The blip syndrome.
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Cardiac Complexes, Premature↗
Biomedical subjects
K J Hellestrand
Publications and source records attributed to K J Hellestrand.
Clinical benefit of transdermal glyceryl trinitrate when used with an eight hour patch-free period.
The 24-hour application of transdermal nitrate patches has been associated with rapid development of therapeutic tolerance. Recent reports suggest maintenance of clinical benefit by introducing a daily patch-free period. This study investigates, by means of serial treadmill testing, the efficacy of a new transdermal delivery system when used with an eight hour patch-free period in 16 subjects with chronic stable angina. Concomitant antianginal therapy was permitted. After demonstration of exercise test reproducibility and nitrate responsiveness, subjects entered a double-blind randomised placebo-controlled crossover trial comprising one week of active nitroglycerin patches (10mg/24hrs) and one week of an identical placebo patch. Exercise tests were conducted four hours after patch application on the last day of each of the treatment arms. Daily angina frequency and nitroglycerin consumption were also monitored. There was significant improvement in total exercise duration (16.5%), time to onset of angina (26%), time to 1mm ST depression (22%), and peak heart rate blood pressure product with active patch application. Angina frequency was reduced during the week of active therapy. These results demonstrate the additional efficacy of intermittent transdermal nitroglycerin in a group of subjects with continuing angina despite therapy with beta-blockers and calcium antagonists.
Administration, Cutaneous↗
Intravenous flecainide acetate for supraventricular tachycardias.
Flecainide acetate, 2 mg/kg body weight, given intravenously at 10 mg/min was administered to 128 (74 male and 54 female) patients whose ages ranged from 11 to 86 years (mean 44). All patients had supraventricular tachycardias (SVT) that developed spontaneously or were induced during electrophysiologic study. There were 26 patients with atrial flutter, 34 with atrial fibrillation, 7 with ectopic atrial tachycardia, 41 with atrioventricular (AV) reentrant tachycardia and 40 with AV nodal reentrant tachycardia. Twenty patients had more than 1 variety of SVT. Flecainide was administered during SVT to 9 patients with atrial flutter, 11 with atrial fibrillation, 7 with atrial tachycardia, 38 with AV reentrant tachycardia and 34 with AV nodal reentrant tachycardia. In the remaining 31 patients with inducible SVT at electrophysiologic study, flecainide was administered during sinus rhythm. Reinitiation of SVT was attempted in these patients after completion of flecainide administration. Flecainide successfully terminated atrial flutter in 2 patients (22%), atrial fibrillation in 9 (82%), atrial tachycardia in 5 (71%), AV reentrant tachycardia in 32 (84%) and AV nodal reentrant tachycardia in 30 (88%). Reinitiation of SVT was possible in 10 of 26 patients with atrial flutter (38%), 5 of 34 with atrial fibrillation (15%), 3 of 7 with atrial tachycardia (43%), 14 of 41 with AV reentrant tachycardia (34%) and 11 of 40 with AV nodal reentrant tachycardia (27%). In patients with AV reentrant tachycardia and AV nodal reentrant tachycardia, reinitiation occurred when retrograde anomalous pathway refractoriness was not significantly prolonged by intravenous flecainide.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Intravenous flecainide acetate for the clinical management of paroxysmal tachycardias.
Intravenous flecainide acetate (2 mg/kg) was administered to 40 patients undergoing routine electrophysiological evaluation for the investigation of recurrent paroxysmal tachycardias. Ten patients had recurrent atrial flutter, 11 patients had recurrent atrial fibrillation, one of whom also had paroxysmal left atrial tachycardia, and 19 patients had recurrent ventricular tachyarrhythmias (17 with recurrent ventricular tachycardia and 2 with recurrent fascicular tachycardia). Flecainide was administered during tachycardia (over 5 to 10 minutes) to all patients with atrial flutter, to 10 patients with atrial fibrillation, and to 17 patients with ventricular tachyarrhythmias. In the remaining 3 patients with ill-sustained arrhythmias flecainide was administered during sinus rhythm and reinitiation of tachycardia was then attempted. Flecainide restored sinus rhythm in only 2 patients with atrial flutter (20%), in 9 patients with atrial fibrillation (90%), in 12 patients with ventricular tachycardia (80%), and in one of the 2 patients with fasicular tachycardia. Flecainide also successfully terminated the left atrial tachycardia. Two patients experienced proarrhythmic side effects during flecainide administration, one of whom required intervention by cardioversion. Minor dose effects included oral paresthesia, transient drowsiness or dizziness, and occasional visual blurring. Flecainide acetate is an effective antiarrhythmic agent for the acute termination of recent onset paroxysmal atrial and ventricular tachyarrhythmias.
