Electrical Conversion Of Atrial Fibrillation Research Articles

Defibrillation of Atrial Fibrillation is not Associated with Increased Risk of Ventricular Fibrillation – The VCD-Trial (Clinical Trial of Electrical Therapy for Atrial Fibrillation using R-wave Guided Cardioversion Versus Defibrillation)

Background: Because of a possible risk of induction of Ventricular Fibrillation (VF) by defibrillation of atrial fibrillation (AF) postulated by LOWN and coworkers, synchronized cardioversion is used worldwide. This prospective, randomized study assessed the efficacy and safety between R-wave controlled cardioversion and defibrillation of AF at 2 study centers in Cologne, Germany. Hypothesis: Defibrillation is not significantly different from cardioversion primarily in the occurrence of VF or sustained Ventricular Tachycardia (VT) and secondarily in restoring sinus rhythm, inducing non-sustained VT, asystole, or bradycardia. Methods: 146 patients at an outpatient practice and 122 at the university hospital were randomized to cardioversion (n = 140) or defibrillation (n = 124). Results: Cardioversion was successful in 92.1% of cases and defibrillation in 87.1%. The difference in efficacy was not statistically significant. In n = 1 patients receiving defibrillation, VF occurred after the first shock (200J) and immediate defibrillation (200J) restored sinus rhythm. In the n = 1 case, asystole occurred during cardioversion which terminated spontaneously. In n = 1 patients cardioverted and n = 2 who were defibrillated, sinus bradycardia occurred requiring Atropine in two cases. There were no thromboembolic events within 10 days. N = 9 patients reverted to AF within two hours. No patients died. Conclusion: Electrical conversion of AF can be performed with similar results and low risk with both R-wave-triggered cardioversion and defibrillation. In particular, defibrillation with higher energies (> 100J) can be performed as effectively and safely without a statistically significant increased risk of VF or VT. There was no difference in efficacy and risk between electrotherapy performed in the outpatient and inpatient settings.

Changes in cardiac output, rhythm regularity, and symptom severity after electrical cardioversion of atrial fibrillation

Objectives Symptoms in atrial fibrillation (AF) range from none to disabling. The physiological correlates of AF symptoms are not well characterized. This study investigated the association between physiological parameters and symptom severity before and after electrical cardioversion (EC) of AF. Design We studied 44 patients with persistent AF (age 66.2 ± 7.9 years, 16% females) 4 ± 2 days before and 5 ± 2 days after EC. Physiological parameters included cardiac output (CO; non-invasive inert gas rebreathing), heart rate (HR), RR variability and resting and ambulatory blood pressure (BP). Symptoms and quality of life (QoL) were assessed by the modified European Heart Rhythm Association score (mEHRA), the Atrial Fibrillation Effect on Quality of Life (AFEQT) and the Symptom Checklist for frequency and severity of symptoms (SCL). Results 28 of 44 patients were still in sinus rhythm (SR) at post EC evaluation. Those in SR had a decreased HR (-15.4 ± 13.1 bpm, p < 0.001), and an increased CO (+0.8 ± 0.7 L/min, p < 0.001) as compared to those with recurrent AF. Changes in CO after EC correlated with symptom improvement as scored by AFEQT (r = 0.36; p < 0.05), AFEQT symptoms subscore (r = 0.46; p < 0.01), SCL for frequency (r = 0.62; p < 0.01) and severity (r = 0.33; p < 0.05) of symptoms, and the mEHRA score (r = 0.50; p < 0.01). A decrease in RR variability showed similar correlations with these measures of symptom improvement. Conclusions Improvements in symptoms and quality of life experienced by patients after electrical conversion of atrial fibrillation are correlated with an increase in CO and a decreased RR variability.

