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1.
Electrophysiologic properties of flecainide acetate   总被引:1,自引:0,他引:1  
Preliminary clinical experience indicates that flecainide is a useful antiarrhythmic agent for the suppression of spontaneous ventricular arrhythmias. The drug also exerts marked effects on accessory atrioventricular (AV) pathway and retrograde fast AV nodal pathway refractoriness, and therefore may be effective in treatment and prevention of reentrant supraventricular tachycardias. Electrophysiologic studies indicate that flecainide slows atrial, AV nodal, His-Purkinje and intraventricular conduction and, to a far lesser degree, prolongs refractory periods in these tissues. The effect of the drug in slowing conduction within the His-Purkinje system is particularly marked and is commonly associated with prolongation of the HV interval beyond the normal range. Flecainide causes a small but significant increase in the QT interval duration, which results largely from prolongation of the QRS interval. Significant prolongation of the sinus node recovery time has been observed in patients with preexisting sinus node dysfunction. Available electrophysiologic data suggest that flecainide should not be administered to patients with advanced disease of the His-Purkinje system or sinus node. The safety of the drug in patients with mild to moderate abnormalities of His-Purkinje conduction or sinus node function awaits further study.  相似文献   

2.
Flecainide is effective against certain supraventricular arrhythmias (atrial fibrillation and atrioventricular [AV] node reentrant tachycardia), but its mechanisms of action are unknown. Previous in vitro work suggests that flecainide attenuates rate-dependent action potential duration shortening, producing tachycardia-dependent prolongation of the refractory period. This study was designed to assess whether similar changes occur in vivo and whether the effects of flecainide on AV node conduction depend on heart rate and on direction of propagation (anterograde vs. retrograde). The effects of flecainide at three clinically relevant concentrations were assessed in open chest, morphine-chloralose-anesthetized dogs. Flecainide increased atrial refractory period in a concentration- and rate-related fashion (e.g., dose 3 increased the atrial effective refractory period by 9 +/- 4% at a cycle length of 1,000 ms but by 36 +/- 5% and 55 +/- 10% at a basic cycle length of 400 and 300 ms, respectively; p less than 0.001 for each). Flecainide attenuated the action potential duration accommodation (measured by monophasic action potentials) to heart rate, causing tachycardia-dependent action potential duration prolongation and accounting for most of the rate-dependent atrial effective refractory period changes. Flecainide increased Wenckebach cycle length, but the concentration-response curve was much steeper in the retrograde (slope 41 +/- 7 ms/mumol.liter-1) than in the anterograde direction (17 +/- 4 ms/mumol.liter-1; p less than 0.01), indicating more potent effects on retrograde conduction. The depressant action of the drug on the AV node was also rate dependent, with an effect on the AH interval at a basic cycle length of 400 ms that averaged 1.8, 1.5 and 2 times that at a basic cycle length of 1,000 ms for doses 1 (p less than 0.05), 2 (p less than 0.01) and 3 (p less than 0.001), respectively. Conclusions: 1) Flecainide suppresses atrial action potential duration accommodation to heart rate changes in vivo, leading to rate-dependent atrial effective refractory period prolongation, which may be important in suppressing atrial fibrillation. 2) The drug has frequency- and direction-dependent effects on AV node conduction, which may lead to selective antiarrhythmic actions during AV node reentry.  相似文献   