Adolescent↗
Clinical usefulness of flecainide acetate in the treatment of paroxysmal supraventricular arrhythmias.
Flecainide acetate depresses both the upstroke of the intracellular action potential and the rate of diastolic depolarisation in isolated tissue preparations of atrial myocardium. It produces no consistent effect on action potential duration. Predictably, in the human heart, studied by clinical cardiac electrophysiological techniques, conduction velocity through atrial myocardium, the atrioventricular (AV) node and anomalous tissue is depressed following flecainide administration. Refractoriness of normal atrial or AV nodal myocardium is not prolonged but the recovery time of anomalous or abnormal tissue is lengthened by the drug. In response to the intravenous injection of flecainide, atrial fibrillation (90%), atrial tachycardia (100%), intra-AV nodal tachycardia (89%) and atrioventricular re-entrant tachycardia (80%) are generally terminated, and although atrial flutter is slowed, only a small proportion (20%) is terminated. There is little experience of the long term treatment of supraventricular tachycardia with oral flecainide. However, preliminary results suggest that flecainide is equally effective in the treatment of both supraventricular and ventricular arrhythmias. Thus, flecainide acetate is a 'broad spectrum' antiarrhythmic agent.
Animals↗
The proarrhythmic effects of flecainide.
Flecainide acetate, a new potent class I antiarrhythmic agent, was administered to 152 patients (orally to 46, intravenously to 106) over a period of 22 months. Seven patients developed proarrhythmic effects. The only conduction abnormalities induced were PR interval prolongation and QRS complex widening, and no patient developed significant sinus bradyarrhythmias; patients with known serious abnormalities of impulse generation or conduction were excluded from this study. Five patients, of whom only 3 had pre-existing ventricular arrhythmias, developed ventricular tachycardia or ventricular fibrillation. QT and QTc interval prolongation was observed, but was due to QRS complex widening rather than an increase in the JT interval. A patient with Wolff-Parkinson-White syndrome had an inducible orthodromic atrioventricular tachycardia before flecainide administration, but only an antidromic tachycardia was induced after taking the drug. In 1 patient, flecainide administration resulted in an increase of atrial flutter cycle length, which resulted in the development of 1:1 atrioventricular conduction rate, and, overall, a faster ventricular rate. Two patients who developed ventricular arrhythmias were taking other antiarrhythmic agents, and in this series proarrhythmic effects occurred with both normal and high flecainide concentrations. Other published series are also summarised.
Adult↗
Electrophysiologic effects of flecainide acetate on sinus node function, anomalous atrioventricular connections, and pacemaker thresholds.
The acute electrophysiologic effects of i.v. flecainide acetate (2 mg/kg body weight) were assessed in 71 patients undergoing electrophysiologic study. Ten patients underwent investigation for sinus node dysfunction. Sinus cycle length shortened slightly, from 980 +/- 292 to 931 +/- 276 ms (p less than 0.01). Uncorrected or corrected sinus node recovery times or sinoatrial conduction time (according to the methods of Strauss and Narula) did not change in 6 patients with normal sinus node function and in 3 of 4 patients with abnormal sinus node function at rest. In the remaining patient maximal sinus node recovery time increased from a value at rest of 5,185 ms to 23,460 ms after flecainide. In the same patient sinoatrial conduction times at rest increased from 159 ms (Strauss method) and 143 ms (Narula method) to 1,398 and 1,455 ms, respectively, after flecainide. Thirty-three patients underwent electrophysiologic evaluation of anomalous atrioventricular (AV) pathways and reentrant tachycardias. Flecainide significantly prolonged accessory AV pathway anterograde and retrograde refractoriness. Anterograde accessory pathway block occurred in 33% of patients and retrograde accessory pathway block in 44%. Flecainide was successful in the acute termination of 86% of orthodromic atrioventricular reentrant tachycardias. In 15 patients with dual AV nodal pathways, only retrograde "fast" AH pathway refractoriness was significantly increased by flecainide, which was successful in the acute termination of 88% of intra-AV nodal reentrant tachycardias. In 28 patients who underwent endocardial pacing threshold assessment before and after i.v. flecainide, the acute threshold rose by a maximum of 117%, whereas the chronic threshold rose by a maximum of 83%.(ABSTRACT TRUNCATED AT 250 WORDS)
Adolescent↗
The electrophysiologic characteristics of the transplanted human heart.
