When should heparin preferably be administered during radiofrequency catheter ablation?

RF catheter ablation is complicated by thromboembolism in about 1% of patients. Limited knowledge exists concerning when and how to use anticoagulation or antithrombotic treatment. We studied the activation of coagulation (prothrombin fragment 1 + 2 [PF1 + 2] and D-dimer), platelets (beta-thromboglobulin [beta-TG]) and fibrinolysis (plasmin-antiplasmin complexes [PAP]) during RF ablation of accessory pathways in 30 patients. They were randomized to receive heparin (100 IU/kg, intravenously) (1) immediately after introduction of the femoral venous sheaths (group I) or (2) after the initial electrophysiological study, prior to the delivery of RF current (groups II and III). Group II additionally received saline irrigation of all femoral sheaths. After the initial bolus, 1,000 IU of heparin was supplied hourly in all groups. Within groups II and III, median plasma values of PF1 + 2 and beta-TG more than tripled (P < or = 0.007) during the diagnostic study and gradually declined during heparin administration despite RF current delivery. Median D-dimer tripled (P = 0.005) and PAP doubled (NS) before heparin administration; then both remained around the upper reference values. In the early heparin group, however, PF1 + 2, D-dimer, and PAP did not rise at all, and beta-TG showed only a slight increase towards the end of the procedure. The differences between group I versus groups II and III were statistically significant prior to the first RF current delivery (PF1 + 2, D-dimer, and beta-TG) and by the end of the procedure (PF1 + 2, D-dimer, and PAP). In conclusion, "late" heparin administration allows hemostatic activation during the initial catheterization and diagnostic study. By administering intravenous heparin immediately after introduction of the venous sheaths, hemostatic activation is significantly decreased. Saline irrigation of the venous sheaths added nothing to late heparin administration.

The activation of platelet function, coagulation, and fibrinolysis during radiofrequency catheter ablation in heparinized patients.

INTRODUCTION: Catheter ablation may be complicated by clinical thromboembolism in about 1% of patients. METHODS AND RESULTS: We studied the activation of coagulation (prothrombin fragment 1+2 [PF1+2]), platelets (beta-thromboglobulin [beta-TG])) and fibrinolysis (plasmin-antiplasmin complexes [PAP] and D-dimer) during radiofrequency (RF) ablation in 13 patients. They received heparin 100 U/kg intravenously after the initial electrophysiologic study, prior to the delivery of RF current; thereafter 1,000 U/hour throughout the procedure. PF1+2 increased fourfold (P < 0.001) during the diagnostic study, but gradually declined to upper reference value during heparin administration. There was a strong correlation between procedure duration prior to heparin bolus (range 39 to 173 min); and (a) the maximal rise of PF1+2 (r = 0.83, P < 0.001) and (b) the increase of PF1+2 from baseline to end of the procedure (r = 0.74, P = 0.004). There was no correlation between postheparin changes of PF1+2 and (a) postheparin procedure duration (range 40 to 317 min), (b) number of RF pulses (range 1 to 16), or (c) RF current duration (range 46 to 687 sec). Plasma beta-TG concentration showed similar trends. Fibrinolytic activity increased moderately from baseline until heparin administration; then remained around the upper reference values. PAP at the end of procedure and D-dimer at the time of heparin administration both correlated with preheparin procedure duration (r = 0.70, P = 0.007 and r = 0.69, P = 0.01, respectively). All parameters were normal the next morning. CONCLUSION: Procedure duration prior to heparin administration, and not the delivery of RF current per se, determines activation of hemostasis and fibrinolysis during RF ablation.

Radiofrequency catheter ablation of two right Mahaïm-like accessory pathways in a patient with Ebstein's anomaly.

A 17-year-old woman with Ebstein's anomaly and recurrent episodes of antidromic tachycardia with two distinct morphologies is described. The tachycardias were produced by two separate Mahaïm-like accessory pathways. These were localized by their activation potentials at the anterolateral ventricular margin of the tricuspid annulus and ablated in a single session using radiofrequency current.

[Radiofrequency ablation of arrhythmia--considerable progress]. / Radiofrekvensablasjon av arytmier--et stort fremskritt!

Today, the majority of paroxysmal tachycardias can be cured by radiofrequency catheter ablation, obviating the need to use anti-arrhythmia drugs or open heart surgery. The history, the indications, the results and complications of current practice are reviewed.

[Ablation of the bundle of His in atrial arrhythmia. A solution when the drugs fail]. / Ablasjon av His-bunten ved atriale arytmier. En utvei når medikamentene ikke virker.

Radiofrequency ablation of the bundle of His was performed in 33 patients with intractable atrial arrhythmias (fibrillation in 23, flutter in seven, atrial tachycardia in three). Complete AV block was produced in 30 patients, and clinically satisfactory incomplete block in another two. All were subsequently treated by pacemaker. The ablation was a failure in one patient with hypertrophic cardiomyopathy. Today ablation can be targeted at atrial tachycardias and flutter, and ablative modification of the AV node can reduce ventricular rate in chronic atrial fibrillation. However, His bundle ablation is still the treatment of choice in drug refractory atrial fibrillation when no other measure can provide adequate rate control.

[Radiofrequency ablation of heart arrhythmias. Results in the first 150 patients treated at the Arrhythmia center in Oslo]. / Radiofrekvensablasjon av hjertearytmier. Resultater hos de første 150 pasienter behandlet ved Arytmisenteret i Oslo.

