Effects of digitalis on atrial vulnerability

Engel, Toby R.; Gonzalez, Ana Del C.

doi:10.1016/0002-9149(78)90625-2

Cited by 53 publications

(8 citation statements)

References 23 publications

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“…In a randomized, placebo-controlled trial of patients with atrial fibrillation and normal left ventricular function, digoxin did not increase the number of conversions to sinus rhythm; moreover, in that study SDC was higher than the levels found in this investigation [3]. However, two experimental studies in dogs [4][5], one of which showed a relation between the conversion of atrial fibrillation to the inotropic actions of acetyl strophanthidin I5], an electrophysiologic study in humans [6], and several clinical trials demonstrating the efficacy of prophylactic digoxin in preventing postoperative atrial fibrillation indicate that the controversy is still not resolved. In any case, when digoxin and quinidine are used in the treatment of atrial fibrillation or flutter, elevation of SDC by quinidine does not appear to play an important role in the return to sinus rhythm.…”

Section: Sumatilal Shah and Howard S Friedmanmentioning

confidence: 70%

The relation of quinidine-Induced elevation of serum digoxin concentration to the conversion of atrial fibrillation-flutter: A pilot study

Shah

Frıedman

1989

Cardiovasc Drug Ther

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Similarly, some of the apparent therapeutic effects of digoxin might also be related to the elevation of SDC by quinidine.Atrial fibrillation that fails to revert to sinus rhythm after digoxin administration will sometimes convert soon after quinidine administration. Because quinidine can influence SDC within 30 minutes of its administration, even before appreciable amounts are detected in the blood by standard laboratory methods [2], elevation of SDC by quinidine might be the cause of such occurrences. Although the role of digitalis in the conversion of atrial fibrillation to sinus rhythm is still not clear, knowing whether SDC elevations accompany the conversion of arrhythmias after quinidine administration in patients who have received digoxin would be of interest. The findings of a preliminary study undertaken to examine this question are presented.Nineteen patients comprised the study group. All were hospitalized because of atrial fibrillation or flutter of apparent recent onset and converted to sinus rhythm following the administration of digoxin (group I) or following the administration of digoxin and quinidine (group II).Digoxin was measured by radioimmunoassay and quinidine by spectrofluorometric assay. SDC was measured just before administration of the first dose of quinidine and at the time of conversion to sinus rhythm. The serum quinidine concentration was measured at the time of conversion. Student's t test was used to assess changes. Values are expressed as mean _+ standard error of the mean. P < 0.05 was considered statistically significant.Nine patients (group I I converted to sinus rhythm after receiving digoxin and no quinidine: Seven of these patients converted within 11/2 days of admission (in six, less than 24 hours), after receiving an average of 0.8 +-0.2 mg (0.t25 -1.5 mg) of digoxin. One converted on the third day and one on the sixth day; both had been receiving 0.25 mg per day of digoxin, but the former had also received a beta blocker and antithyroid medication for hyperthyroidism.Ten patients (group II) who did not convert to sinus rhythm while receiving digoxin converted after the administration of quinidine. Four had been receiving digoxin when the arrhythmia developed; their SDC before quinidine administration was 0.4-0.6 ng/ml. Six had received 1.6 _+ 0.2 mg (0.825-1.75 mg) digoxin over 3.8 -+ 0.7 days (2-5 days) without converting to sinus rhythm. Quinidine sulfate, 200-300 mg, every 6 hours, and digoxin, 0.125-0.25 mg per day --if there was no conversion 24 hours after beginning quinidine administration --were administered to these ten patients. Three patients converted within 24 hours of beginning quinidine therapy; their SDC changed by -0.2-0.4 ng/ml and their serum quinidine concentration (SQC) measured 1.5-3 ~tg/ml at the time of conversion. Six converted after 2-3 days of the regimen; their SDC changed from -0.3-1.0 ng/ml, and their SQC measured 2.7-6.2 ~g/ml at the time Address tbr correspondence and reprint requests: Howard S. Friedman, MD, Chief of CardioloKv, The Brook...

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Section: Sumatilal Shah and Howard S Friedmanmentioning

confidence: 70%

The relation of quinidine-Induced elevation of serum digoxin concentration to the conversion of atrial fibrillation-flutter: A pilot study

Shah

Frıedman

1989

Cardiovasc Drug Ther

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“…In previous reports'0 [15][16][17] In summary, as with clinical paroxysms of AFF, vulnerability to AFF was not associated with unique abnormalities of atrial refractoriness.…”

Section: Dispersion Of Atrial Refractoriness/luck and Engelmentioning

confidence: 70%

Dispersion of atrial refractoriness in patients with sinus node dysfunction.

