more than 48 hours and without previous AC can be considered as a method that is both safe and effective.

Maintenance of sinus rhythm after electrical cardioversion of persistent atrial fibrillation; sotalol vs bisoprolol.

AIMS: The purpose of the study was to compare the efficacy and safety of sotalol and bisoprolol in the maintenance of sinus rhythm after electrical cardioversion of atrial fibrillation. METHODS: Patients (n=128) were randomized to sotalol (80 mg b.i.d.) or bisoprolol (5 mg x day(-1)). Patients with contraindications to beta-blockers, class III antiarrhythmic drugs or prior treatment with use of study medication for prevention of atrial fibrillation were excluded. Follow-up clinical evaluation was performed 1 day and 1 month after cardioversion and thereafter at 3-month intervals. RESULTS: There were no group differences in baseline clinical characteristics. After a follow-up of 12 months, 59% of all patients were still in sinus rhythm. The fraction remaining in sinus rhythm was calculated for the two groups by Kaplan--Meier analysis. During follow-up, 41% of patients on sotalol and 42% on bisoprolol developed atrial fibrillation (ns). In two patients (3.1%) on sotalol, life-threatening proarrhythmias (torsade de pointes tachycardias) occurred, whereas none were found in the bisoprolol group. Symptomatic bradycardias occurred in two patients on sotalol and three on bisoprolol. CONCLUSION: This study demonstrates that sotalol (160 mg x day(-1)) and bisoprolol (5 mg x day(-1)) are equally effective in maintaining sinus rhythm. Because of the side effects of sotalol, bisoprolol seems to be advantageous for maintenance of sinus rhythm after cardioversion of atrial fibrillation.

Value of programmed ventricular stimulation for prophylactic internal cardioverter-defibrillator implantation in postinfarction patients preselected by noninvasive risk stratifiers.

OBJECTIVES: The aim of this prospective study was to evaluate the role of programmed ventricular stimulation (PVS) after noninvasive risk stratification to identify a subgroup of acute myocardial infarction (AMI) survivors considered at risk for ventricular arrhythmias and whether these patients could benefit from internal cardioverter-defibrillators (ICDs). BACKGROUND: The predictive value of noninvasive and invasive risk stratifiers after AMI has been questioned. The question of whether the group of patients with inducible monomorphic ventricular tachycardia (VT) after AMI could profit from ICD implantation is unanswered. METHODS: A consecutive series of 1,436 AMI survivors was screened noninvasively by Holter monitoring, heart rate variability, ventricular late potentials, and ejection fraction. A subgroup of 248 patients (17.3%) were identified as high-risk patients and scheduled for PVS. Due to the study design, 54 patients >75 years were excluded; thus, 194 patients were eligible for PVS. Triple extrastimuli at two paced cycle lengths (600 ms and 400 ms) were applied. RESULTS: In a subgroup of 98 (51%) high-risk patients, PVS was performed; 21 patients had an abnormal response, and in 20 patients an ICD was implanted. During a mean follow-up of 607 days the arrhythmic event rate (sudden cardiac death, symptomatic VT, cardiac arrest) was 33% with a positive electrophysiological test versus 2.6% (p < 0.0001) with a negative electrophysiological test. A subgroup of 96 high-risk patients declined electrophysiological study. In this nonconsent group, cardiac mortality (combined sudden and nonsudden) was significantly higher (log-rank chi-square 9.38, p = 0.0022, relative risk 4.7, 1.6 to 13.9) compared to the group guided by electrophysiological testing and consecutive ICD implantation. CONCLUSIONS: After a two-step risk stratification, PVS is helpful in selecting a subgroup of AMI survivors without spontaneous ventricular arrhythmias who benefit from prophylactic ICD implantation.

Effects of implantable cardioverter defibrillator implantation and shock application on biochemical markers of myocardial damage.

