Electrophysiologic effects of oral theophylline in sinus bradycardia

Alboni, Paoló; Rossi, Paolo; Ratto, B.; Pedroni, P.; Gatto, E; Antonioli, G

doi:10.1016/0002-9149(90)91012-u

Cited by 20 publications

(12 citation statements)

References 12 publications

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“…In this study 117 patients with symptomatic sick sinus syndrome (age 73 11 years) were randomized to no treatment (control group, n=35), dual-chamber rateresponsive pacemaker therapy (n=36) and oral theophylline (n=36), a drug which improves sinus node function [25] and increases sinus rate during long-term follow-up [26][27][28] . Patients were evaluated for randomization if they met all of the following criteria: (1) age d45 years; (2) mean resting sinus rate <50 beats .…”

Section: The Theopace Studymentioning

confidence: 99%

Is sinus bradycardia a factor facilitating overt heart failure?

Alboni¹

1999

European Heart Journal

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Section: The Theopace Studymentioning

confidence: 99%

Is sinus bradycardia a factor facilitating overt heart failure?

Alboni¹

1999

European Heart Journal

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“…[21][22][23] Several studies demonstrated theophylline's chronotropic effect in non-SCI patients with bradycardia secondary to atrioventricular nodal block, heart transplantation, chronic symptomatic bradycardia, vasodepressor syncope, and bradysystolic cardiac arrest. [24][25][26][27][28][29][30] However, the pathophysiology of autonomic dysfunction in patients with acute SCI is vastly different from that of the other conditions listed above. 1 We theorized that an increase in sympathetic nervous system activity from aminophylline administration was associated with successful prevention of bradycardic events without a resulting increase in resting heart rate in our patient.…”

Section: Discussionmentioning

confidence: 99%

Efficacy of Aminophylline for Treatment of Recurrent Symptomatic Bradycardia After Spinal Cord Injury

Whitman

Schroeder²,

Ploch

et al. 2008

Pharmacotherapy

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Cardiac dysrhythmias and cardiac arrest can occur after acute spinal cord injury (SCI). Disrupted sympathetic innervation after SCI results in unopposed parasympathetic activity leading to baseline bradycardia. Hence, vagal stimulation can result in episodes of exaggerated symptomatic bradycardia. Data supporting pharmacologic intervention for treatment of symptomatic bradycardia after SCI are limited. We describe a patient who sustained a high cervical SCI and subsequently developed episodic symptomatic bradycardia. The addition of aminophylline to the patient's therapeutic regimen was associated with resolution of the bradycardia. Throughout her treatment course, the patient's serum theophylline concentrations were 1.9-3.4 mg/L. These levels were consistent with those identified in other case reports describing treatment with methylxanthines to prevent episodic bradycardia after SCI. Our understanding of drug pharmacokinetics and pharmacodynamics in patients with acute SCI is limited and provides an ideal opportunity for further study in this area.

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“…The most probable mechanism by which the drug exerts this action is the antagonism of the cardiac effect of adenosine, which has been found to depress sinus node automaticity 15 , 16 ) . Several electrophysiology studies reported that theophylline improves sinus node function in subjects with sinus bradycardia and enhances nodal conduction 17 , 18 ) . In uncontrolled studies performed in patients with symptomatic SND, oral theophylline increased the resting and exercise heart rate, improved symptoms, and reduced sinus pauses during the follow-up period 19 ) .…”

Section: Discussionmentioning

confidence: 99%

Clinical Characteristics of Hypervagotonic Sinus Node Dysfunction

Park

Cho

Yum

et al. 2004

Korean J Intern Med

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BackgroundSinus node dysfunction (SND) is caused not only by intrinsic sinus node disease, but also by the extrinsic factors. Among the extrinsic factors, autonomic imbalance is most common. Symptomatic SND usually requires permanent pacemaker therapy. However, the clinical characteristics and patient response to medical therapy for hypervagotonic SND have not been properly clarified.Materials and MethodsThirty two patients (14 men, 18 women, 51 ± 14 years) with hypervagotonic SND were included in this study, but those patients who had taken calcium antagonists, beta-blockers or other antiarrhythmic drugs were excluded. Hypervagotonic SND was diagnosed if the abnormal electrophysiologic properties of the sinus node were normalized after the administration of atropine (0.04 mg/kg).ResultsThe presenting arrhythmias were 16 cases of sinus bradycardia (50.0%), 12 of sinus pause (37.5%), 3 of sinoatrial block (9.4%) and 1 of tachy-bradycardia (3.1%). Nine (28.1%) patients had hypertension, 7 (21.9%) smoked, 2 (6.3%) had diabetes mellitus, and 1 (3.1%) had hypercholesterolemia. Among the patients, 3 had no remarkable symptoms, 13 had dizziness, 7 had syncope, 3 had weakness and 6 had shortness of breath. Twenty five (78.1%) patients were treated with theophylline, 1 patient with tachy-bradycardia syndrome was treated with digoxin and propafenone, and 6 (18.8%) were treated with no medication. During the 43±28 month follow-up, 25 patients remained asymptomatic, but 6 who took no medication developed mild dizziness. One patient needed permanent pacemaker implantation owing to recurrent syncope despite of theophylline treatment.ConclusionThese results show that hypervagotonic SND has a benign course and most of the patients can be managed safely without implanting a pacemaker. (Ed note: I like the abstract. It is short and direct, as it should be.)

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Electrophysiologic effects of oral theophylline in sinus bradycardia

Cited by 20 publications

References 12 publications

Is sinus bradycardia a factor facilitating overt heart failure?

Is sinus bradycardia a factor facilitating overt heart failure?

Efficacy of Aminophylline for Treatment of Recurrent Symptomatic Bradycardia After Spinal Cord Injury

Clinical Characteristics of Hypervagotonic Sinus Node Dysfunction

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