Cryoablation as standard treatment of atrial flutter: a prospective, 2-center study (CASTAF).

BACKGROUND: Cryoablation (CRYO) of cavotricuspid isthmus (CTI)-dependent atrial flutter (AFL) has been shown to be non-inferior to radiofrequency ablation (RF) in terms of ablation success and is associated with less pain. However, procedural time has been significantly longer with CRYO compared to RF. A possible explanation for this could be that operators had less experience with CRYO than with RF. The purpose of this study was to test the hypothesis that in the hands of experienced operators, cryoablation of CTI-dependent AFL is effective with procedure-time similar to what is reported for RF. METHODS: This prospective 2-center study included 184 patients with CTI-dependent AFL - median age 66 years (range 28-83), 159 men (86%). Cryoablation was performed using a 9 F, 8 mm tip catheter (Freezor MAX, Medtronic, Inc, MN, USA). Ablation endpoint was bidirectional CTI-block. Pain was evaluated with a visual analogue scale (VAS 0-10). All operators had experience of at least 25 previous CTI-ablations with CRYO. RESULTS: The acute success rate was 89%. Procedural time including an observation period of 30 min, was 115 ± 36 min which is similar to procedural times for RF in previous studies. Fluoroscopy time was 11 ± 9 min. Cryoablation was perceived as almost pain- free by the patients, VAS (mean) 1.8 ± 1.2. Success rate at 12-month follow-up (FU) was 88% in patients with primary success. No major adverse events occurred. CONCLUSIONS: Cryoablation of CTI-dependent AFL is effective, with a low level of procedure-related pain. In experienced hands, the procedure time in this prospective non-randomised trial seems to be in the level of reported procedure times for RF. The long-term relapse rate appears to be higher than for RF.

Elevations in antidiuretic hormone and aldosterone as possible causes of fluid retention in the Maze procedure.

BACKGROUND: Reduced levels of atrial natriuretic peptide (ANP) has been suggested as a cause of fluid retention after combined Maze and valvular surgery. This study aimed to assess hormonal activation in the perioperative setting of isolated Maze procedures. METHODS: Changes in ANP, brain natriuretic peptide (BNP), antidiuretic hormone (ADH), aldosterone, and angiotensin II were measured in 16 patients (mean age 53+/-9 years) without concomitant heart disease undergoing the Maze (III) procedure. Ten matched patients (mean age 56+/-9 years) undergoing multivessel coronary artery bypass grafting served as controls. Measurements with hemodynamic correlates were obtained at baseline and after ventricular pacing (100 stimulations/minute), directly preoperatively, postoperatively and the first postoperative day. Weight gain and diuretic requirements were recorded. RESULTS: The major differences in hormonal response were significantly higher plasma levels of ADH (Maze preoperative 1.1+/-0.4, postoperative 24.9+/-16.7 pmol/L; controls preoperative 1.1+/-0.1, postoperative 3.7+/-3.5 pmol/L) and aldosterone (Maze preoperative 106+/-94, postoperative 678+/-343 pmol/L; controls preoperative 124+/-79, postoperative 171+/-93 pmol/L) in the Maze group on the first postoperative day (p < 0.001). Preoperative baseline plasma levels of ANP and pulmonary capillary wedge pressures (PCWP) were higher in the Maze group but this difference was abolished by pacing, and postoperatively, ANP levels changed in parallel to the PCWP in both groups. Diuretic requirements were significantly higher in the Maze group. CONCLUSIONS: Substantial increases in ADH and aldosterone were observed after the Maze procedure, indicating these hormones as important determinants in postoperative fluid retention. The role for ANP in this setting may be a less prominent than previously reported.

The Maze operation for treatment of atrial fibrillation. Early clinical experience in a Scandinavian institution.

The Maze operation is a potentially curative surgical option in patients with disabling atrial fibrillation (AF) refractory to conventional treatment. The aim of this study was to evaluate the initial 4-year Maze experience in our institution. The study included 26 patients (19 males, mean age 55 years) who had undergone the Maze (III) operation between 1994 and 1998. Nine patients had surgery for concomitant heart disease. Follow-up was 3-55 (median 18) months. No deaths or neurological complications occurred; 22 patients are at present in regular sinus-, or junctional rhythm, 2 patients have permanent atrial pacing for symptomatic sinus node dysfunction, and 2 patients have had persistent AF, post surgery. Sinus node dysfunctions were detected in five patients, though not requiring pacemakers. Out of the total 26 patients, 23 are free of anti-arrhythmic drugs. Echocardiographic signs of left atrial contraction were recorded in 50% of the patients. The Maze operation offers a safe alternative to conventional therapy, with attractive results justifying expansion in the use of this treatment for AF.