BACKGROUND: Implantable cardioverter defibrillator (ICD) implantation is a common approach in patients at high risk of sudden cardiac death. To check for normal function, it is necessary to test the ICD. For this purpose, repetitive induction and termination of ventricular fibrillation by direct current shocks is required. This may lead to minor myocardial damage. Cardiac troponin T (cTnT) and I (cTnI) are specific markers for the detection of myocardial injury. Because these proteins usually are undetectable in healthy individuals, they are excellent markers for detecting minimal myocardial damage. The objective of this study was to evaluate the effect of defibrillation of induced ventricular fibrillation on markers of myocardial damage. METHODS: This study included 14 patients who underwent ICD implantation and intraoperative testing. We measured cTnT, cTnI, creatine kinase MB (CK-MB) mass, CK activity, and myoglobin before and at definite times after intraoperative shock application. RESULTS: Depending on the effectiveness of shocks and the energy applied, the cardiac-specific markers cTnT and cTnI, as well as CK-MB mass, showed a significant increase compared with the baseline value before testing and peaked for the most part 4 h after shock application. In contrast, the increases in CK activity and myoglobin were predominantly detectable in patients who received additional external shocks. CONCLUSIONS: ICD implantation and testing leads to a short release of cardiac markers into the circulation. This release seems to be of cytoplasmic origin and depends on the number and effectiveness of the shocks applied.

The recording of monophasic action potentials with fractal-coated iridium electrodes in humans.

The present study was designed to evaluate the feasibility of the recording of monophasic action potentials (MAP) with fractal-coated iridium electrodes in a clinical setting. In 18 patients who underwent an electrophysiological study for various arrhythmias, we performed MAP recordings with both 1.3-mm2 and 6-mm2 tip surface area fractal-coated iridium and standard silver--silver chloride (Ag/AgCl) electrodes in the high right atrium and two ventricular positions. Amplitude and MAP duration at 90%, 50%, and 25% of repolarization were calculated during steady-state pacing at 600, 500, and 400 ms cycle lengths with extrastimuli application. Morphology comparisons of MAP signals recorded with both types of electrodes were performed by regression analysis using 5% of the repolarization segments of the MAP trajectory. Differences between MAP duration at 90%, 50%, and 25% of repolarization recorded with fractal-coated and Ag/AgCl electrodes were statistically insignificant. Amplitude values recorded with 6-mm2 tip electrodes were significantly smaller than those recorded with Ag/AgCl electrodes for all comparisons. During steady-state pacing, the correlation coefficients between Ag/AgCl and fractal-coated 1.3-mm2 and 6-mm2 tip electrodes were within the range of 0.93-0.999 and 0.87-0.999, respectively. The correlation of MAP amplitude and duration at 90%, 50%, and 25% of repolarization following the extrastimulus S2, recorded with both types of electrodes, was significantly weaker for right atrial recordings (r value range 0.78-0.92) as compared to ventricular recordings (r value range 0.92-0.99). The MAP sensing features of fractal-coated iridium and Ag/AgCl electrodes are comparable. The best results for recording of MAPs with fractal-coated electrodes can be achieved with small surface area tip electrodes.

Marked reduction in atrial defibrillation thresholds with repeated internal cardioversion.

