Monophasic Action Potential Duration at the Crista Terminalis in Patients With Sinus Node Disease

Abstract

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...

Role of Oxidation-Dependent CaMKII Activation in the Genesis of Abnormal Action Potentials in Atrial Cardiomyocytes: A Simulation Study

“…The resting membrane potential (RMP), maximum upstroke velocity (dV/dt max ), action potential amplitude (APA), and action potential duration at 90% repolarization (APD 90 ) were measured as −75.2 mV, 160 mV/ms, 110 mV, and 312 ms, respectively. These parameters were consistent with previous models developed by Grandi et al [33], Courtemanche et al [43], and Nygren et al [44], and APD 90 was within the scope of previously reported experimental data [45][46][47][48], as listed in Table 1.…”

Pro‐arrhythmogenic effects of atrial fibrillation‐induced electrical remodelling: insights from the three‐dimensional virtual human atria

“…Note that the RAA model was validated using experimental data from human (APD 90 in the model is 230 ms at a BCL of 1000 ms, compared to 255 ± 45 ms observed by Bosch et al . (1999)) and other models were validated by their APD relative to the RAA using either human or canine data (as necessitated by human data availability or lack thereof; Feng et al 1998; Li et al 2001; Burashnikov et al 2004; Katoh et al 2005; Gong et al 2008). Additional details of the AP morphology validation are presented in the Online Supplement (Figs S8–S12).…”

“…The absence of particular experimental data sets is a common limitation of modelling studies accounting for regional heterogeneity in the human atria, and, in common with the present investigation, the approach of incorporating data from alternative species has been implemented in previous studies (Courtemanche et al 1998; Seemann et al 2006; Aslanidi et al 2011 b ; Dorn et al 2012). It is encouraging that such an approach has resulted in models that can replicate regional APD and AP morphology differences observed in both the human and the canine atria (Feng et al 1998; Burashnikov et al 2004; Katoh et al 2005; Gong et al 2008). It should be noted that major results of the present study were confirmed by replacing the updated CRN‐based models with a different family of human atrial AP models developed recently by Dorn et al (2012).…”

Clinical and Electrophysiological Characteristics of Binodal Disease

“…Baba et al, 15 who compared 90 SSS patients and 14 healthy subjects, found that the high right atrium (HRA) -HBE interval and HRA -coronary sinus interval were significantly prolonged in the SSS group, and Katoh et al 16 reported that the monophasic action potential duration at the crista terminalis in the SSS group (n=13) was significantly prolonged compared with the control group (n=13). Both studies described a significant disturbance of intraatrial conduction in patients with SSS.…”