Pharmacological and Electrical Conversion of Atrial Fibrillation to Sinus Rhythm Is Worth the Effort

Current treatment guidelines for atrial fibrillation (AF) base decisions on the triad of prevention of symptoms and protection from stroke and tachycardia-mediated cardiomyopathy. Conceptually, all of these objectives could be satisfied by either timely cardioversion and subsequent rhythm control, or the admittedly easier (for the patient and the physician) rate control strategy. We feel strongly that pharmacological or electrical cardioversion is worth the effort and should in fact usher in a new paradigm for AF disease management, rather than the passive and defeatist approach currently in place. Response by Wyse on p 1443 AF is the most frequent arrhythmia in clinical practice and a major cause of morbidity and mortality.1 More than 100 years after Sir James Mackenzie first described a pulse irregularity associated with disappearance of the “a” wave from the jugular pulse and paralysis of the atria,2 the pathophysiology of AF remains incompletely understood. However, over the last half century it was realized that electrical, contractile, and structural remodeling are fundamental contributors to the disease process of AF, potentially allowing improved and more specific therapies. Traditional therapy for AF consists of empirically tested ion channel blockers, offered without a real understanding of the pathophysiologic basis of the disease. It is therefore not surprising that pharmacological therapies for AF are neither as effective nor as safe as we would like. In major clinical trails, which have traditionally based success on absence of symptoms alone, antiarrhythmic drugs (AADs) prevent recurrent AF in 50% to 65% over short-term follow-up. It is largely due to frustration from current AADs that studies comparing rate control with rhythm control were conducted. Although the debate of rhythm versus rate control continues, it is important to realize that with either therapy, mortality trends in patients with AF remained unabated. In a longitudinal cohort study …

Dofetilide: a class III anti-arrhythmic drug for the treatment of atrial fibrillation

Dofetilide is a class III anti-arrhythmic drug that has been approved for the treatment of atrial fibrillation. Two clinical studies, which enrolled 996 patients, demonstrated pharmacological conversion to sinus rhythm to occur in 30% of patients. Following pharmacological or electrical conversion, median time to relapse exceeded one year. Two large clinical studies that enrolled 3028 patients have been performed in high-risk patients with severe heart failure and large myocardial infarctions. The outcomes of these studies were neutral with respect to survival and demonstrated the safety of dofetilide. After pharmacological or electrical conversion of atrial fibrillation to sinus rhythm in these studies, the probability of remaining in sinus rhythm during the following year was 75%. Dofetilide has a single significant side effect: risk of developing torsade de pointes ventricular tachycardia. Therefore, dosage must be carefully adjusted to the length of QTc interval, calculated creatinine clearance and the presence of heart failure or recent infarction. In addition, treatment must be initiated in hospital with three days of continuous telemetry. Dofetilide can be co-administered with digoxin and β-blockers. Other anti-arrhythmic drugs, as well as drugs that interfere with the renal elimination or the metabolism of dofetilide, must be avoided. Dofetilide is an option when persistent atrial fibrillation is a clinical problem. In the setting of severe heart failure and large myocardial infarctions, only amiodarone and dofetilide have proven safety and dofetilide is a strong candidate for first choice treatment when the aim is to achieve sinus rhythm.

Low‐Energy Transvenous Cardioversion of Atrial Fibrillation Using a Single Atrial Lead System

Clinical studies have shown that electrical conversion of atrial fibrillation (AF) is feasible with transvenous catheter electrodes at low energies. We developed a single atrial lead system that allows atrial pacing, sensing, and defibrillation to improve and facilitate this new therapeutic option. The lead consists of a tripolar sensing, pacing, and defibrillation system. Two defibrillation coil electrodes are positioned on a stylet-guided lead. A ring electrode located between the two coils serves as the cathode for atrial sensing and pacing. We used this lead to cardiovert patients with acute or chronic AF. The distal coil was positioned in the coronary sinus, and the proximal coil and the ring electrode in the right atrium. R wave synchronized biphasic shocks were delivered between the two coils. Atrial signal detection and pacing were performed using the proximal coil and the ring electrode. Eight patients with acute AF (38 +/- 9 min) and eight patients with chronic AF (6.6 +/- 5 months) were included. The fluoroscopy time for lead placement was 3.5 +/- 4.3 minutes. The atrial defibrillation threshold was 2.0 +/- 1.4 J for patients with acute AF and 9.2 +/- 5.9 J for patients with chronic AF (P < 0.01). The signal amplitude detected was 1.7 +/- 1.1 mV during AF and 4.0 +/- 2.9 mV after restoration of sinus rhythm (P < 0.001). Atrial pacing was feasible at a threshold of 4.4 +/- 3.3 V (0.5-msec pulse width). Atrial signal detection, atrial pacing, and low-energy atrial defibrillation using this single atrial lead system is feasible in various clinical settings. This system might lead to a simpler, less invasive approach for internal atrial cardioversion.