3.
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)  相似文献   

4.
Drugs that affect the autonomic nervous system can influence the Q-T interval directly or by changing the heart rate. Bazett's formula to correct for rate may be misleading after certain drug interventions. This hypothesis was tested in 20 patients receiving both propranolol (0.15 mg/kg intravenously) and atropine (0.03 mg/kg intravenously). Six patients received propranolol first, 7 patients received atropine first, and 7 patients received atropine plus propranolol simultaneously. During control and after drug intervention, the Q-T interval was measured directly in sinus rhythm and during a fixed atrial paced rate, and was calculated using Bazett's formula. The ventricular effective refractory period was also determined in 6 patients after administration of atropine plus propranolol. The sinus cycle length (836 ± 156 to 648 ± 84 ms, mean ± standard deviation), measured Q-T interval (367 ± 26 to 329 ± 26 ms), and atrially paced Q-T interval (330 ± 28 to 315 ±27 ms) shortened after atropine plus propranolol (p <0.001), but the corrected Q-T interval with use of Bazett's formula did not change (402 ± 33 to 412 ± 24 ms). The ventricular effective refractory period also shortened from 241 to 20 to 218 ± 21 ms after atropine plus propranolol (p <0.02). The sinus cycle length increased after propranolol (750 ± 97 to 907 ± 108 ms, p <0.001), but no change occurred in the measured Q-T interval or atrial paced Q-T interval although the corrected Q-T interval using Bazett's formula was greatly shortened (428 ± 15 to 391 ±22 ms, p <0.001). The sinus cycle length, measured Q-T interval, and atrially paced Q-T interval decreased after atropine (p <0.01), but the corrected Q-T interval lengthened (375 ± 29 to 418 ± 28 ms, p <0.01).In summary, atropine and atropine plus propranolol shorten the Q-T interval independent of rate, demonstrating a direct vagal effect on the Q-T interval. Bazett's formula inaccurately predicts the Q-T interval after administration of atropine, propranolol, and atropine plus propranolol.  相似文献   

5.
Flecainide acetate, an investigational class 1 antiarrhythmic agent, undergoes biotransformation in man with production of 2 major metabolites: meta-O-dealkylated flecainide (S-24623) and the meta-O-dealkylated lactam of flecainide (S-26191). This study compared the effects of flecainide, S-24623 and S-26191 on cardiac electrophysiologic characteristics in the anesthetized dog. Each dog received 2 dose levels of 1 of the 3 test compounds after control measurements. Flecainide (2 and 4 mg/kg in 8 dogs), S-24623 (4 and 8 mg/kg in 8 dogs) and S-26191 (4 and 10 mg/kg in 7 dogs) were administered intravenously in dilute solution. Of the 3 compounds, only flecainide significantly prolonged sinus cycle length (p less than 0.01). However, both flecainide and S-24623 significantly prolonged minimum atrial paced cycle length with 1:1 atrioventricular conduction, atrioventricular nodal effective and functional refractory periods, and right ventricular effective refractory period. Metabolite S-26191 exhibited qualitatively similar but much weaker electrophysiologic actions. The maximal electrophysiologic effects of flecainide and S-24623 were approximately equivalent, but the metabolite was about one-half as potent on a milligram-permilligram basis, and lacked marked effects on infranodal (HV interval) conduction. S-26191 was less than one-tenth as potent as flecainide. Therefore, since both flecainide metabolites occur primarily in the conjugated form in plasma (i.e., free metabolite concentrations are low), it is unlikely that these compounds either potentiate flecainide's antiarrhythmic action or increase susceptibility to drug toxicity in the clinical setting.  相似文献   

6.
Four patients with recurrent, symptomatic ventricular tachycardia (VT) refractory to conventional antiarrhythmic agents were given flecainide acetate to control arrhythmias. Ventricular stimulation studies were performed in all patients before and 1 to 2 weeks after initiation of oral flecainide therapy. Before flecainide, all patients had easily inducible VT that was morphologically identical to their spontaneously occurring arrhythmia. Flecainide increased the mean PR interval (from 0.17 to 0.23 second), mean QRS duration (from 0.08 to 0.12 second) and mean ventricular effective refractory period (from 235 to 270 ms). Mean corrected QT interval did not change (0.51 second).In 2 patients, VT could not be induced during follow-up stimulation studies. One patient has been treated successfully for 10 months, with no clinically apparent episodes of VT. One patient had recurrent nonsustained VT and was withdrawn from the study as a treatment failure after 6 months of therapy. Two patients had inducible, polymorphous VT that degenerated into ventricular fibrillation that required 2 countershocks before the successful restoration of sinus rhythm. One of these patients had VT stimulation by atrial pacing at a cycle length of 320 ms in the postflecainide electrophysiologic study. VT was not inducible by atrial pacing during this patient's preflecainide study.Thus, sustained oral flecainide administration may precipitate serious electrical instability in susceptible patients, and ventricular stimulation studies and other clinical variables may be useful in selecting patients with recurrent VT who may benefit or may be endangered by oral flecainide therapy.  相似文献   