[A new surgical technique in atrial fibrillation. The maze procedure restores sinus rhythm]. / Ny hjärtkirurgisk metod vid förmaksflimmer. Maze-operation återställer sinusrytm.

Atrial fibrillation (AF) is a common arrhythmia associated with significant morbidity and increased mortality, partly due to the increased risk of stroke. The maze procedure, introduced by James Cox of the USA, is an internationally established surgical alternative in cases of unsuccessful medical or catheterised treatment of paroxysmal or chronic AF. It is an open heart procedure, involving multiple transmural incisions and continuous suture lines in both atria. By creating a maze of atrial tissue, the re-entrant circuits causing the AF are interrupted, hence re-establishing regular sinus rhythm and atrioventricular synchronization. The article reviews the initial 3-year experience of the procedure in 10 patients with AF, either paroxysmal (n = 5) or chronic (n = 5). The indications for surgery were disabling symptoms in all 10 cases, medical treatment failure in nine cases, previous AF-associated stroke in three cases, and a significant atrial septal defect in one case. All patients underwent extensive investigation both pre- and post-operatively. Postoperatively, nine of the 10 patients manifested regular sinus or atrial rhythm and freedom from or amelioration of preoperative symptoms associated with AF. There were no deaths, neurological complications or long-term recurrence of arrhythmia. One patient had an early recurrence of AF that was not amenable to medical treatment, and was subsequently treated with His' bundle ablation. Of the remaining nine patients, seven manifested signs of some postoperative atrial contraction at echocardiography, the occurrence of which needs to be borne in mind with a view to reducing the risk of future thromboembolic events. We recommend the maze procedure as an attractive surgical option in cases of unsuccessful medical treatment of paroxysmal or chronic AF.

Changes in arrhythmia profile and heart rate variability during abrupt withdrawal of antiepileptic drugs. Implications for sudden death.

Sudden unexpected death (SUD) has been associated with low or undetectable concentrations of antiepileptic drugs in patients with epilepsy suggesting that a sudden fall in plasma levels of these drugs might be a critical factor for the occurrence of SUD. We studied the changes in arrhythmia profile and heart-rate variability, during abrupt withdrawal of carbamazepine and phenytoin treatment in 10 patients with side effects on these drugs. Continuous ECG recording and daily measurements of drug plasma concentrations were performed from the last day of steady-state treatment and the following 4 days. Three patients had a 10-fold increase in ventricular premature beats. In addition, there was a significant reduction in heart-rate variability, assessed over 24 hours, in both the time (SDNN index, P = 0.03) and frequency domains from days 1-5. In the frequency domain analysis there was a significant reduction in total power (P = 0.01), very-low-frequency power (P = 0.004) and in low-frequency (LF) power (P = 0.01). Similar reductions in heart-rate variability and increases in ventricular automaticity have been associated with increased mortality in other patient groups. Two factors that might contribute to the increased rate of SUD in patients with epilepsy have thus been identified.

Arrhythmia, heart rate variability, and antiepileptic drugs.

This article reviews the clinical evidence for cardiac arrhythmias and alterations in heart rate variability (HRV) induced by antiepileptic drugs (AEDs). The medical literature was searched for cases with documented arrhythmias induced by AEDs at therapeutic doses, for systematic studies of the prevalence of arrhythmias related to AED therapy, and for studies on HRV in relation to AED treatment. Phenytoin has been associated predominantly with bradyarrhythmias, some of which were fatal. This has occurred almost exclusively with i.v. administration of the drug. Several reports demonstrate car-bamazepine's depressant effects on the cardiac conduction system. This has occurred mainly in the elderly or in otherwise predisposed patients. There were no reports of arrhythmias induced by other AEDs. Although information on HRV is scarce, treatment with carbamazepine appears to be associated with a decreased HRV. AED-induced cardiac arrhythmias are rare and occur mainly in patient populations different from those with a high incidence of sudden unexpected death. Further studies of HRV and AEDs are needed.

Electrophysiological evaluation of the sodium-channel blocker carbamazepine in healthy human subjects.

