Acute resumption of conduction in the cavotricuspid isthmus after catheter ablation in patients with common atrial flutter. Real-time evaluation and long-term follow-up.

AIMS: Cavotricuspid isthmus conduction (CIC) is closely associated with the maintenance and recurrence of common atrial flutter (AFL). This study systematically sought to assess the prevalence and characteristics of acute CIC recovery during AFL ablation and to define its predictors and its relationship with the results of long-term follow-up. METHODS AND RESULTS: A total of 124 consecutive patients (105 men, 19 women, mean age 58 +/- 11 years) who underwent successful AFL ablation were included. The procedure endpoint was defined as complete bi-directional CIC block. During an observation period of 30 min, the incidence of CIC restoration was 34.% in patients and 39.8% in applications. It increased with increasing block time and decreased over time during the observation period. Block time in successful burns followed by persistent block was shorter than in those followed by CIC resumption (12 +/- 6 vs 33 +/- 12 s, P<0.0001). A negative correlation between block time and resumption time was found (r = - 0.57, P<0.001). Patients with permanent pacemakers had a higher incidence of acute CIC resumption than those without pacemakers (5/7 vs 29/117, P = 0.007). The AFL recurrence rate was 4.8% during a mean follow-up period of 21 +/- 8 months. Our results suggest that acute CIC resumption may be a potential risk for clinical AFL recurrence during long-term follow-up. CONCLUSIONS: Acute CIC resumption in common AFL ablation varies in terms of incidence and time course. Block time has a predictive value for acute CIC recovery. Observation time can be shortened if block time is short. With longer block time, it is essential to observe for a longer period in order to minimize CIC resumption.

[Atrial flutter--diagnosis and therapeutic possibilities]. / Atrieflutter--diagnostikk og behandlingsmuligheter.

BACKGROUND: Atrial flutter and atrial fibrillation are among the most common heart rhythm disturbances in the population, with an assumed prevalence of 1-2%. About 40,000-60,000 Norwegians endure such rhythm disorders, with an increasing occurrence in the elderly population. MATERIAL AND METHODS: Surface ECG remains the corner-stone for the clinical diagnosis. We describe the various mechanisms, clinical presentation, and diagnosis based on modern invasive electrophysiological methods of atrial flutter. RESULTS: The available therapeutic modalities for conversion during episodes and prophylaxis with drugs, various pacing techniques, DC conversion and surgical therapy are discussed. INTERPRETATION: Radiofrequency catheter ablation is the only available method to cure the patient in a gentle manner.

[Radiofrequency catheter ablation of atrial flutter]. / Radiofrekvenskateterablasjon av atrieflutter.

BACKGROUND: The anatomical structure of atrial flutter is now well recognized, and treatment with radiofrequency catheter ablation (RFA) is established. Several recording and ablation techniques can be applied. MATERIAL AND METHODS: An increasing number of patients have been treated with RFA at the Arrhythmia Centre at Haukeland University Hospital over the last six years. During the two-year period 1999 and 2000, a total of 108 procedures were performed for atrial flutter in a total of 84 patients. A total of 543 RFA procedures for various forms of re-entry tachycardias were performed during the same period; hence, atrial flutter comprised about 20% of RFA procedures. Altogether 71 men and 14 women with a mean age of 57 +/- 12 years were treated. The mean history of atrial flutter had a duration of nine years, maximum 43 years with several hospital admissions, drug trials, overdrive pacing and DC conversion until they were ultimately cured with RFA. RESULTS: The success rate during first time treatment was 96.5%. No serious complications were observed. INTERPRETATION: RFA should be the treatment of first choice in patients with recurrent or incessant atrial flutter.

RV function in stable and unstable VT: is there a need for hemodynamic monitoring in future defibrillators?

