inus arrest and sinoatrial block (sinus node disease: SND) decrease cardiac output and elicit AdamStokes syndrome. To improve the activities of daily life of patients with SND, pacemaker therapy is used, but because the incidence of SND increases with age, the number of the patients and cost of pacemaker therapy are increasing in developed countries.SND occurs because of either a decrease in the pacemaker potential to a level below the threshold of overshoot of the action potential or exit block of the pacemaker activity to the surrounding atrial muscle. Recently, an electroanatomical mapping technique demonstrated that structural and electrical abnormalities of the atrium characterized SND. 1 However, the properties of repolarization, based on structural differences of the right atrium (RA), have not been clarified in SND patients.The monophasic action potential (MAP) of the human heart enables us to estimate the repolarization of the human ventricle 2 and atrium 3 in the clinical setting. In this study, we developed a new technique of recording the MAP at the crista terminalis (CT) in the superior vena cava -RA junction. Using this method, we estimated the properties of the Circulation Journal Vol. 69, November 2005 MAP at the CT in the SND patients and compared it with the conventional indices of sinus node function. Also, we demonstrated the effect of adenosine triphosphate, known to enhance sinus arrest or sinoatrial block, 4 on the MAP at the CT in the SND patients.
Methods
Patient PopulationThirteen consecutive SND patients and 13 age-and sexmatched control patients were enrolled. All subjects underwent diagnostic electrophysiological studies (EPS) while in a postabsorptive nonsedated state. SND patients were defined as those having a ventricular pause lasting for more than 3 s because of either sinus arrest or sinoatrial block with symptoms related to a pause (Rubinstein type II or III). Control patients were defined as having none of those findings. Patients with (1) sinus bradycardia less than 50 beats/min in mean heart rate (Rubinstein type I), (2) atrial fibrillation, atrial flutter or atrial tachycardia during the monitoring described later, (3) a past history of heart failure and (4) ongoing cardiac ischemia were excluded because we wanted to focus on the characteristic of the MAP related to the particular type of ventricular pause. All patients underwent electrocardiography and ambulatory 24 h-Holter electrocardiogram (ECG) at least twice in the outpatient clinic. In addition, ambulatory monitoring by ECG for 24-48 h after admission and before the EPS was performed. All antiarrhythmic or cardioactive medications were ceased for at least 5 times the biological half-life of the drugs.Written informed consent from the patients and approval
Monophasic Action Potential Duration at the Crista Terminalis in Patients With Sinus Node DiseaseHiroshi Katoh; Tsuyoshi Shinozaki, MD*; Shigeo Baba, MD*; Shoichi Satoh, MD**; Yutaka Kagaya, MD*; Jun Watanabe, MD*; Kunio Shirato, MD* Background The repolarizati...