OBJECTIVES: This study was performed to assess the atrial defibrillation threshold in patients with recurrent atrial fibrillation (AF) using repeated internal cardioversion. BACKGROUND: Previous studies in patients with chronic AF undergoing internal cardioversion have shown this method to be effective and safe. However, current energy requirements might preclude patients with longer-lasting AF from being eligible for an implantable atrial defibrillator. METHODS: Internal shocks were delivered via defibrillation electrodes placed in the right atrium (cathode) and the coronary sinus (anode) or the right atrium (cathode) and the left pulmonary artery. After cardioversion, patients were orally treated with sotalol (mean 189 +/- 63 mg/day). Eighty consecutive patients with chronic AF (mean duration 291 +/- 237 days) underwent internal cardioversion, and sinus rhythm was restored in 74 patients. Eighteen patients underwent repeated internal cardioversion using the same electrode position and shock configuration after recurrence of AF (mean duration 34 +/- 25 days). RESULTS: In these 18 patients, the overall mean defibrillation threshold was 6.67 +/- 3.09 J for the first cardioversion and 3.83 +/- 2.62 J for the second (p = 0.003). Mean lead impedance was 55.6 +/- 5.1 ohms and 57.1 +/- 3.7 ohms, respectively (not significant). For sedation, 6.7 +/- 2.9 mg and 3.9 +/- 2.2 mg midazolam were administered intravenously (p = 0.003), and the pain score (0 = not felt, 10 = intolerable) was 5.1 +/- 1.9 and 2.7 +/- 1.8 (p = 0.001). Uni- and multivariate analyses revealed only the duration of AF before cardioversion to be of relevance, lasting 175 +/- 113 days before the first and 34 +/- 25 days before the second cardioversion in these 18 patients (p = 0.002). CONCLUSIONS: If the duration of AF is reduced, a significant reduction in defibrillation energy requirements for internal cardioversion ensues. This might extend the group of patients eligible for an implantable atrial defibrillator despite relatively high initial defibrillation thresholds.

Initial experience with a new balloon-guided single lead catheter for internal cardioversion of atrial fibrillation and dual chamber pacing.

BACKGROUND: Based on the observation that internal cardioversion (IntCV) of atrial fibrillation is effective with electrodes in the right atrium and pulmonary artery, a new balloon-guided catheter and external defibrillation device with optional dual chamber pacing was evaluated. METHODS: IntCV was attempted in 27 patients (age: 57 +/- 10 years, duration: 14 +/- 18 months, left atrial diameter 56 +/- 8 mm) using a new defibrillation device (Alert, EP MedSystems, Inc., NJ, USA) that allows the delivery of biphasic shocks (0.5-15 J, variable tilt), atrial and ventricular pacing, and online signal recording. Pacing and defibrillation shocks were applied via a 7.5 Fr balloon-guided catheter (EP MedSystems, Inc.). Pacing, sensing, and triggering were established through the proximal atrial array and an electrode ring between both defibrillation arrays and a single ventricular electrode ring. Catheters were inserted from the antecubital vein. RESULTS: In 25 of 27 patients sinus rhythm was restored with a mean energy of 6.7 +/- 4.5 J. In five patients, atrial postshock pacing was required for bradycardia and atrial premature beats. The mean fluoroscopy time was 2.0 +/- 1.3 minutes. CONCLUSION: The high success rate, ease of application, and backup dual chamber pacing suggest that this system is an alternative to established methods of cardioversion. In certain indications, such as failure of prior external cardioversion and situations in which a standard pulmonary balloon catheter is needed, this system would be advantageous.

Noninvasive localization of accessory pathways in patients with Wolff-Parkinson-White syndrome with the use of myocardial Doppler imaging.

This study sought to examine the diagnostic accuracy of noninvasive prediction of accessory pathway localization in patients with manifest Wolff-Parkinson-White syndrome with the use of myocardial Doppler imaging as a new noninvasive mapping procedure. Myocardial Doppler imaging measures myocardial velocities and therefore can determine the site of earliest ventricular activation in patients with accessory bypass tracts. Twenty-five patients with manifest preexcitation were studied with the use of pulsed wave and M-mode myocardial Doppler imaging for the evaluation of the shortest electromechanical time interval in 9 basal myocardial segments. The new diagnostic test was compared with 3 electrocardiographic algorithms. An invasive mapping procedure served as reference standard. Abnormally short electromechanical time intervals were found in preexcited segments (27 +/- 12 ms vs 64 +/- 27 ms). Myocardial Doppler imaging correctly localized 84% of the accessory pathways and electrocardiographic algorithms only 48% to 60% of cases. Noninvasive prediction of accessory pathway localization by myocardial Doppler imaging is accurate and proved to be superior to prediction based on electrocardiographic algorithms.

Internal cardioversion of atrial fibrillation with a single lead configuration in a patient with massive diaphragmatic herniation.