7.
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.  相似文献   

8.
To study the effects of digitalis on the sinus node and the mechanisms involved, 16 patients with the sick sinus syndrome had electrophysiologic assessment of sinus nodal function during (1) control study, (2) after pharmacologic autonomic blockade with propranolol (0.2 mg/kg body weight and atropine sulfate 0.04 mg/kg intravenously), and (3) 10 minutes after 0.01 mg/kg of intravenous ouabain. The study was completed within 30 minutes of pharmacologic autonomic blockade. During the control study 50 percent of patients had an abnormal corrected sinus nodal recovery time or abnormal sinoatrial conduction time, or both. The effects of ouabain on sinus nodal function were compared with those after pharmacologic autonomic blockade. Ouabain significantly increased both intrinsic sinus cycle length (ouabain 975 ± 194 ms [mean ± standard deviation]; autonomic blockade 1,025 ± 218 ms, probability [p] < 0.001) and corrected sinus nodal recovery time (ouabain 615 ± 503 ms; autonomic blockade 575 ± 536 ms, p < 0.05). In contrast there was no significant change in sinoatrial conduction time after ouabain (ouabain 141 ± 56 ms; autonomic blockade 132 ± 45 ms; difference not significant). The effects of ouabain were similar in patients with both normal and abnormal sinus nodal function.These findings suggest that (1) digitalis in therapeutic doses has a depressant effect on intrinsic sinus nodal automaticity in patients with normal as well as abnormal sinus nodal function; (2) digitalis has no significant effects on sinoatrial conduction; and (3) the effects of digitalis on sinus nodal automaticity are primary and independent of its vagal and antiadrenergic effects.  相似文献   

9.
ObjectivesWe studied the effects of rate and some cardioactive drugs on the atrial surface electrocardiogram (ECG).BackgroundIn atrioventricular block, atrial surface ECG is unmasked. The effect of rate alone permits detection of the effect of other exogenous stimulations such as drugs in the presence of rate alterations.MethodsHigh fidelity, high gain ECG leads I, II and III were recorded from 51 patients with heart block. Durations of P and Ta waves and the total PTa interval were measured from nonconducted atrial events.ResultsNo relationship was found between sinus cycle length and PTa, P or Ta in 31 patients. In 20 patients, progressively decreasing the atrial pacing cycle length from 853 ms to 381 ms resulted in a linear reduction of the PTa interval from 444 to 291 ms (rho = 0.76, slope = 0.24). This was largely due to shortening of Ta. A linear rate correction formula was derived: corrected PTa = PTa − 0.24 (PP − 1000). Atropine (0.02 mg/kg) shortened the PP interval (p < 0.001) and the PTa interval (p < 0.01). Propranolol (0.1 mg/kg) prolonged the PP interval (p < 0.001) but did not alter the PTa interval. Neither disopyramide (2.0 mg/kg) nor flecainide acetate (2.0 mg/kg) altered the PP interval, but both prolonged the PTa interval (p < 0.001). This was largely due to P wave lengthening after flecainide (p < 0.001) and to Ta prolongation after disopyramide (p < 0.001).ConclusionsIn heart block, PTa, P and Ta waves can be measured reliably. The effects of pacing and some antiarrhythmic drugs on the atrial myocardium are similar to those known at the ventricular level.  相似文献   

10.
Aims Atrial fibrillation (AF) shortens the atrial action potential and the atrial refractory period. These changes promote persistence of AF. Pharmacological prolongation of atrial action potential duration (APD) may therefore help to prevent recurrent AF. In addition to prolonging APD, sodium channel blockers may prevent AF by inducing post–repolarization refractoriness (PRR). We studied whether two antiarrhythmic drugs (sotalol, flecainide) prolong APD or induce PRR in the fibrillating human atrium. Methods In 12 patients with persistent AF (11 male, 58 ± 5 yrs, 27 ± 7 months duration of AF), we recorded monophasic action potentials from the right atrial appendage and inferior right atrium at baseline and 15 minutes after intravenous administration of sotalol (1.5 mg/kg) or flecainide (2 mg/kg). APD and effective refractory periods (ERP) were determined. Results Both drugs prolonged APD90 during AF (flecainide from 109 ± 7 ms to 137 ± 10 ms, sotalol from 108 ± 6 ms to 131 ± 8 ms, both p < 0.05 vs. baseline). Sotalol prolonged ERP in parallel to APD (from 119 ± 8 ms to 139 ± 8 ms, p < 0.05). Flecainide induced PRR by prolonging ERP more than APD90 (from 134 ± 9 ms to 197 ± 28 ms, p < 0.05 vs. baseline and vs. sotalol). Conclusions Flecainide and sotalol prolong the atrial action potential during atrial fibrillation in humans. In addition, flecainide induces atrial PRR. These electrophysiological effects may reduce AF recurrences and prevent their persistence.Drs. Kirchhof, Engelen and Breithardt are Members of the Kompetenznetz Vorhofflimmern  相似文献   