Pharmacologic enhancement of atrial electrical defibrillation efficacy: role of ibutilide.

The study was designed to identify the influence of ibutilide on activation during atrial fibrillation (AF) and determine its role in enhancing the efficacy of electrical conversion of AF. Vagally-mediated acute AF was induced in 12 anesthetized dogs. In 5 dogs, a cross-shaped epicardial patch containing 16 recording electrodes was placed on the right atrium. In 7 dogs, defibrillation patch electrodes overlying both atria were used to deliver biphasic shocks (50% tilt; 90 microF). Measurements were made at baseline and following ibutilide (0.075 mg/kg bolus followed by 0.075 mg/kg infusion over 10 minutes). Right atrial multisite electrogram recordings revealed significant prolongation in AF cycle length at all sites following ibutilide. In all dogs, AF cycle length increased with ibutilide from 90 +/- 23 to 130 +/- 49 ms (p < 0.005). Whereas, atrial defibrillation threshold decreased from 0.83 +/- 0.5 to 0.53 +/- 0.29 J (p = 0.020). In conclusion, ibutilide prolongs cycle length of canine vagally-mediated acute AF. Furthermore, ibutilide facilitates electrical conversion of AF by lowering energy requirement. Thus, controlled drug infusion in conjunction with electrical defibrillation may be useful for managing AF.

Ventricular proarrhythmic effects of ventricular cycle length and shock strength in a sheep model of transvenous atrial defibrillation.

Synchronized cardioversion is generally accepted as safe for the treatment of ventricular tachycardia and atrial fibrillation when shocks are synchronized to the R wave and delivered transthoracically. However, others have shown that during attempted transvenous cardioversion of rapid ventricular tachycardia, ventricular fibrillation (VF) may be induced. It was our objective to evaluate conditions (short and irregular cycle lengths [CL]) under which VF might be induced during synchronized electrical conversion of atrial fibrillation with transvenous electrodes. In 16 sheep (weight, 62 +/- 7.8 kg), atrial defibrillation thresholds (ADFT) were determined for a 3-ms/3-ms biphasic shock delivered between two catheters each having 6-cm coil electrodes, one in the great cardiac vein under the left atrial appendage and one in the right atrial appendage along the anterolateral atrioventricular groove. A hexapolar mapping catheter was positioned in the right ventricular apex for shock synchronization. In 8 sheep (group A), a shock intensity 20 V less than the ADFT was used for testing, and in the remaining 8 sheep (group B), a shock intensity of twice ADFT was used. With a modified extrastimulus technique, a basic train of eight stimuli alone (part 1) and with single (part 2) and double (part 3) extrastimuli were applied to right ventricular plunge electrodes. Atrial defibrillation shocks were delivered synchronized to the last depolarization. In part 4, shocks were delivered during atrial fibrillation. The preceding CL was evaluated over a range of 150 to 1000 milliseconds. Shocks were also delayed 2, 20, 50, and 100 milliseconds after the last depolarization from the stimulus (parts 1 through 3) or intrinsic depolarization (part 4). The mean ADFT for group A was 127 +/- 48 V, 0.71 +/- 0.60 J and for group B, 136 +/- 37 V, 0.79 +/- 0.42 J (NS, P > .15). Of 1870 shocks delivered, 11 episodes of VF were induced. Group A had no episodes of VF in part 1, two episodes of VF in part 2 (CL, 240 and 230 milliseconds with 2-millisecond delay), and one episode each in parts 3 (CL, 280 milliseconds with 2-millisecond delay) and 4 (CL, 240 milliseconds with 100-millisecond delay). Group B had two episodes in part 1 (CL, 250 and 300 milliseconds with 20-millisecond delay), three episodes in part 2 (CL, 230, 230, and 250 milliseconds with 2-millisecond delay), and one episode each in parts 3 (CL, 260 milliseconds with 2-millisecond delay) and 4 (198 milliseconds with 100-millisecond delay). No episodes of VF were induced for shocks delivered after a CL > 300 milliseconds. Synchronized transvenous atrial defibrillation shocks delivered on beats with a short preceding ventricular cycle length (< 300 milliseconds) are associated with a significantly increased risk of initiation of VF. To decrease the risk of ventricular proarrhythmia, short CLs should be avoided.