The electrophysiologic characteristics of the denervated human heart were assessed in 14 cardiac transplant recipients. Conduction intervals and refractory periods were measured at pacing cycle lengths of 500 msec and 400 msec. The faster pacing rate caused lengthening of the AH interval (83 +/- 23 msec to 116 +/- 41 msec, p less than 0.01) and shortening of the QT (338 +/- 27 msec to 313 +/- 22 msec, p less than 0.001) and JT (249 +/- 21 msec to 229 +/- 19 msec, p less than 0.001) intervals. There was no change in the SA, HV, or QRS durations. Wenckebach periodicity occurred at a longer cycle length in the retrograde than in the anterograde direction (409 +/- 96 msec vs 318 +/- 46 msec, p less than 0.01) and anterograde conduction was better than retrograde conduction in 13 of the 14 patients (93%). Increasing pacing cycle length resulted in shortening of the atrial effective (203 +/- 28 msec to 190 +/- 25 msec, p less than 0.001), ventricular effective (224 +/- 18 msec to 211 +/- 17 msec, p less than 0.01), and AV nodal functional (367 +/- 38 msec to 357 +/- 36 msec, NS) refractory periods. The AV nodal effective refractory period lengthened (294 +/- 31 msec to 314 +/- 52 msec, p less than 0.05). There was a close correlation between AV Wenckebach cycle length and the functional refractory period of the AV node (r = 0.853, p less than 0.001). These results are qualitatively and quantitatively similar to those reported in the innervated heart. The autonomic nervous system appears to have little influence on the resting electrophysiologic characteristics of the atrioventricular conduction system in the innervated heart.
Adult↗
Proarrhythmic effects of the new antiarrhythmic agent flecainide acetate.
Flecainide acetate, a new potent class I antiarrhythmic agent, was given to 152 patients (46 orally and 106 intravenously) over a period of 22 months. Seven patients developed proarrhythmic effects. The only conduction abnormalities induced were PR interval prolongation and QRS complex widening, and no patient developed significant sinus bradyarrhythmias; patients with known serious abnormalities of impulse generation or conduction were excluded from this study. Five patients developed ventricular tachycardia or ventricular fibrillation of whom only three had preexisting ventricular arrhythmias. QT and QTc interval prolongation was observed but was due to QRS complex widening rather than to an increase in the JT interval. A patient with the Wolff-Parkinson-White syndrome had an inducible orthodromic atrioventricular (AV) tachycardia prior to flecainide, but only an antidromic tachycardia was induced after the drug. In one patient flecainide administration resulted in an increase of atrial flutter cycle length which resulted in development of 1:1 AV conduction and overall faster ventricular rate. Two patients who developed ventricular arrhythmias were taking other antiarrhythmic agents, and in this series proarrhythmic effects occurred with both normal and high flecainide concentrations.
Administration, Oral↗
Sinoatrial function after cardiac transplantation.
The function of both the denervated donor and innervated recipient sinus nodes of 14 asymptomatic cardiac transplant recipients was assessed. Tests of sinoatrial function were performed in 14 donor and 10 recipient atria. The mean spontaneous cycle length of the recipient atria was significantly longer than that of the donor atria (944 +/- 246 versus 663 +/- 158 ms, p less than 0.01). Donor sinus node recovery time was prolonged in four patients (greater than 2,500 ms in two) and recipient recovery time was prolonged in six patients. In those patients with normal sinus node function tests, the recovery time of the recipient sinus node was longer than that of the donor sinus node (1,170 +/- 207 versus 864 +/- 175 ms, p less than 0.02). The pattern of response of recovery times to increasing pacing rate was predictable and organized in the donor but chaotic in the recipient, and the longest sinus node recovery time occurred at the shortest pacing cycle length used in 12 of the 14 donor atria but in only 1 of the 10 recipient atria (p less than 0.001). Secondary pauses occurred in none of the normal donor atria and in all of the abnormal donor atria (p less than 0.001); however, they occurred in both normal and abnormal recipient atria. The recipient and donor atria were paced alone and synchronously in the same patients. Synchronous pacing had no effect on the recovery times of the donor sinus node but significantly lengthened those of the recipient (sinus node recovery time: 1,266 +/- 218 to 1,547 +/- 332 ms, p less than 0.02; corrected recovery time: 322 +/- 102 to 686 +/- 188 ms, p less than 0.01). In the donor atria, abnormal recovery time was invariably associated with abnormal sinoatrial conduction time. There was a strong correlation between sinoatrial conduction time measured by the methods of Strauss and Narula and their coworkers in the donor atria (r = 0.98, p less than 0.001) but not in the recipient atria (r = 0.72). In the absence of autonomic influences, tests of sinus node function of the donor atria produce predictable and consistent results and, therefore, may be more clinically reliable than in intact human subjects. There is a high incidence of recipient sinus node dysfunction in asymptomatic long-term survivors of cardiac transplantation.