11.
We studied the effects of intravenous fiecainide (2 mg.kg–1)on atrial and ventricular refractoriness and conduction duringsinus rhythm, induced atrial fibrillation and atrial pacingat rates of 100, 120 and 150 ppm, in 14 patients with normalleft ventricle. Flecainide caused a significant increase inQRS duration during sinus rhythm (mean ± SD: 87.2 ±8.4 ms vs 102.8 ± 9.1 ms, P<0.001) atrial fibrillation(87.8 ± 10.0 ms vs 108.8 ± 13.7 ms, P<0.001)and at all paced rates. The duration of the atrial electrogramwas significantly increased during sinus rhythm (54.9 ±13.2 ms vs 64.8 ± 16.6 ms, P=0.003) and at all pacingrates. The PA interval was also signficantly prolonged, as wasthe pacing stimulus-to-atrial-electrogram interval at all pacingrates. There was increased QRS duration and atrial electrogramprolongation at higher pacing rates. Atrial refractoriness wasprolonged during sinus rhythm (216.4 ± 28.2 vs 228.6± 36.1, P=0.02), but not during atrial pacing at anyrate. The QT interval, but not the JT interval or ventricularrefractoriness, was significantly prolonged during sinus rhythmand at all pacing rates. Flecainide slows atrial conductionin a use-dependent manner and increases atrial refractorinessduring sinus rhythm but not during faster atrial pacing, thusnot displaying a use-dependent effect. QRS duration is prolongedin a use-dependent manner without a commensurate increase inventricular refractoriness. In the presence of rapidly conductedatrial fibrillation, which was not found to be slowed by flecainide,this effect may constitute a proarrhythmic mechanism even inpatients with no apparent myocardial abnormality.  相似文献   

12.
Ventricular arrhythmias after Q-T prolongation by drugs could result from a nonhomogeneous increase in refractoriness (dispersion). Dispersion of effective refractory periods (ERP) was measured before and after infusion of 1 g of procainamide using twice-threshold extrastimuli applied in sinus rhythm and with 500 ms ventricular drive cycle length at 3 right ventricular sites (2 patients) or 2 right and 1 left ventricular site (10 patients). Procainamide prolonged ERP. In drive, average ERP was 247 ± 5 ms (standard error of the mean) before and 277 ± 7 ms after procainamide (p < 0.001). The Q-T interval was prolonged by 50 ms in drive (p < 0.001), but Q-T prolongation did not reflect the increased ERP (r = ?0.05). However, procainamide did not alter measured dispersion (54 ± 16 to 44 ± 14 ms in sinus, 48 ± 14 to 47 ± 13 ms in drive). Polymorphic ventricular tachycardia (VT) was induced in 6 patients in whom drive itself generally failed to reduce dispersion, and failure to induce tachycardia or shorter runs after procainamide was associated with narrowed dispersion. Polymorphic VT was not induced after procainamide in 2 patients with clinical episodes of torsades de pointes caused by type I agents. The mechanism of torsades de pointes was not explained by dispersion of refractoriness or by polymorphic VT initiated by premature beats after a type I drug.  相似文献   

