The aim of this clinical crossover study was to elucidate the effects of atrioventricular (AV) synchronous pacing on cardiac function in patients with sick sinus syndrome (SSS). Thirty SSS patients, each with dual chamber pacemaker (DDD), were enrolled and divided into two groups based on echocardiographic findings. Group A (n = 16) had hypertensive heart disease (wall thickness 11 approximately 12 mm) or mitral or aortic regurgitation (Grade I or II). Group B (n = 14) had no organic heart disease. Three successive 3-month pacing periods were tested. For the first 3 months, long AV delay that achieved > 80% ventricular sensing was chosen. For the next 3 months, AV delay was abbreviated to achieve > 80% ventricular pacing at an optimal AV interval. For the final 3 months, the first setting was resumed. At the end of each period, M mode echocardiography, pulsed-Doppler study, and measurement of plasma brain natriuretic peptide (BNP) level were conducted. In both groups, echocardiographic parameters were not significantly changed during the evaluation. In group A, plasma BNP level was significantly higher at the end of the short AV delay period than at the long AV delay period (P = 0.009), while in group B it did not differ during each period. AV synchronous pacing (> 80% ventricular pacing) in the SSS patients with a DDD pacemaker implanted could increase the ventricular load, and it is better to preserve the spontaneous QRS with the DDD mode with prolonged AV delay in patients with mild hypertensive or valvular disease.

yncope is often encountered in an emergency room, but its etiology is not always clear. Neurally mediated syncope, which is characterized by abnormal vagal reflex, has been recently recognized as a major cause of syncopal episodes, 1-3 and it can be provoked repeatedly by the head-up tilt test with fairly good sensitivity. 2,4 A paroxysmal attack of atrial fibrillation (AF) is another pathological entity that can be concomitant with increased vagal tone, 5 but because this arrhythmia hardly ever causes collapse while the patient has a structurally normal heart, syncope induced by the interaction of these 2 diseases has been neglected as a diagnosis. [6][7][8] We describe a patient who suffered from syncope only in the presence of AF. The head-up tilt test was negative, but the induction of AF caused faintness or syncope in an upright position. Case ReportA 64-year-old male was admitted to hospital because of repeated episodes of syncope during palpitation attacks for the past 7 months. He would lose consciousness abruptly, but recovered within 1 min without neurological symptoms. His history showed that he had had palpitation attacks for 20 years under the diagnosis of 'arrhythmia'. He had general fatigue, and occasional sweating, with the palpitations, but had never had syncope or faintness until recently.Physical examination showed mild hepatomegaly, possibly related to alcohol intake (800-900 ml of Japanese sake daily for 40 years), but otherwise normal findings.Laboratory tests revealed hyperlipidemia (triglyceride, 240 mg/dl; total cholesterol, 208 mg/dl) and hyperuricemia (8.6 mg/dl). Liver enzymes (aspartate aminotransferase, alanine aminotransferase, -glutamyl transpeptidase) were normal. Blood pressure was 132/70 mmHg, and heart rate was regular at 85 beats/min. The ECG was normal, as was ultrasonic echocardiography. Ambulatory ECG monitoring revealed occasional episodes of AF concurrent with palpitation (Fig 1). Paroxysmal AF (heart rate ~150 beats/min) was recorded during an episode of dizziness with collapse. Neither bradycardia nor long pause was recorded. The electroencephalogram was normal, which excluded epilepsy. Because no episode of syncope was detected during the hospital stay, a cardiac electrophysiological study was performed. Maximum sinus node recovery time was 1,240 ms and corrected sinus node recovery time was 420 ms. Sino-atrial conduction time was 114 ms. Atrioventricular conduction was normal (effective refractory period: 240 ms, functional refractory period: 390 ms, basic cycle length 500 ms). No arrhythmia was induced by the extrastimulus method, but AF was easily induced by rapid

A 69-year-old womanwas admitted to our hospital for the examination of syncope. Whenshe ate solid food, she had dizziness or loss of consciousness. The ambulatory ECG suggested sino-atrial block during swallowing with a maximumsinus pause of 6 seconds. An electrophysiologic study revealed pre-existing sinus node dysfunction, which was exaggerated by the balloon inflation in the esophagus. Atropine counteracted the slowing of the basal sinus rate induced by esophageal pressure, but it did not block the effect on the maximumsinus node recovery time. This observation suggested that the syncope was mediated partly by a non-vagal mechanism. (Internal Medicine 41: 207-210, 2002)

bstein anomaly is characterized by apical displacement of the septal or posterior leaflet of the tricuspid valve and may be related to abnormal cell death. Furthermore, conduction abnormalities associated with this anomaly are often confined to the atrioventricular junction. We report a rare case of Ebstein anomaly associated with an unusual conduction delay in the whole heart, as well as systolic dysfunction of both ventricles, which indicates that the entire myocardium can be impaired globally in this anomaly. Case ReportA 64-year-old man was admitted to our hospital because he had often felt palpitation and dyspnea on effort, and he had facial edema. On admission, the 12-lead electrocardiogram (ECG) revealed atrial tachycardia with 2:1 conduction and intraventricular conduction delay; his heart rate was 75 beats/min (atrial rate: 150 beats/min) (Fig 1). The cardiothoracic ratio was 61% on chest rentogenogram. Echocardiography showed severe enlargement of the right atrium and ventricle, decreased systolic function of both ventricles (end-diastolic and end-systolic left ventricular dimensions were 48 mm and 41 mm, respectively), apical displacement of the septal leaflet of the tricuspid valve by 16 mm (10.5 mm/m 2 ), and mild tricuspid regurgitation with a peak velocity of 0.78 m/s and pressure gradient of 2.4 mmHg (Fig 2). The diagnosis was Ebstein anomaly.An electrophysiological study revealed that the atrial rhythm was common atrial flutter. Atrial mapping showed a counterclockwise rotation of excitation along the tricusCirculation Journal Vol.68, July 2004 pid annulus; the atrial flutter cycle length was 400 ms (Fig 3). The post pacing interval after an extra-stimulation at the proximal coronary sinus and the low lateral right atrium was the same as the atrial flutter cycle length. Right atrial mapping showed that the slowest atrial conduction existed between RA3 and RA1 (Fig 3), located on the inferior vena cava -tricuspid annulus isthmus where low A 64-year-old man was admitted to our hospital because of palpitation, dyspnea on effort, and facial edema. The echocardiographic diagnosis was Ebstein anomaly. Although the 12-lead electrocardiogram showed an atrial rate of 150 beats/min and no typical flutter wave, the electrophysiological study showed counterclockwise rotation of excitation along the tricuspid annulus. Because of sinus arrest and syncope, a permanent pacemaker was implanted, but the right atrium was not captured by electrical stimulation at 5V/0.4 ms, except for the orifice of coronary sinus, and the intracardiac P wave was only 0.2 mV or less. This is a rare case of Ebstein anomaly characterized by unusually prolonged conduction in the atrium, the basis of which was global myocardial damage, including the ventricles.