The authors review the first 150 patients with cardiac arrhythmias who were treated with radio-frequency ablation at a Norwegian arrhythmia centre. The clinical success rate (either electrophysiological cure or a dramatic reduction in the severity and frequency of the attacks) was 97%. 11 patients were treated for two or more arrhythmias. In 27 patients two, occasionally three, sessions were required to obtain a satisfactory clinical result. Repeat ablation is scheduled for three cases where the treatment was unsuccessful. Among 190 ablations, 13 complications occurred, none of which resulted in permanent sequelae. The time spent on each procedure, and particularly the long time spent on fluoroscopy during the earlier procedures, demonstrates the existence of a learning curve for ablation. This lends support to the authorities' restriction of treatment of arrhythmias by ablation to only two laboratories in a population of four million.

[Guidelines for use of amiodarone (Cordarone). A potent anti-arrhythmic agent that may have problematic adverse effects]. / Retningslinjer for bruk av amiodaron (Cordarone). Et potent antiarytmikum som kan gi problematiske bivirkininger.

The authors discuss the potent antiarrhythmic drug amiodarone, with emphasis on indications, efficacy and side effects. At present the drug can be prescribed only by specialists in internal medicine. In order to monitor the efficacy of the drug and any side effects the patient should preferably be evaluated every three to six months. Use of intravenous amiodarone in hospital is effective in many cases but, so far, documentation on this treatment is limited.

Effects of flecainide on termination of atrial flutter by rapid atrial pacing.

Rapid atrial pacing is effective in terminating atrial flutter, but often results in transient or permanent atrial fibrillation rather than sinus rhythm. Class Ia antiarrhythmic drugs have earlier been shown to facilitate the direct conversion of atrial flutter to sinus rhythm. The present study was performed to test the hypothesis that flecainide, a group 1c antiarrhythmic drug, increases the direct conversion to sinus rhythm. In a series of 30 consecutive clinical episodes of atrial flutter treated with rapid atrial pacing, 12 episodes were in patients on flecainide treatment (group A), while in 13 episodes no patients were on group I antiarrhythmic drugs (group B). Direct conversion to sinus rhythm was achieved more often in group A (75%) than in group B (31%) P = 0.034. Both the flutter rates and the pacing rates used were lower in group A, 240 vs 280 beat.min-1 and 375 vs 430 b.min-1, respectively. Patients with atrial flutter in whom rapid atrial pacing is to be performed should be considered for pretreatment with flecainide.

[Atrial flutter with 1:1 AV conduction during intravenous flecainide treatment]. / Atrieflutter med 1:1 AV-overledning under intravenøs flekainidbehandling.

Acute drug treatment of recent onset atrial flutter may reduce the ventricular rate by increasing block in the A-V node (digitalis/verapamil) or act by directly affecting the atria by reducing the atrial rate or converting flutter to sinus rhythm (1a and 1c antiarrthythmic drugs). Treatment that reduces the atrial rate may cause 1:1 A-V conduction. Quinidine and disopyramide are well known for increasing A-V conduction to 1:1 in some patients, because of their anticholinergic effect on the A-V node. Flecainide, a 1c antiarrhythmic drug, slows down atrial conduction, reducing flutter rate by 1/3. Clinical studies have shown flecainide to be effective in converting atrial fibrillation, atrial tachycardia, A-V reentry and A-V nodal reentry tachycardias to sinus rhythm. The effect on atrial flutter has been less impressive. Flecainide prolongs A-V conduction and increases Wenckebach cycle length. In spite of this, 1:1 A-V conduction may occur during treatment with intravenous flecainide for atrial flutter. We present a case where this is demonstrated and review the literature.

A double-blind, crossover comparison of flecainide acetate and disopyramide phosphate in the treatment of ventricular premature complexes.

The efficacy and safety of flecainide, 200 mg twice daily, was compared with disopyramide, 150 mg 4 times daily, in a randomized, double-blind, crossover study in 25 patients (19 men and 6 women, aged 20 to 71 years, mean 52.5) with more than 1,000 ventricular premature complexes (VPCs) in a pretrial 24-hour Holter monitoring screen. Each 14-day active treatment period was preceded and followed by a 7-day placebo period. Ambulatory ECGs were recorded at the end of each study week and analyzed blindly. Average VPCs recorded during each of the 2 active periods were compared with average VPCs in the placebo periods. Twenty-two of 25 patients attained therapeutic plasma levels of both drugs. The occurrence of VPCs was significantly less during flecainide than during disopyramide treatment, 92 and 39%, respectively (p less than 0.01). Complex arrhythmic events were significantly more suppressed with flecainide than with disopyramide. No difference was observed between the 2 drugs in the incidence or severity of reported side effects. PQ, QRS and QT intervals increased beyond normal limits on both drugs in some patients, significantly more with flecainide than with disopyramide. The JT interval did not change or decrease; hence, all changes in the QT interval were attributable to a widening of the QRS complex. Neither drug showed any significant effect on blood pressure or heart rate. Flecainide may be a well-tolerated and valuable alternative to currently available antiarrhythmic agents.

Iohexol in coronary angiography. A double blind investigation.

Iohexol 350 mg I/ml (Omnipaque) was compared with the routine contrast medium meglumine, Na-Ca-metrizoate 370 mg I/ml (Isopaque Coronar) in coronary angiography in 30 patients. A randomized, double blind, crossover design was employed. Angiographic image quality, ECG, heart rate, aortic blood pressure and adverse reactions were recorded. Excellent image quality was obtained with both media. Except for one single event of hypotension, only few and minor changes in the parameters measured were recorded. No distinct difference between the two media was found. Iohexol seems to be suitable for selective coronary angiography.