An anatomically related circumstance is reported as indication for the internal low energy cardioversion instead of an external approach. A new single lead electrode configuration is described.

Does radiofrequency catheter ablation induce a deterioration in sympathetic innervation? A positron emission tomography study.

Radiofrequency catheter ablation (RFCA) is an effective treatment for the interruption of accessory bypass tracts in WPW syndrome or the modification of the AV-nodal conduction system in patients with AV-nodal tachycardias. However RFCA may also damage cardiac innervation. The purpose of this pilot study was to assess possible changes in sympathetic innervation after RFCA as evaluated by the cathecholamine analog carbon-11-hydoxyephedrine (HED) positron emission tomography (PET) which allows the visualisation of sympathetic nerve terminals. We investigated nine patients with supraventricular tachycardias before and two to six weeks after RFCA. Myocardial perfusion was depicted by n-13-ammonia-PET. In addition to visual analysis, HED retention was quantified in the myocardial quadrant distal to the location of intervention; these results were compared with values in remote areas. Before RFCA, myocardial perfusion showed homogenous distribution in 8 of 9 patients. One patient showed a perfusion defect in the posterior wall. HED retention matched perfusion distribution in all patients. After RFCA there was no significant change observed either in ammonia or in HED distribution. Quantitative HED retention data showed no significant change before versus after RFCA. Thus, HED-PET does not demonstrate any abnormalities of tracer uptake indicating integrity of sympathetic nerve terminals after radiofrequency ablation therapy.

Effect of electrode position on outcome of low-energy intracardiac cardioversion of atrial fibrillation.

The aim of this study was to evaluate the new method of low-energy, catheter-based intracardiac cardioversion in patients with chronic atrial fibrillation (AF) and to compare 2 different lead positions. Accordingly, we prospectively studied 80 consecutive patients with chronic AF (9.8 +/- 7.9 months) who were randomly assigned to undergo internal cardioversion either via defibrillation electrodes placed in the right atrium and coronary sinus (coronary sinus group) or via defibrillation electrodes placed in the right atrium and left pulmonary artery (pulmonary artery group). Intracardiac shocks were delivered by an external defibrillator synchronized to the QRS complex. After conversion, all patients were treated orally with sotalol (mean daily dose, 189 +/- 63 mg/day). For conversion to sinus rhythm, the overall mean energy requirement was 5.6 +/- 3.1 J. In the coronary sinus group, cardioversion was achieved in 35 of 38 patients at a mean energy level of 4.1 +/- 2.3 J (range 1.0 to 9.9), and in the pulmonary artery group in 39 of 42 patients with 7.2 +/- 3.1 J (range 2.5 to 14.8). Although there was no difference with regard to success rate, the energy differed significantly between the 2 groups (p < 0.01). Mean lead impedance was 56.4 +/- 7.0 omega and 54.6 +/- 8.5 omega, respectively (p = NS). No serious complications were observed in either lead group. At a mean follow-up of 14.2 +/- 7.0 months, 54% and 56%, respectively, of patients who had been converted successfully remained in sinus rhythm. Thus, low-energy biphasic shocks delivered between the right atrium and coronary sinus or pulmonary artery are equally effective for cardioversion of patients with chronic AF. The energy requirements for conversion from a pulmonary artery electrode position are higher than for the coronary sinus position.

[Torsade de pointes tachycardia during administration of quinidine and verapamil in atrial fibrillation]. / Torsade-de-pointes-Tachykardie unter Einnahme von Chinidin und Verapamil bei Vorhofflimmern.

