Even short-term high-rate atrial excitation could differentially alter the mRNA levels of Kv1.5, Kv4.2, and Kv4.3 in a rate-dependent manner. In particular, increased Kv1.5 gene expression, having a transient nature, implied the possible biochemical electrical remodeling unique to paroxysmal tachycardia.

No abstract

No abstract

SUMMARYProlonged QT interval is suggested to indicate an increased risk of sudden cardiac death in certain clinical conditions such as diabetes mellitus. We investigated whether the individual QT interval is an indicator of an autonomic state. An ambulatory 24-hour ECG was recorded in 53 subjects from different clinical backgrounds. Power spectral components of heart rate variability (HRV) and the QT interval were regressively obtained at a heart rate of 60, 70, 80, 90, or 100 beats per minutes (bpm). Log values of the high-frequency component of HRV (HF: 0.15-0.50 Hz, a scale of cardiac parasympathetic tone) failed to show a relationship with the QT interval. In contrast, the QT interval at a heart rate of 90 bpm and 100 bpm showed a significant correlation with the log values of the low-frequency component (LF: 0.04-0.15 Hz) and the log[LF / HF], i.e., a putative scale of sympathetic tone (100 bpm: QT vs logLF: r = 0.414, p < 0.005, QT vs log[LF / HF]: r = 0.416, p < 0.002). Also, attenuated rate-dependent QT shortening was associated with greater logLF and log[LF / HF] values at a heart rate of 80, 90, or 100 bpm. These results suggest that the QT interval at a moderate heart rate (approximately 90-100 / min) and the degree of rate-dependent QT shortening are related to individual sympathetic tone. (Jpn Heart J 2000; 41: 713-721) Key words: Diabetes mellitus, Coronary artery disease, Ambulatory ECG monitoring, Heart rate variability, Sympathetic nerve, Parasympathetic nerve PPROLONGED QT intervals have been shown to be related to an increased risk of sudden cardiac death in apparently healthy subjects 1) in addition to patients with coronary artery disease (CAD)2) or diabetes mellitus (DM).3) To clarify the underlying pathogenic mechanism of these clinical observations, it appears important to understand whether the QT interval is associated with a particular cardiac autonomic state or not. However, the response of the QT interval to pharmacological autonomic modifications is often conflicting.4-10) Also, an intricate sympathovagal interaction 11) blurs the respective contribution of each limb of the autonomic nerve system to the QT interval. Thus, it is not readily predictable how the autonomic state is reflected on the QT interval in conditions without specific

We present a 57-year-old man with Wolff-Parkinson-White syndrome who exhibited a wide "gap" in retrograde conduction through a concealed atrioventricular accessory pathway. The appearance of the wide "gap" depended on the ventricular pacing sites. While ventricular extrastimuli at a basic cycle length of 600 msec from the right ventricular outflow tract consistently conducted to the atria, retrogradely through the accessory pathway, those from the right ventricular apex repeatedly revealed disappearance of the retrograde conduction at the wide coupling intervals from 550 to 380 msec. The mechanisms of this rare "gap"-like phenomenon are discussed in this paper.