During electrophysiological investigation of 22 patients with VT or aborted sudden cardiac death, arterial and RV pressures were measured. The time courses of mean arterial pressure (MAP), RV pulse pressure (RVPP), RV pulse pressure integral (RVPPI), and maximum right ventricular dP/dt (RV dP/dtmax) were followed during the first 15 seconds after VT induction. Compared to basal (preinduction) conditions, the RVPPI decreased by 41+/-10% (mean +/- SD) after 10-15 seconds of VT in 11 patients with stable VT and by 75+/-8% in 11 patients with unstable VT (MAP < 60 mmHg 15 s after VT onset). RVPP decreased by 13+/-11% after 10-15 seconds of VT in the stable VT group and by 50+/-16% in the unstable VT group. For RV dP/dtmax, these decreases were 4+/-22% in the stable VT group and 37+/-24% in the unstable VT group. There was a good correlation between percent decrease in MAP and percent decrease in RVPPI, RVPP, and RV dP/dtmax at 5-10 seconds (r = 0.86, 0.81, and 0.73, respectively) and 10-15 seconds (r = 0.84, 0.82, and 0.69, respectively) after VT onset. There was hardly any overlap of distributions of the individual values with the RVPPI parameter between the two VT groups. Comparing and correlating the percent decrease in mean arterial pressure with the RVPPI, RVPP, and RV dP/dtmax during induced VT, RVPPI demonstrated the most significant and specific changes in discriminating stable from unstable rhythms. However, by comparing RVPPI and RVPP using the area under the receiver operating characteristic curves, there was no significant statistical difference between the two parameters. By integrating rate criteria, electrogram signal analysis, and RVPPI or RVPP as a hemodynamic criterion, detection and treatment algorithms could improve the performance of future implantable defibrillators and avoiding shocks in VTs that can be terminated by antitachycardia pacing.

A typical P-wave morphology in incessant atrial tachycardia originating from the right upper pulmonary vein.

Automatic atrial tachycardias often originate from the ostia of the pulmonary veins. P-wave morphology during tachycardia may indicate from which pulmonary vein the tachycardia originates. Two patients with pulmonary vein tachycardias demonstrating atypical P-wave morphology were investigated. One of the patients had a tachycardia with two different cycle lengths. P-wave morphology was evaluated in 12-lead ECGs from two patients with incessant atrial tachycardia, during tachycardia and sinus rhythm. Their tachycardias were successfully ablated at the mouth of the right upper pulmonary vein. Previous studies have demonstrated a positive or negative P-wave configuration in lead aVL originating from this area and a change from a biphasic P-wave in V1 during sinus rhythm to a positive P-wave configuration during tachycardia. Neither of our two patients had such a change in lead V1. One our patients had two tachycardias with different cycle lengths originating from the same area. It is concluded that if an atrial tachycardia with P-wave morphology resembling that of sinus rhythm cannot be located to the right atrium, its origin may be the right upper pulmonary vein.

An algorithm for automatic measurement of stimulation thresholds: clinical performance and preliminary results.

We have developed an algorithmic method for automatic determination of stimulation thresholds in both cardiac chambers in patients with intact atrioventricular (AV) conduction. The algorithm utilizes ventricular sensing, may be used with any type of pacing leads, and may be downloaded via telemetry links into already implanted dual-chamber Thera pacemakers. Thresholds are determined with 0.5 V amplitude and 0.06 ms pulse-width resolution in unipolar, bipolar, or both lead configurations, with a programmable sampling interval from 2 minutes to 48 hours. Measured values are stored in the pacemaker memory for later retrieval and do not influence permanent output settings. The algorithm was intended to gather information on continuous behavior of stimulation thresholds, which is important in the formation of strategies for programming pacemaker outputs. Clinical performance of the algorithm was evaluated in eight patients who received bipolar tined steroid-eluting leads and were observed for a mean of 5.1 months. Patient safety was not compromised by the algorithm, except for the possibility of pacing during the physiologic refractory period. Methods for discrimination of incorrect data points were developed and incorrect values were discarded. Fine resolution threshold measurements collected during this study indicated that: (1) there were great differences in magnitude of threshold peaking in different patients; (2) the initial intensive threshold peaking was usually followed by another less intensive but longer-lasting wave of threshold peaking; (3) the pattern of tissue reaction in the atrium appeared different from that in the ventricle; and (4) threshold peaking in the bipolar lead configuration was greater than in the unipolar configuration. The algorithm proved to be useful in studying ambulatory thresholds.

Clinical performance of steroid-eluting pacing leads with 1.2-mm2 electrodes.