The following case report shows that life threatening arrhythmias with fatal consequences may occur after treatment with Cordichin a combination of 80 mg verapamil and 160 mg quinidine. A 65-year-old woman was treated with Cordichin due to atrial fibrillation lasting for 3 months. After the first day of treatment the patient suddenly collapsed with loss of consciousness. The patient was resuscitated 15 min later. The emergency physician diagnosed a cardiac arrest. After cardiopulmonary resuscitation and intubation stable circulation was restored. When the patient was admitted in our hospital the ECG showed numerous ventricular extrasystoles, marked prolongation of the QT interval (700 ms) (Figures 1a and b) and nonsustained polymorphic ventricular tachycardias (Figure 2). The arrhythmias could be suppressed by right ventricular stimulation after inserting a pacemaker lead. After a period of 12 h a normal QT interval was restored (Figure 3). Unfortunately the patient died 3 days later due to irreversible cerebral damage. The concept of suppressing proarrhythmic effects of quinidine by calcium antagonists is discussed. Despite theoretical advantages of a combination therapy this case report shows that life threatening dysrhythmias cannot be prevented by additional calcium antagonism.

Initial experience with implantation of internal cardioverter/defibrillators under local anaesthesia by electrophysiologists.

This study was designed to evaluate the implantation of internal cardioverter/defibrillators under local anaesthesia by electrophysiologists and to compare this to our former experience of implants with general anaesthesia. Forty-seven internal cardioverter/defibrillators were implanted at our institution by electrophysiologists. Twenty-nine operations were performed under general anaesthesia (isoflurane 0.4-0.6%), and 18 under local anaesthesia (mepivacain 1%). The defibrillator leads were introduced by venotomy of the cephalic vein (n = 25), puncture of the subclavian vein (n = 17) or both (n = 5). All devices were implanted beneath the pectoral muscles. The mean operation time was 99 +/- 29 min. In the group with local anaesthesia the operation time was significantly shorter than with general anaesthesia (86 +/- 20 min vs 107 +/- 31 min; P = 0.027). The defibrillation threshold with biphasic shock application was below 24 J in all patients; thus, the implantation of an additional subcutaneous patch electrode was unnecessary. There were no major complications in either group. However, modifications were required in four patients: in one a set screw had to be re-tightened after delivery of an erroneous shock in the early postoperative phase; in another, device migration occurred several weeks after implantation, but no therapeutic intervention was required; in another, a rise in pacing threshold and partial sensing loss were noted ten days postoperatively; in the fourth, a minor pneumothorax occurred after subclavian puncture, but no further treatment was necessary. There was no intra-operative or postoperative mortality in either group. Implantation of internal cardioverter/defibrillators under local anaesthesia and mild sedation is feasible, and can be safely performed by electrophysiologists experienced in basic surgery. The newly developed smaller devices allow implantation in the subpectoral region, and with "active can' configuration and biphasic shock application, subcutaneous patch electrodes become unnecessary.

Low energy intracardiac cardioversion after failed conventional external cardioversion of atrial fibrillation.

OBJECTIVES: This study was designed to evaluate the efficacy of intracardiac cardioversion in patients with chronic atrial fibrillation after unsuccessful external cardioversion. BACKGROUND: Previous studies in patients with atrial fibrillation undergoing intracardiac cardioversion have suggested that intracardiac cardioversion is highly effective and safe. However, the characteristics of patients who benefit most from this invasive technique are unknown. METHODS: We prospectively studied 25 consecutive patients with chronic atrial fibrillation (11 +/- 9 months). All patients had undergone at least three attempts at conventional external transthoracic cardioversion by means of paddles in an anteroposterolateral position applying energies up to 360 J without success. Intracardiac shocks were delivered by an external defibrillator through defibrillation electrodes placed in the right atrium and coronary sinus or in the right atrium and left pulmonary artery. After conversion, all patients were treated orally with sotalol (mean 194 +/- 63 mg/day). RESULTS: Internal cardioversion was successful in 22 of 25 patients at a mean defibrillation threshold of 6.5 +/- 3.0 J. Mean lead impedance was 56.4 +/- 7.4 omega. No severe complications were observed. At a mean follow-up of 15 +/- 12 months, 12 (55%) of the patients treated successfully remained in sinus rhythm. CONCLUSIONS: In patients with failed external cardioversion, internal cardioversion offers a new option for restoring sinus rhythm. Intracardiac cardioversion is an effective and safe method and can be easily performed in patients with minimal sedation.