A cross-over trial of long and short acting quinidine preparations for the maintenance of sinus rhythm after defibrillation

A second part of a cross-over study was performed for fifteen months in 16 patients to compare the efficiency of long-acting and conventional quinidine in maintaining sinus rhythm after electrical conversion of atrial fibrillation. Both quinidine preparations in adequate dosage were capable of maintaining sinus rhythm. The long-acting form of quinidine produced more stable blood levels with less fluctuation in concentration. The long-acting preparation caused fewer side effects than the conventional form of quinidine sulphate.

The efficacy of antiarrhythmic drugs in the prevention of recurrence of aconitine-induced atrial fibrillation after electrical conversion

We have developed an experimental model to assess the ability of drugs to maintain slow supraventricular rhythm after electrical conversion of atrial fibrillation. Fibrillation was produced by application of a saturated solution of aconitine to the surface of the right atrium of open-chest dogs. Right and left atrial electrograms, the lead II electrocardiogram, and blood pressure were recorded. A capacitor discharge (30 watt-seconds) was applied through electrodes placed on the right atrium and the left ventricle. Atrial rhythm was improved for 1 to 20 s following defibrillation; then atrial fibrillation returned owing to the continued presence of aconitine. Quinidine in doses up to 4 mg/kg did not convert the arrhythmia but increased the duration of recovery after defibrillation up to 49 s. Pronethalol in doses up to 8 mg/kg and propranolol in doses up to 0.8 mg/kg occasionally converted atrial fibrillation to normal rhythm, but had no effect upon the duration of recovery after defibrillation. Diphenylhydantoin was tested in doses up to 20 mg/kg. Rapid injection of doses above 10 mg/kg slowed or converted the arrhythmia. Slow injections of diphenylhydantoin had no direct effect on the atrial fibrillation, but the period of recovery after defibrillation was prolonged up to 700 s. These experiments show that drugs can enhance the ability of the heart to maintain a slow rhythm following electrical conversion of atrial fibrillation. Those agents which most effectively convert atrial fibrillation are not the most effective agents for preventing the return of fibrillation after conversion.

Electrical conversion of atrial fibrillation: A one year follow-up study: Donaldson, P. and Kavanagh-Gray, D. Canad. Med. Ass. J. 100: 370, 1969. (St. Paul's Hosp. 1081 Burrard St., Vancouver 2, Canada)

Electrical conversion of atrial fibrillation: A one year follow-up study: Donaldson, P. and Kavanagh-Gray, D. Canad. Med. Ass. J. 100: 370, 1969. (St. Paul's Hosp. 1081 Burrard St., Vancouver 2, Canada)

The efficacy of anticoagulant therapy in preventing embolism related to D.C. electrical conversion of atrial fibrillation

Among 437 patients in whom electrical conversion of atrial arrhythmia was attempted 228 were on long-term anticoagulant therapy and 209 were not given anticoagulants. Thirteen (3 per cent) had an embolic episode, 2 of the 186 patients in the anticoagulant group and 11 of the 162 patients in the comparative group whose arrhythmias were converted. This difference is statistically significant at the 5 per cent level ( p = 0.012). Three of 11 patients with a history of embolic episodes, whose arrhythmia was converted without anticoagulants, had a new episode after conversion, compared to none of the 55 patients with previous episodes who were receiving anticoagulant therapy. We attach importance to the significant difference in embolic episodes between the two groups even if the patients were not allocated at random, perhaps even greater importance, because the difference in composition of the two groups produced a bias against the anticoagulant group. For example, patients with a history of previous embolic episodes and those with rheumatic valvular disease were considerably over-represented in this group. In both of these categories an increased risk of embolism is present. Our results lead to the conclusion that prophylactic anticoagulant therapy is clearly indicated before and after attempts to convert atrial fibrillation in patients with a history of previous embolic episodes. In our opinion such prophylaxis should preferably be given in connection with attempts at conversion in all cases.