To raise pacing impedance and reduce battery current drain, new tined steroid-eluting leads were developed with 1.2-mm2 hemispherical electrodes, instead of conventional 5-8 mm2. Twenty-two unipolar J-shaped atrial leads and 25 unipolar ventricular leads (models 4533 and 4033, respectively) were implanted in 33 consecutive patients and followed for a mean of 25 months (range 18-29). Handling characteristics of atrial leads were found favorable. The leads slipped easily into the right atrial appendage and were easy to position. Handling characteristics of ventricular leads were satisfying, but more efforts had to be applied to cross the tricuspid valve. Special care was taken to avoid perforation of the myocardium due to the small lead tip. Following implantation, four ventricular and one atrial lead exhibited instability of pacing thresholds that resolved spontaneously within 1-3 days of implantation. Except for this, no lead malfunctioned. The reoperation rate was zero. The mean electrogram amplitudes of 15 mV (ventricle) and 4 mV (atrium), and the mean chronic pacing threshold of 0.085 ms at 1.6 V (app. 0.43 V at 0.5 ms) were comparable with the best values seen in the literature on passive fixation leads. The rest of the electrophysiological parameters were enhanced: mean pacing impedances were 984 omega (acute) and 900 Q (chronic), mean slew rates 3.26 V/s (ventricle) and 1.75 V/s (atrium), mean acute voltage threshold at 0.5 ms was 0.25 V, mean current and energy thresholds calculated at 0.5 ms were 260 microA and 32 nJ (acute) and 478 microA and 103 nJ (chronic). The electrical characteristics of these leads provide for increased pacemaker longevity in combination with substantial safety margins for pacing and sensing.

Mini-tip leads: stimulation impedance trends and daily variations

In a clinical study of a unipolar tined porous steroid-eluting lead with the cathode electrode surface area of only 1.2 mm2 (CapSure tm Z models 4533 and 4033, medtronic Inc), a total of 19 leads, ten atrial and nine ventricular, were implanted in 12 patients. Pulse generators capable of automatic measurement and recording of pacing impedance over a long-term period (Thera, Medtronic Inc) were used. The mean impedance during the first six months after implant, with all the leads included, was consientlly 900. Observed daily variations were also consistent, and the six-month average ranged rom 50 to 280 in different leads. The variations were not considered to indicate lead instability.

The acute effects of induced tachycardia on coronary sinus and arterial plasma levels of atrial natriuretic peptide and on arterial catecholamines.

Atrial natriuretic peptide (ANP) was measured in coronary sinus (CS) plasma in seven patients with induced tachycardia. Right atrial pressure (RAP) and femoral artery (FA) levels of ANP, noradrenaline (NA) and adrenaline (A) were measured before and after 5 min with tachycardia. During tachycardia, ANP in CS plasma increased from 381 +/- 273 (mean +/- SD) to 1376 +/- 1191 pmol l-1 (p < 0.0001), and ANP levels in FA plasma from 89 +/- 48 to 231 +/- 151 pmol l-1 (p < 0.005). A significant increase was observed for peak RAP, whereas mean RAP remained unaltered. While no correlation existed between the increase in CS plasma ANP level and RAP, significant correlations were found between the changes in FA plasma ANP and RAP, and between FA plasma levels of ANP and NA. Following tachycardia, significant correlations were found both between ANP in CS and FA plasma and between the changes in these plasma levels. Whereas the changes in FA plasma levels of ANP during tachycardia seems dependent of RAP and arterial plasma levels of NA, the CS plasma ANP level appears to be independent of the two factors, probably because CS plasma ANP are drained mainly from the left side of the heart.

[Treatment of ventricular tachyarrhythmias with an implantable pacemaker-cardioverter-defibrillator]. / Behandling av ventrikulaere takyarytmier med implanterbar pacemaker-kardioverter-defibrillator.

During the period from November 1989 to January 1992, 17 patients with ventricular tachyarrhythmias received an implantable pacemaker-cardioverter-defibrillator. The material consists of three female and 14 male patients with an age range of 13-66 years, mean 50.8 +/- 16.6 years. 13 patients had coronary artery disease, one cardiomyopathy, one a myocarditis sequela and two primary rhythm disorder. Four patients received epicardial and 13 endocardial electrode systems. The observation period varied from 4-30 months (april 1992), mean 15.2 +/- 8.8 months. 11 out of 17 patients (65%) experienced one or more episodes of tachyarrhythmias which was treated successfully with overdrive pacing (ramp or burst), cardioversion or defibrillation. One patient died of heart failure after an observation period of 13 months. His pacemaker-cardioverter-defibrillator had been activated more than 100 times. Two children, 13 and 15 years, were treated successfully for ventricular fibrillation four and five months after implantation of the device. The actual one year survival is 100%. Assuming that therapy with a device had not taken place, and that the six patients who experienced episodes of ventricular fibrillation died, the hypothetical probability of survival would have been 62.1 +/- 12.3%.

[Sudden cardiac death]. / Plutselig hjertedøod.