Adult↗
Comparison of the efficacy of newly developed antiarrhythmic drugs in the treatment of ventricular tachyarrhythmias.
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Anilides↗
Class 1 antiarrhythmic drugs--characteristic electrocardiographic differences when assessed by atrial and ventricular pacing.
Class 1 antiarrhythmic drugs have been subdivided into 1a, 1b and 1c according to their effect on the action potential duration. The effects on the surface electrocardiogram of one drug from each subgroup were investigated in nine patients. Electrocardiographic recordings were taken during sinus rhythm and at identical atrial and ventricular paced rates. Disopyramide (1a) significantly prolonged the QT interval during sinus rhythm and at the identical paced rates, by increasing both the QRS duration and JT interval. Lignocaine (1b) significantly reduced the QT interval during sinus rhythm and at the identical paced rates, by reducing the JT interval. Lignocaine had no effect on the QRS duration. Flecainide (1c) significantly prolonged the QRS duration during sinus rhythm, but not the QTc. However the QT interval at the paced rates prolonged significantly, due entirely to an increase of the QRS duration. Flecainide had no effect on the JT interval. These characteristic electrocardiographic differences support the differentiation of class 1 drugs into three separate subgroups.
Action Potentials↗
Response of an abnormal sinus node to intravenous flecainide acetate.
A patient with sinus node disease underwent provocative testing with flecainide, a new Vaughan Williams class IC antiarrhythmic agent. There were dramatic increases in sinus node recovery times and in sinoatrial conduction times, and the magnitude of the response could only be witnessed because of the emergence of a subsidiary junctional pacemaker without retrograde conduction to the atria.
Aged↗
Fatal ventricular tachycardia in association with propafenone, a new class IC antiarrhythmic agent.
A man with a past history of malignant ventricular arrhythmias occurring late after myocardial infarction was admitted for assessment. Monitoring revealed frequent ventricular premature beats and occasional non-sustained runs of ventricular tachycardia. Other drugs having failed, he was started on oral propafenone which is a new Vaughan Williams class IC antiarrhythmic agent. Several hours after starting this drug he had incessant ventricular tachycardia and subsequently died. Other class IC agents have been shown to have a high incidence of proarrhythmic effects, and particular care should be taken with these potent new drugs.
Anti-Arrhythmia Agents↗
Cardiac electrophysiologic effects of flecainide acetate for paroxysmal reentrant junctional tachycardias.
Intravenous flecainide acetate was administered to 33 patients undergoing routine electrophysiologic study: 18 patients had a direct accessory atrioventricular (AV) pathway and 15 patients had functional longitudinal A-H dissociation (dual A-H pathways). Flecainide was given to 14 patients during sustained AV reentrant tachycardia and to 9 patients during sustained intra-AV nodal reentrant tachycardia. AV reentrant tachycardia was successfully terminated in 12 of 14 patients. Tachycardia termination was due to retrograde accessory pathway block in 11 patients and AV nodal block in 1. During flecainide administration, tachycardia cycle lengths increased (327 +/- 55 to 426 +/- 84 ms) principally because of retrograde conduction delay in the accessory pathway (127 +/- 34 to 197 +/- 67 ms). After flecainide administration, tachycardia reinitiation was not possible in 6 patients. In all 18 patients with accessory AV pathway conduction, flecainide significantly increased both anterograde and retrograde accessory pathway effective refractory periods, with anterograde accessory pathway block in 3 patients and retrograde accessory pathway block in 8. Intra-AV nodal reentrant tachycardia was successfully terminated in 8 of 9 patients. Tachycardia termination was due to retrograde "fast" A-H pathway block in 7 patients and anterograde "slow" A-H pathway block in 1 patient. During flecainide administration, tachycardia cycle lengths increased (326 +/- 50 to 433 +/- 64 ms) due to both anterograde, A-H and H-V (AV 242 +/- 97 to 343 +/- 75 ms), and retrograde, earliest ventricular to earliest atrial (51 +/- 14 to 70 +/- 23 ms) conduction delay. After flecainide administration, reinitiation of intra-AV nodal reentrant tachycardia was not possible in 4 patients. In all 15 patients with dual A-H pathways, flecainide selectively prolonged the retrograde effective refractory period of the fast A-H pathway, having little effect on anterograde fast A-H pathway refractoriness or on anterograde and retrograde slow A-H pathway refractoriness. Anterograde fast A-H pathway block occurred in 1 patient and retrograde fast A-H pathway block occurred in 6 patients. No serious adverse effects were encountered during the study. Flecainide acetate is an effective agent for the acute termination of both orthodromic AV and intra-AV nodal reentrant tachycardias. This antiarrhythmic action appears to be mediated through a predominant effect on either accessory AV pathway or retrograde fast A-H pathway refractoriness.