Determination of Cardiac Output by Indocyanine Green-Dilution Method and Its Clinical Applications

A new method of serial determination of cardiac output has been employed to evaluate the cardiac function. It is based on the indocyanine green dye-dilution method with sampling from the systemic artery after injection of the dye into the right atrium. The purpose of the present study is to verify the reliability and reproducibility of this method, and to investigate the influence of cardiac glycoside and adrenergic β-receptor blockade upon the cardiac and renal functions, and also to determine the hemodynamic effect of electrical conversion of atrial fibrillation to sinus rhythm in patients with operated mitral stenosis. Part I. The Basic Studies for the Determination of Cardiac Output by Indocyanine Green-Dilution Method Materials and Methods. Indocyanine green in doses of I to 1.5 mg was injected into the right atrium through a 7F Lehman catheter inserted into the antecubital vein. Blood was sampled from the brachial or femoral artery through an indwelling arterial needle employing a Gilford constant withdrawal pump (Model 105S) and a cuvette densitometer (Model 1031R). The dye dilution curve was recorded on an 8-channel photographic recorder (Sanborn 4568A) with an electrocardiogram. The dye concentrations were replotted on a semilogarithmic paper. The curve was calibrated by whole blood and integrated sampling methods. The cardiac output was calculated according to Hamilton's formula. Two successive determinations of cardial indicies within 3 to 5 minutes were made in a total of 31 cases with or without heart disease. Results and Discussion: Fick and dye determination of cardiac output were carried out in 16 subjects. The average dye cardiac index was 2.74 ± 0.20 L/min/m2 and the Fick was 2.94 ± 0.23 L/min/m2. The correlation coefficient for Fick to dye was 0.88 (P <0.001). There was no significant difference between the mean values of these two groups. These results showed reliability of the dye method. The average cardiac index in the first determination of the two successive measurements within 3 to 5 minutes in 31 subjects was 2.86 ± 0.15 L/min/m2. The average in the second determination was 2.88 ± 0.16 L/min/m2. The percent difference between two successive determinations ranged from -13.3 to ± 10.5%. About 94% of all determinations were within ± 10% of the line of identity. The correlation coefficient was 0.99 (P <0.001). These results revealed good reproducibility of the dye-dilution method. The differences may be mainly due to the physiological changes rather than technical errors.

Alterations in cardiac function immediately following electrical conversion of atrial fibrillation to normal sinus rhythm.

An assessment was made of cardiac function by means of right heart catheterization before and immediately after conversion of atrial fibrillation to sinus rhythm in 11 studies on 10 human subjects. Comparable data during exercise were available in five studies. Medical management of patients in this study was identical to that employed routinely for this procedure. After conversion to normal sinus rhythm cardiac output response was significantly increased only during exercise. The relationship of mean right atrial and mean pulmonary wedge pressures to right and left ventricular stroke work was uniformly improved both because of decreases in these pressures and increases in work. Indirect evidence of mitral valvular regurgitation was diminished to absent after conversion. "A" waves and the pulse pressure of atrial contraction were very small in the right atrial tracings after conversion and these contours were usually inapparent on pulmonary wedge tracings. It is concluded that over-all cardiac performance was improved with re-establishment of sinus rhythm and that diminutions in atrial-venous pressure behind each ventricle may be important in explaining symptomatic improvement following electroconversion. Measures of both pressure and flow were required for complete description of the alterations induced by this intervention.

Haemodynamic studies before and after electrical conversion of atrial fibrillation and flutter to sinus rhythm.

Haemodynamic studies before and after electrical conversion of atrial fibrillation and flutter to sinus rhythm.

Alterations in Cardiac Function Following Electrical Conversion of Atrial Fibrillation to Normal Sinus Rhythm.

Excerpt Evaluation of cardiac performance requires analysis of both pressure and flow data. Eleven right heart catheterizations were performed (six included exercise observations) to compare measur...

Electrical Conversion of Atrial Fibrillation

Excerpt For many years the major therapeutic approach for reverting atrial fibrillation to sinus rhythm has been through the use of quinidine. In 1962 Lown, Amarasingham, and Neuman (1) introducted...