Clinical Characteristics of Hypervagotonic Sinus Node Dysfunction.
- Author:
Hyung Wook PARK
1
;
Jeong Gwan CHO
;
Ju Hyup YUM
;
Young Joon HONG
;
Ji Hyun LIM
;
Han Gyun KIM
;
Ju Han KIM
;
Weon KIM
;
Young Keun AHN
;
Myung Ho JEONG
;
Jong Chun PARK
;
Jung Chaee KANG
Author Information
1. Department of Internal Medicine, Division of Cardiology, Chonnam National University Medical School, Gwangju, Korea. chojg@unitel.co.kr
- Publication Type:Original Article
- Keywords:
Sick sinus syndrome;
Vagus;
Autonomic hyperactivity;
Electrophysiologic study
- MeSH:
Dizziness/etiology;
Dyspnea/etiology;
Female;
Humans;
Male;
Middle Aged;
Muscle Weakness/etiology;
Sick Sinus Syndrome/*complications/drug therapy;
Syncope/etiology;
Theophylline/therapeutic use;
Vasodilator Agents/therapeutic use
- From:The Korean Journal of Internal Medicine
2004;19(3):155-159
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND: Sinus 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 METHODS: Thirty 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). RESULTS: The 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. CONCLUSION: These 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.)