13.
This study examines the efferent mechanisms of carotid sinus baroreflex influence on ventricular repolarization and refractory period compared with effects on atrioventricular (AV) nodal conduction. Pressure was controlled in both carotid sinuses by the Moisejeff technique in 16 chloralose-anesthetized dogs. Increases in carotid sinus pressure during pacing produced graded prolongation of AV nodal conduction, ventricular repolarization and refractory period with a threshold at a carotid sinus pressure of 120 mm Hg and a peak response at 200 mm Hg. Atropine, 0.4 mg/kg, attenuated the peak percent change in ventricular repolarization interval by only 12 ± 14% (± standard error of the mean) despite a significantly greater attenuation (48 ± 11%, p <0.05) in peak percent change in AV nodal conduction. However, stellate ganglionectomy attenuated the peak percent change in ventricular repolarization (42 ± 19%), similar to effects on AV nodal conduction (59 ± 21%, p >0.25). Changes in mean arterial pressure, ventricular end-diastolic segment length or segment length shortening with systole (sonomicrometer technique) did not account for the electrophysiologic responses. Latency to peak effect on ventricular repolarization (43 ± 7 seconds) was slower than that on AV nodal conduction (23 ± 6 seconds, p <0.05). This difference in time course was not abolished by atropine. Thus, the carotid sinus baroreflex prolongs ventricular repolarization and refractoriness mainly by withdrawal of sympathetic influence; AV nodal conduction is prolonged by both vagal activation and sympathetic withdrawal. In addition, differences in time course between ventricular and AV nodal electrophysiologic responses are not explained by different efferent autonomic mechanisms.  相似文献   

14.
Background: The Long QT Syndrome (LQTS) is a genetic channelopathy with life‐threatening implications. The LQT3 form of this disease is caused by mutations of the SCN5A sodium‐channel gene. A specific mutation, SCN5A:ΔKPQ, is associated with repetitive reopenings of the sodium channel and prolonged inward current. This dominant inward current is manifest on the electrocardiogram as QT prolongation. Flecainide is a potent blocker of the open sodium channel. Methods and Results: The effect of flecainide on the duration of the QT‐interval and the T‐wave morphology was systematically evaluated in five male patients age 2–64 years having the SCN5A:ΔKPQ mutation. After baseline electrocardiograms were obtained, low‐dose oral flecainide was administered for 48 hours. Serial electrocardiograms and blood flecainide levels were obtained during flecainide therapy. The QTc interval decreased on average by 104 ms, from a baseline value of 565 ± 60 ms to 461 ± 23 ms (P < 0.04) at a mean flecainide level of 0.28 ± 0.08 mg/L, with shortening of the QTonset interval (P < 0.003) and normalization of T‐wave morphology. The effects of flecainide were compared with oral mexiletine in two patients, with flecainide showing greater QTc shortening and more complete normalization of repolarization. No adverse side effects or proarrhythmia were observed with flecainide in this study. Conclusion: Low‐dose, oral flecainide consistently shortened the QTc interval and normalized the repolarization T‐wave pattern in five LQT3 patients with SCN5A:ΔKPQ mutation. This preliminary study indicates that low‐dose flecainide is a promising therapeutic agent for LQTS patients with the SCN5A:ΔKPQ sodium channel mutation. A.N.E. 2001;6(2):153–158  相似文献   

15.
The electrophysiological effects of prenalterol, a new beta-receptoragonist, in a dose of 100 µg/kg body weight given intravenouslyfor 5 min, were studied in 13 patients with signs of sinus nodedysfunction and/or conduction defects within or distal to theatrioventricular (AV) node. In nine patients with signs of sinus node dysfunction a significantreduction was found in corrected sinus node recovery time, onan average by 1955±640ms (–61%, P<0.05) andin atrial refractoriness, by 61 ±21 ms (–20%, P<0.05).Similar but insignificant changes were also seen in the fourpatients with normal sinus node function. In eight patientswith AV nodal dysfunction, a significant increase was foundin the Wenckebach point, by 51±10b.p.m (+52%. P<0.01)and a decrease in the AH interval, by 23±9ms(–14%,P<0.05). AV nodal refractoriness tended to decrease by 115±58ms(–24%, NS). Similar changes were found in the five patientswith normal AV conduction. Heart rate increased in all 13 patients,on an average by 28±5 b.p.m. (+44%, P<0.001) and systolicblood pressure by 18±8 mmHg (+13% P0.01). In conclusion, prenalterol increased sinus node automaticityand atrial and AV nodal conductivity, but did not improve infranodalconduction. Thus, the drug might be useful in the treatmentof patients with sinus node dysfunction as well as in patientswith spontaneous or induced atrioventricular conduction abnormalities.  相似文献   