Carbamazepine (CBZ) is a sodium-channel blocker used mainly for the treatment of epileptic seizures and neuralgias. It may impair the function of the cardiac conduction system in susceptible patients, but its electrophysiological effects have not been thoroughly assessed in the normal heart, which was the aim of the present study. Ten healthy volunteers, mean age 32 years, underwent two electrophysiological investigations at baseline and three at different dose levels of CBZ. The transesophageal atrial stimulation technique was used to evaluate sinus node function, refractoriness of the atrial myocardium, atrioventricular conduction, and ventricular depolarization and repolarization (as reflected by the QRS, JT, and QT intervals) at spontaneous rhythm and after atrial pacing. Atropine was administered to facilitate 1:1 conduction and assessment of rate-dependent effects. At the highest CBZ dose (800 mg/day), which gave plasma concentrations within the upper therapeutic range, the PQ interval was mildly prolonged (151 vs. 159 msec; p < 0.01). In addition, the shortening of the JT interval normally seen at higher pacing rates was counteracted by high-dose CBZ, as demonstrated by a lower mean slope of the regression line after atropine and CBZ than after atropine alone (0.17 vs. 0.20; p < 0.05). No other effects were detected. At therapeutic levels CBZ had minimal effects on the healthy conduction system, supporting its safe use in the absence of cardiac disease.

Carbamazepine induced bradycardia--a problem in general or only in susceptible patients? A 24-h long-term electrocardiogram study.

Carbamazepine is a first line drug in the treatment of epilepsy and trigeminal neuralgia, but may exert negative chronotropic and dromotropic effects on the cardiac conduction system. Bradyarrhythmias of different types and severity have been described, especially in the elderly, but the prevalence of arrhythmias in a larger group of carbamazepine treated patients is unknown. Forty-eight patients, 40 years of older, on continuous carbamazepine treatment because of various neurologic disorders were investigated by interview, physical examination, 12-lead surface electrocardiogram, and 24-h long-term electrocardiogram recording. The prevalence of bradyarrhythmias was compared with that in an age-stratified reference group. There was no differences between the two groups, either in the number or the duration of pauses or in the type of pauses. In conclusion, carbamazepine does not increase the risk of bradyarrhythmias in the vast majority of patients.

Electrophysiologic effects and clinical hazards of carbamazepine treatment for neurologic disorders in patients with abnormalities of the cardiac conduction system.

Carbamazepine, a first-line drug for the treatment of epilepsy and neuralgia, may exert hazardous effects on the cardiac conduction system. Standard ECG and long-term ECG monitoring and invasive electrophysiologic testing were carried out in 10 patients who required this drug for neurologic disorders, but in whom its safe use had been questioned because of symptoms of ECG abnormalities. We observed depression of sinus node function and an atrioventricular conduction delay with a significant prolongation of the PQ interval of 16 msec (9%; 95% confidence interval: 1.9% to 16.5%; p less than 0.05), of which the HV interval was significantly prolonged but not the PA and AH intervals. These effects are in accordance with previously shown class 1A properties. However, the lack of effects on QRS, JT, and QT intervals at normal heart rates is a class 1B characteristic. Thus carbamazepine seems to have composite electropharmacologic actions. A cause effect relationship between carbamazepine treatment and significant arrhythmias was established in five patients. Thus the negative chronotropic and dromotropic effects of carbamazepine may, at least in predisposed patients, induce symptoms confusingly similar to the epileptic seizures it is used to prevent.

Prevalence of cardiac conduction disturbances during carbamazepine treatment: preliminary data.

Twenty-five epileptic patients chronically treated with carbamazepine underwent 24 h electrocardiogram (ECG) monitoring in order to evaluate the prevalence of cardiac conduction abnormalities. Plasma levels of carbamazepine and its metabolite, carbamazepine-10,11-epoxide, were determined by liquid chromatography. Six patients had mild ECG abnormalities. These patients did not differ from the others with respect to plasma concentrations of the drug and its metabolite.

Long-term ECG recordings in thyroxine-substituted hypothyroid subjects.

Bradyarrhythmias are sometimes observed in hypothyroid patients. This phenomenon could either be due to the disease process with structural changes of the heart or to an abnormal hormone level. The purpose of the present paper was to study the prevalence of bradyarrhythmias in hypothyroid patients on long-term substitution therapy. Nineteen subjects were studied 9-53 months after they had reached the final thyroxine substitution level. Ambulatory ECG registrations were performed during 48 hours. Ventricular ectopic beats were observed in 10 of the 19 patients, but no bradyarrhythmias were detected. The results support the notion that arrhythmias found in hypothyroid patients are at least mainly due to the low thyroid hormone level.