Abstract
In this study, both acute electrophysiologic actions of intravenously administered theophylline and clinical effects of chronic oral theophylline therapy were assessed in 10 young patients (aged 9 to 41 years) without clinically significant cardiac disease, in whom recurrent symptoms of syncope and dizziness were attributed to transient bradyarrhythmias (sinus pauses, marked sinus bradycardia or paroxysmal atrioventricular [AV] block). Intravenous theophylline infusion (serum concentration range 9.5 to 12.0 mg/liter) shortened means sinus cycle length (control 973 ± 285 ms versus theophylline 880 ± 226 ms, p <0.005) and decreased both the estimated sinoatrial conduction time (control 169 ± 56.0 ms versus theophylline 143 ± 55.3 ms, p <0.05) and the maximum corrected sinus node recovery time (control 442 ±251.0 ms versus theophylline 255 ± 146.2 ms, p <0.05). In addition, theophylline infusion shortened the minimum atrial paced cycle length with sustained 1:1 AV conduction (control 414 ± 86 ms versus theophylline 379 ± 97 ms, p <0.05) and consistently reduced AV node functional refractory periods. Subsequent chronic oral theophylline therapy (serum levels 9 to 12 mg/liter) was tolerated in 8 patients (80%). During a follow-up of 5 to 24 months, suppression of symptoms was achieved in 6 of the 8 patients. Thus, theophylline exhibits positive chronotropic and dromotropic effects in man at serum concentrations in the usual therapeutic range (10 to 15 mg/liter). Furthermore, suppression of symptoms during follow-up suggests that theophylline treatment may be a useful therapeutic consideration in some patients with recurrent symptomatic bradyarrhythmias.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 1223-1229 |
| Number of pages | 7 |
| Journal | The American Journal of Cardiology |
| Volume | 52 |
| Issue number | 10 |
| DOIs | |
| State | Published - Dec 1 1983 |
Bibliographical note
Funding Information:From the Departments of Medicine, Surgery and Pediatrics, University of Minnesota, Mlnneapolls, Minnesota, and the Department of Medicine, University of California, San Francisco, California. This work was supported in part by both a Grant-in-Aid (DGB) and a Fellowship award (MRP) from the American Heart Association (Minnesota Affiliate), Minneapolis, Minnesota, and by Grant lF32 HL06097-01 (JK) from the National Institutes of Health, Bethesda, Maryland. Dr. Benditt is an Established Investigator of the American Heart Association. Manuscript received February 22, 1963; revised manuscript received August 1. 1963, accepted August 5, 1963.