Yohichiro Furuta

Termination of Ventricular Tachycardia by an Implantable Atrial Pacemaker and External Pacemaker Activator

An atrial pacemaker was implanted in a patient who had dilated cardiomyopathy, sinus node dysfunction, and drug‐resistant ventricular tachycardia (VT). VT episodes were terminated by atrial overdrive pacing using an implanted pacmaker and a newly developed handheld external programmer/transmitter. Although successful cases of termination of intractable VT by ventricular pacing have recently been reported, the ventricular method might increase the risk of accelerating VT. Atrial overdrive pacing is a safer method since it minimizes the possibility of tachycardia acceleration and, combined with antiarrhythmic drugs, it appeared to be a unique and useful approach for the treatment of drug‐resistant VT.

Cardiac Adaptation to Dynamic Exercise in Pacemaker Implanted Patients

To clarify the mechanism of cardiac adaptations to dynamic exercise excluding chronotropic effect, supine bicycle ergometer exercise with 2-dimensional echocardiogram was performed in 27 pacemaker implanted patients (PMI-pts), whose heart rate were constant during exercise, and six healthy subjects (control: C). Simultaneously, cuff-blood pressure (BP) and serum catecholamine were measured. Patients were divided into two groups by exercise capacity in the sitting bicycle ergometer. Group I (G-I) consisted of 15 patients with relatively good physical work capacity (maximal load: 80 watt ≦ in male, 60 watt ≦ in female) and group II (G-lI) of 12 patients with depressed physical work capacity (maximal load: 60 watt ≧ in male, 40 watt ≧ in female). The resting left ventricular function was impaired in group II. During the initial stage of exercise, left ventricular enddiastolic dimension (EDD) and percent fractional shortening (%FS) in group I increased significantly greater than those in the other two groups, and left ventricular end-systolic dimension (ESD) in group I decreased greater than that in the other groups (G-I ≫ G-II > C). Increase of systolic BP, posterior wall velocity and systolic BP/ESD ratio in group I and controls were greater than those in group II (G-I = C > G-II). At the last stage of exercise, increases of ESD and systolic BP/ESD ratio in group I were lower than those in controls. Plasma norepinephrine levels in PMI-pts were significantly higher than in controls at rest and during exercise (G-II ≫ G-I > C). Thus, group I adapts to exercise mainly due to the Frank-Starling mechanism, and to a lesser degree due to an augmentation of contractility corresponding to an increase of circulatory catecholamines. On the other hand, group II can not adapt sufficiently to exercise because of near limitation of preload-reserve and contractility reserve at rest, in spite of a remarkable activation of sympathetic nervous system.