Luck¹,

Engel²

1979

Circulation

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SUMMARY Abnormal atrial refractoriness was examined as a cause of atrial fibrillation/flutter (AFF) in patients with bradycardia. Refractory periods at three disparate right atrial sites were compared in 17 patients with sinus node dysfunction (SND) and 16 controls. Atrial pacing shortened refractory periods, but failed to decrease dispersion of refractoriness significantly. During sinus rhythm, duration and dispersion of refractoriness were greater in SND patients than in controls. These differences persisted with atrial pacing. For example, at the paced rate, dispersion of effective refractory periods in SND patients was greater than in controls (62.9 ± 34 vs 36.6 ± 21 msec,p < 0.01). Six SND patients had AFF, but they did not have greater dispersion than other SND patients, or unusually short or long refractory periods. Thus, prolonged and nonuniform refractoriness were features of SND. Abnormal refractoriness in SND reflected atrial disease and persisted with pacing. These abnormalities were not unique to patients with AFF.EARLY ATRIAL EXTRASYSTOLES are critical to the initiation of atrial fibrillation and flutter (AFF).1, 2 According to one theory, AFF results from nonuniform recovery of excitability3 4 and nonhomogeheous spread of the early excitation.5 Thus, AFF results when there is dispersion of atrial refractoriness. Because slower heart rates have been shown to increase the normal dispersion of canine atrial refractoriness,6 bradycardia should predispose to ectopic atrial rhythms.7 A clinical model of this theory would be the bradycardia-tachycardia sequences in some patients with sinus node dysfunction (SND).6 9 HIowever, faster heart rates curtail atrial refractoriness in man, exposing the vulnerable zone to excitation.'0 Thus, vulnerability to AFF from early extrasystoles could reflect a shortened refractory period rather than dispersion of refractory periods. Alternative explanations for atrial tachycardias include enhanced automaticity or tachycardias triggered from afterpotentials." These mechanisms suggest that faster, not slower heart rates, predispose to AFF.In this investigation we assess atrial refractoriness in patients with SND to delineate the role of bradycardia in determining dispersion of refractoriness and arrhythmia in man. In this preliminary investigation, measurements were limited to the right atrium of patients without obvious hemodynamic abnormalities.

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“…Such findings might have implications for the clinical observation that atrial fibrillation may terminate after administration of digitalis [3,4], especially when heart failure improves [4]. A reduced tendency to induce nonsustained atrial fibrillation after digitalis administration has also been demonstrated in apparently normal atria [8]. Thus, in atrial fibrillation cardiac glycosides not only exert inotropic and dromotropic effects, but they also have a complex effect on atrial fibrillation itself which under certain conditions might even be antifibrillatory as well.…”

Section: Discussionmentioning

confidence: 91%

“…The influence of cardiac glycosides on atrial fibrillation has previously been tested by determining the energy requirements for its induction [7], measuring the duration of the vulnerable period [8], or, indirectly, by assessing the electrophysiologic conditions that might favor its occurrence, such as whether there had been a shortening of the atrial refractory period [9]. In this study, duration of atrial fibrillation after its induction by rapid atrial electrical stimulation was used as the standard for determining change in the predilection for this arrhythmia.…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, in humans, atrial effective/or functional refractory periods have been found either to lengthen, in the neurally intact heart [8], or to show no change, both in the intact and denervated heart [15], after digitalis administration. The direct atrial fibrillationenhancing effects of cardiac glycosides, and even their neurohumoral-mediated actions, may therefore relate more to their producing a greater dispersion of atrial refractoriness, perhaps caused by a variable response of the atrial myocardium to these stimuli [11,14], than to any global electrophysiologic changes.…”

Section: Theoretical Considerationsmentioning

confidence: 99%

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Effects of acetyl strophanthidin on duration of atrial fibrillation in the neurally-intact and blockaded dog

Mokraoui

Frıedman

Melniker

et al. 1988

Cardiovasc Drug Ther

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Although the inotropic and dromotropic effects of cardiac glycosides in atrial fibrillation (AF) are well recognized, their action on AF itself is not clear. Accordingly, to determine whether cardiac glycosides prolong AF, the duration of electrically induced AF, atrioventricular conduction, and left ventricular function were assessed for 30 minutes before and for 30 minutes following intravenous administration of acetyl strophanthidin (AS), 20 micrograms/kg, in neurally intact, beta-blocked, and beta-blocked and vagotomized dogs. In the intact dog, AS, 20 micrograms/kg, increased peak dp/dt by 132 +/- 35 mmHg.sec-1, p less than 0.05, and slowed ventricular response by 16 +/- 7 min-1, p less than 0.05, but had a variable effect on AF duration. While the increased left ventricular peak dp/dt persisted for 15 minutes after AS, an increased duration of AF was evident only at 20 minutes, when the effects of AS on left ventricular (LV) inotropy were no longer apparent. Moreover, the subset of dogs that did not demonstrate prolongation of average duration of AF after AS had a greater increment of peak dp/dt than those that showed prolongation, 237 +/- 52 versus 53 +/- 31 mmHg.sec-1, p less than 0.05. An additional 20 micrograms/kg, which produced ventricular extrasystoles, prolonged AF duration when compared to both control and 30-minute measurements. Acetyl strophanthidin, 20 micrograms/kg, had a variable effect on duration of AF with beta-blockade but prolonged duration by 114 +/- 34%, p less than 0.05, with both vagotomy and beta-blockade.(ABSTRACT TRUNCATED AT 250 WORDS)

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Effects of digitalis on atrial vulnerability

Cited by 53 publications

References 23 publications

The relation of quinidine-Induced elevation of serum digoxin concentration to the conversion of atrial fibrillation-flutter: A pilot study

The relation of quinidine-Induced elevation of serum digoxin concentration to the conversion of atrial fibrillation-flutter: A pilot study

Dispersion of atrial refractoriness in patients with sinus node dysfunction.

Effects of acetyl strophanthidin on duration of atrial fibrillation in the neurally-intact and blockaded dog

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