16.
Summary: The cardiac electrophysiological effects of metoprolol were studied in ten patients (pts) aged 22–51 years undergoing intracardiac stimulation studies for paroxysmal palpitations. The following measurements were made: (1) basic sinus cycle length (SCL); (2) sinus node recovery time (SRT) following overdrive pacing; (3) atrio-His (A-H) and His-ventricular (H-V) conduction intervals during regular atrial pacing; (4) effective refractory periods of the atria (AERP), A-V node (AVERP) and ventricular myocardium (VERP); and (5) A-V nodal functional refractory period (AVFRP). All measurements were repeated 10–20 min after a slow bolus intravenous injection of metoprolol (0.2 mg/kg body weight). Results were analyzed by the Wilcoxon Signed Rank test. Highly significant increases in: SRT (932±166 to 1107±225 ms, p<0.001) and A-H (72±14 to 103± 14 ms, p<0.001) were observed. There were also small increases of lesser significance in SCL (794± 160 to 898±190 ms, p<0.01), AVERP (308±46 to 341±66 ms, p<0.02), and AVFRP (376±43 to 416±59 ms, p<0.01). Metoprolol did not affect the H-V interval, the AERP, or the VERP. These results are similar to those of other beta blockers.  相似文献   

17.
His bundle electrograms were obtained in 26 patients before and after intravenous administration of glucagon (50 μg/kg). The group consisted of 4 patients with normal conduction and 22 patients with conduction disease. The P-A interval, measured in all patients, was 35 ± 1.4 msec (mean ± standard error of the mean) before and 30 ± 1.5 msec after infusion of glucagon (P < 0.001). The mean A-H interval during sinus rhythm in all patients and during pacing at 100/min in 21 patients was, respectively, 97 ± 6.0 msec and 114 ± 6.4 msec before, and 96 ± 6.0 msec and 114 ± 6.6 msec after infusion of glucagon (not significant). The mean H-V interval in 25 patients was 48 ± 2.6 msec before and 49 ± 2.0 msec after infusion of glucagon (not significant). The mean sinus rate and sinus recovery times were, respectively, 73 ± 3.0 beats/min and 1,025 ± 42.0 msec before and 81 ± 3.0 beats/min and 919 ± 27.0 msec after infusion of glucagon (P < 0.001 and < 0.01). Functional and effective refractory periods were measured (In milliseconds) with use of the atrial extrastimulus technique. The mean atrial functional and effective refractory periods (21 patients) were, respectively, 273 ± 11.6 and 252 ± 12.0 before and 256 ± 10.0 and 238 ± 9.6 after infusion of glucagon (P < 0.001 and < 0.01). Mean atrloventricular (A-V) nodal functional refractory period (22 patients) and effective refractory period (15 patients) were 465 ± 22.0 and 404 ± 33.0 before and 457 ± 23.0 and 395 ± 32.0 after the infusion (not significant). The mean effective refractory period of the His-Purkinje system (2 patients) was 440 ± 45.0 before and 425 ± 55.0 after infusion of glucagon (not significant).In summary, glucagon increased sinus nodal automaticity, as manifested by an increase in sinus rate and decrease of sinus nodal recovery time, and improved intraatrial conduction as manifested by a reduction of the P-A interval and atrial functional and effective refractory periods. Glucagon had no effect on A-V nodal or intraventricular conduction.  相似文献   