Sudden cardiac death is instant unexpected death that occurs within one hour of an abrupt change in a person's stable clinical state. The mechanism is generally a ventricular tachyarrhythmia. The underlying pathology is usually coronary heart disease. In 1990, 18 patients who survived sudden cardiac death, excluding those with acute myocardial infarction, were evaluated and treated in our institution. 15 patients had coronary heart disease, one had hypertrophic cardiomyopathy, one had dilated cardiomyopathy and one had a replaced aortic valve. Evaluation included heart catheterization and electrophysiological examination. Treatment was specifically tailored to each patient according to etiology, results of all tests and the patient's prognostic factors. Treatment included a permanent pacemaker-cardioverter-defibrillator, antiarrhythmic drug therapy, aortocoronary bypass and betablocker therapy.

Electrophysiologic and clinical effects of flecainide for recurrent paroxysmal supraventricular tachycardia.

The antiarrhythmic effects of flecainide acetate were evaluated in 9 patients with paroxysmal atrioventricular (AV) nodal tachycardia and 17 patients with AV tachycardia. An electrophysiologic study was performed before and after intravenous flecainide acetate, 2 mg/kg body weight, was infused over 15 minutes and was followed by a maintenance infusion of 1.6 mg/kg given over 1 hour to 26 patients and during oral treatment to 15. Treatment with oral flecainide acetate was continued for 14 +/- 5 months. Intravenous flecainide acetate terminated AV nodal tachycardia by blocking the retrograde fast pathway conduction in 7 of 7 patients and AV tachycardia by blocking retrograde conduction in the extranodal pathway in 10 of 10 patients. AV nodal tachycardia and AV tachycardia were noninducible in 8 of 9 patients (90%, p less than 0.001) and 11 of 17 patients (65%, p less than 0.001), respectively. Long-term treatment with oral flecainide acetate suppressed AV nodal tachycardia and AV tachycardia in 8 of 9 patients (90%, p less than 0.001) and 11 of 17 patients (65%, p less than 0.001), respectively. A favorable outcome was associated with block in the accessory pathway after intravenous flecainide acetate and noninducibility during oral treatment. Recurrences preferentially occurred in the younger patients. Flecainide acetate is effective in the acute and long-term management of paroxysmal supraventricular reentry tachycardia by suppressing conduction through the retrograde fast limb of the tachycardia circuit. The clinical effect can be predicted by electrophysiologic testing.

Left main or proximal left anterior descending coronary artery disease: detection by echocardiographic evaluation of interventricular septal function during exercise.

Forty patients with coronary artery disease were studied prospectively to investigate whether stenosis of the left main (LMCA) or left anterior descending coronary artery, proximal to the first septal branch (proximal LAD), could be detected by M-mode echocardiography during exertion. The interventricular septum was visualized in 30 of the patients during bicycle exercise in the semisupine position, all with simultaneous occurrence of electrocardiographic evidence of myocardial ischaemia. Fifteen of these had LMCA or proximal LAD stenosis. Systolic motion and thickening of the septum decreased significantly from rest to peak exercise in patients with LMCA or proximal LAD disease while it increased in those without. The results suggest that M-mode echocardiography during exercise in patients with coronary artery disease might identify those with LMCA or proximal LAD stenosis.

One year's treatment with propranolol after myocardial infarction: preliminary report of Norwegian multicentre trial.

A prospective, randomised, double-blind study was performed to compare the effects of propranolol and placebo on sudden cardiac death in a high-risk group of patients who survived acute myocardial infarction. Altogether 4929 patients with definite acute myocardial infarction were screened for inclusion: 574 (11.6%) died before randomisation, and 3795 (77%) were excluded. Five hundred and sixty patients aged 35 to 70 years were stratified into two risk groups and randomly assigned treatment with propranolol 40 mg four times a day or placebo. Treatment started four to six days after the infarction. By one year there had been 11 sudden deaths in the propranolol group and 23 in the placebo group (p less than 0.038, two-tailed test analysed according to the "intention-to-treat" principle). Altogether there were 25 deaths in the propranolol group and 37 in the placebo group (P less than 0.12), with 16 and 21 non-fatal reinfarctions respectively. A quarter of the patients were withdrawn from each group. Withdrawal because of heart failure during the first two weeks of treatment was significantly more common among propranolol-treated patients than among the controls, but thereafter the withdrawal rate was the same. The significant reduction in sudden death was comparable with that after alprenolol, practolol, and timolol, which suggests that the mechanism of prevention is beta-blockade rather than any other pharmacological property of the individual drugs.