Adult↗
Unusual atrial potentials in a cardiac transplant recipient. Possible synchronization between donor and recipient atria.
It is usual to record independent activity from both the innervated recipient and the denervated donor atria in cardiac transplant recipients except for occasional, short-lived periods of entrainment that may occur during exercise. In this report a case is described in which, following orthotopic cardiac transplantation, the recipient and donor atria remained synchronized during a variety of physiological and non-physiological situations. Under no circumstances did the two sets of atria beat independently. The mechanisms that might be involved in this unique situation are discussed.
Adult↗
A comparison of the antiarrhythmic effects on AV junctional re-entrant tachycardia of oral and intravenous flecainide acetate.
Both the electrophysiological and antiarrhythmic effects of some antiarrhythmic agents may differ markedly depending on their route of administration. Flecainide acetate, a new class 1 agent, was therefore administered both intravenously and orally to 13 patients with recurrent paroxysmal tachycardia to assess whether the acute response to intravenous flecainide accurately predicts the response to oral therapy. Eight patients had atrioventricular re-entrant tachycardia (AVRT) and five patients intra AV nodal re-entrant tachycardia (AVNRT). When administered by either route, flecainide markedly prolonged both the anterograde and retrograde conduction intervals during constant rate pacing and the anterograde and retrograde Wenckebach cycle lengths during incremental pacing. Five of the 13 patients developed complete retrograde block after both routes of administration of the drug. All 13 patients received intravenous flecainide during tachycardia with successful reversion to sinus rhythm in all cases. Tachycardia could be reinitiated in five of the patients with AVRT after intravenous flecainide and in one further patient after oral administration. It was not possible to reinitiate tachycardia in any of the five patients with AVNRT after either intravenous or oral flecainide. The size of the tachycardia initiation windows, by either atrial or ventricular premature stimuli, were significantly reduced by both intravenous and oral flecainide. In those patients in whom tachycardia could be reinitiated, tachycardia cycle length was significantly increased, and to a similar degree, by both routes of administration of the drug. This increase in cycle length was predominantly due to prolongation in retrograde conduction. It is concluded that flecainide acetate is a potent antiarrhythmic agent for use in patients with junctional tachycardia. The intravenous administration of flecainide reliably predicts the subsequent response to oral therapy.
Administration, Oral↗
Effect of the antiarrhythmic agent flecainide acetate on acute and chronic pacing thresholds.
To determine the effect of flecainide acetate, a Class IC antiarrhythmic drug, The medication was given to 28 patients with ventricular pacing electrodes. Eleven patients with temporary pacing electrodes (Group I) received intravenous flecainide (2 mg/kg over 10 minutes). Ten patients with chronic permanent electrodes (Group II) were given the same dose at the time of elective pulse generator change. Seven, with implanted multiprogrammable pacemakers capable of threshold analysis (Group III), were given intravenous flecainide and 5 of these were then given the drug orally for up to 3 weeks (100 mg/day increasing to 400 mg/day). In Group I the threshold measured at a pulse width of 0.5 ms rose from a control value of 0.66 to 1.44 volts after 10 minutes (p less than 0.01). In Group II the threshold rose from 1.73 to 2.13 volts (p less than 0.01) and 2 patients had total suppression of their ventricular escape rhythm for approximately one hour. In Group III patients, intravenous flecainide resulted in a rise escape rhythm for approximately one hour. In Group III patients, intravenous flecainide resulted in a rise of the pulse width threshold measured at 2.7 volts from 0.14 to 0.22 ms (p less than 0.02) and at 4.9 volts from 0.06 to 0.11 ms (p less than 0.05) after 10 minutes. After 3 weeks of oral therapy the threshold at 2.7 volts had risen to 0.11 ms /ms (p less than 0.05 after 10 minutes. After 3 weeks of oral therapy the threshold at 2.7 volts had risen from 0.09 to 0.28 ms (p less than 0.02) and at 4.9 volts from 0.06 to 0.16 ms (p less than 0.05) Flecainide significantly increased both acute and chronic thresholds and the most marked rise (greater than 200%) occurred during chronic oral therapy. Both intravenous and oral flecainide should be used with care in patients with either temporary or permanent pacing systems.
Adolescent↗