[Radiofrequency ablation in permanent ectopic left atrial tachycardia]. / Radiofrequenzablation bei permanenter ektoper linksatrialer Tachykardie.

HISTORY AND FINDINGS: A 35-year-old symptom-free woman was known since childhood to have an increased resting heart rate (130-150/min). In the ECG there was a negative P in leads I and aVL, with a shortened P-Q interval of 90 ms. Previous treatment with beta-receptor blockers and calcium antagonists had failed. Clinical examination and echocardiography, as well as levels of thyroid hormone were unremarkable. During electrophysiological studies the earliest atrial activity was localised by endocardial leads in the region of the distal coronary sinus and the arrhythmia could not be terminated by atrial over-stimulation. TREATMENT AND COURSE: After transseptal puncture the ablation catheter was introduced into the left atrium and, the exact site of the origin of the atrial tachycardia having been established, radiofrequency ablation of this point was successfully performed. Subsequently the patient was always found to be in stable sinus rhythm at around 80/min. CONCLUSION: To prevent tachycardia-induced cardiomyopathy, radiofrequency ablation can be indicated even in symptom-free patients with atrial tachycardia.

Urinary excretion of proteolyzed alpha1-antitrypsin: specificity, quantitation, and relation to therapy response in patients with acute myeloid leukemia.

During remission induction chemotherapy, a 41-kDa cleavage product of alpha1-antitrypsin (alpha1-AT41) can be found in the urine of patients with acute myeloid leukemia. By using immunoblotting with antibodies against this protein, 27 patients with acute myeloid leukemia were screened for the excretion of this fragment and the amount of alpha1-AT41 compared with treatment response assessed by therapy-induced cytoreduction in the bone marrow and time to reach remission. Patients with acute lymphoblastic leukemia, malignant lymphomas, and solid tumors receiving chemotherapy, patients with nonmalignant diseases like sepsis and kidney dysfunction, and healthy subjects were probed to evaluate the specificity of this phenomenon. In 74% of the acute myeloid leukemia patients, the truncated inhibitor was detected. Mean concentration of peak excretion was found to be 6.7 microgram/mg creatinine (range, 1.1-41 microgram/mg). Among the patients treated with induction chemotherapy, those who responded completely (<5% residual marrow blast cells) exhibited significantly higher alpha1-AT41 concentrations than the nonresponders (P < 0.03). Patients who showed a partial response (6-25% residual blasts) excreted intermediate values of the protein. The probability of median time to reach remission was 40 days in patients excreting the truncated inhibitor in measurable amounts compared to 100 days in patients negative for alpha1-AT41 (P < 0.02). The 41-kDa fragment was also found in one of 10 patients with acute lymphoblastic leukemia and in 3 of 18 lymphoma patients but not in those with solid tumors, infections, or kidney disease or in healthy individuals.

Proteolytic inactivation of alpha 1-proteinase inhibitor in vivo: detection, characterization and quantitation of the main fragment excreted in the urine of leukemia patients.

During the search for a therapy response parameter in patients with acute myeloid leukemia, we observed the appearance of a 41 kDa glycoprotein band in the urines of these patients under therapy. To investigate the nature of this molecule and to develop a specific detection system, the protein was isolated and antibodies were raised. Urines and sera of patients and healthy subjects were screened for crossreacting proteins by immunoblotting. Only the leukemia patients showed the urinary 41 kDa protein plus a 53 kDa band. In all sera, including those from healthy donors, a 53 kDa protein was intensely stained. Isolation of the plasma protein and sequence analysis of the urinary protein revealed that alpha 1-proteinase inhibitor is the crossreacting plasma protein and that the 41 kDa molecule is proteolytically modified alpha 1-PI, which has lost its antitryptic activity. Cleavage occurred in the N-terminal part as well as in the reactive site loop of the inhibitor. The 41 kDa truncated inhibitor was also found in the leukemic blast cells. A densitometric method is described for the quantitation of the molecule in the nanomolar range.