18.
Amrinone is an effective inotropic agent, but its electrophysiologic effects in humans have not been previously determined. Fifteen patients with congestive heart failure (CHF) New York Heart Association functional class II to IV, underwent an electrophysiologic study after withdrawal of all other cardioactive drugs before and after 10 to 20 μg/kg/min of intravenous amrinone (doses that increased cardiac index and decreased pulmonary capillary wedge pressure and systemic vascular resistance, p < 0.002). Amrinone caused no change in PR, QRS, QTc, AH or HV intervals or maximal corrected sinus node recovery time and had no significant effect on the ventricular effective refractory periods. Amrinone decreased the atrial effective refractory period from 256 ± 40 to 240 ± 38 ms (p = 0.015), and the atrioventricular (AV) nodal functional refractory period from 374 ± 65 to 356 ± 64 ms (p < 0.05), and enhanced maximal 1:1 AV nodal conduction from 371 ± 46 to 334 ± 47 ms (p = 0.006). Nine patients had baseline HV prolongation; this was not affected by amrinone. The frequency of inducible ventricular tachycardia was not significantly affected by amrinone. Holter recordings (24 to 48 hours) were obtained from 10 patients before and after acute oral amrinone dosing (75 to 150 mg every 8 hours). There was no change in the number of ventricular premature contractions per 24 hours (2,197 ± 3,305 vs 2,616 ± 2,436) or number of runs of ventricular tachycardia per 24 hours (10 ± 12 vs 12 ± 13); however, the number of ventricular couplets per 24 hours increased from 22 ± 34 to 52 ± 55 (p = 0.054). Thus, amrinone is safe to use in patients with intraventricular conduction disturbances. It shortens the atrial effective and AV nodal functional refractory period and enhances AV nodal conduction, and it has minimal effects on ventricular arrhythmogenesis during acute drug administration.  相似文献   

19.
The effect of flecainide in 24 patients with inducible sustained ventricular arrhythmia and a history of remote myocardial infarction was determined. Flecainide was administered in oral doses individually adjusted to suppress all spontaneous ventricular tachycardia and 80% of ventricular premature complexes on 24 hour ambulatory (Holter) electrocardiography. Antiarrhythmic therapy, as assessed by Holter monitoring, was adequate in 20 (83%) of the study patients at a mean dose of 144 +/- 28 mg every 12 hours; the mean plasma flecainide level was 583 +/- 329 ng/ml. In 18 patients, the mean sinus cycle length, sinus node recovery time and atrial, atrioventricular nodal and ventricular refractory periods were unchanged. The AH interval increased by 15 +/- 15%, the HV interval by 35 +/- 32% and the QRS duration by 24 +/- 21%. Toxicity or failure to suppress ventricular premature complexes and ventricular tachycardia by Holter monitoring precluded electrophysiologic study with flecainide in four patients; two patients refused electrophysiologic study with flecainide for nonmedical reasons. Ventricular tachycardia was not inducible in 4 (22%) of 18 patients receiving flecainide. Sustained arrhythmia remained inducible in 14 patients (78%) despite evidence of antiarrhythmic efficacy on Holter monitoring, but the rate of the induced ventricular tachycardia was slower and symptoms were alleviated during ventricular tachycardia in 10 (56%) of 18 patients. The 4 patients who had no inducible ventricular tachycardia with flecainide, and the 10 patients who had inducible ventricular tachycardia with a longer cycle length and alleviation of their symptoms, have been followed up as outpatients for 16 +/- 7 months.(ABSTRACT TRUNCATED AT 250 WORDS)  相似文献   

20.
Encainide is an antiarrhythmic agent under evaluation; it is effective in ventricular and supraventricular arrhythmias. Its electrophysiological effects seem to differ according to the route of administration, oral or intravenous, probably because of the effects of active metabolites. Two electrophysiological studies were carried out in 20 patients, under basal conditions, and after 4 to 10 days oral administration at doses ranging from 75 to 300 mg/day. Encainide depressed intra-atrial conduction (prolongation of the P-A interval from 29,7 +/- 2,2 to 36 +/- 4,5 ms, p less than 0,01), slowed conduction in the atrioventricular mode (prolongation of the A-H interval from 74 +/- 14 to 98 +/- 15 ms, p less than 0,01) and the His-Purkinje system (lengthening of H-V from 50 +/- 3 to 70 +/- 6,2 ms, p less than 0,001). The sinus node function was depressed with lengthening of the corrected sinus node recovery time (297 +/- 64 to 387 +/- 71 ms, p less than 0,01) and of the sinoatrial conduction time (173 +/- 25 to 219 +/- 43, p less than 0,01). The atrial and ventricular refractory periods were significantly longer (245 +/- 16 ms to 273 +/- 10 ms, p less than 0,001, and 237 +/- 12 to 266 +/- 19 ms, p less than 0,01, respectively). This new antiarrhythmic agent therefore seems to act at all levels which suggests that it may have wide ranging antiarrhythmic effects.  相似文献   

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