Tokutada Sato

Mechanism of decrease in the atrial potential after implantation of a single-lead VDD pacemaker: atrial histological changes after implantation of a VDD pacemaker lead in dogs.

HIGASHI, Y., et al.: Mechanism of Decrease in the Atrial Potential After Implantation of a Single‐Lead VDD Pacemaker: Atrial Histological Changes After Implantation of a VDD Pacemaker Lead in Dogs. The single‐lead VDD pacemaker system (VDDPS) enables atrial synchronous ventricular pacing with only one lead in patients with an atrioventricular block. There are some cases in which the atrial potential decreases after implantation of a VDDPS, making physiological pacing difficult. The mechanism of this decrease has not been elucidated yet. To elucidate the possible relationship between the decrease of the atrial potential after implantation of a VDDPS and histopathological changes of the atrium. We implanted a VDDPS from the jugular vein under anesthesia in 10 adult dogs. The tip of the pacing lead was fixed in the right ventricular apex of the heart under fluoroscopic guidance. Then, the lead was ligated and fixed to the jugular vein at a point where a favorable atrial potential was obtained. The end of the lead was passed from the neck to the back subcutaneously; then pulled outside and fixed there to measure the atrial potential. The atrial potential was measured using a pacing system analyzer under anesthesia on days 3 (n = 9) and 7 (n = 8) , as well as on weeks2 (n = 6), 3 (n = 4), and4 (n = 3), after the implantation. The heart was removed from the dogs on day3 (n = 2), day7 (n = 2), week2 (n = 2), and week4 (n = 4)to examine the atrial histological findings. The atrial potential was2.7 ± 0.7 mVat the time of the implantation,1.7 ± 1.1 mV (P < 0.05)on day 3, and1.7 ± 0.7 mVon week 4 after the implantation. Macroscopically, the pacemaker lead was covered with thrombus, and adhered to the atrial wall in 80% of animals. Microscopically, the endocardium was hypertrophic due to fibrous tissue; besides RBC extravasation, inflammatory cells infiltration and degeneration of myocardial cells, were observed under the endocardium. Inflammatory changes developed in the atrial wall after implantation of the VDDPS, and this seemed to be one of the mechanisms for the decrease of the atrial potential of the VDDPS. (PACE 2003; 26:685–691)

Pulmonary vein isolation under direct visual identification of the left atrium—pulmonary vein junction using intra-cardiac echography

Introduction: Intra-cardiac echocardiography (ICE) which has some benefits, can be used to obtain detailed anatomy of the heart chambers or large vessels, and the catheter positions, and it has been considered useful for improving the outcome of the ablation. In the present study, we performed pulmonary vein isolation (PVI) under real time monitoring of ICE imaging utilizing an ICE catheter placed at the junction of the left atrium (LA) and PVs (LA-PV junction).Methods: PVI for atrial fibrillation (AF) was performed in 30 cases with drug-resistant AF (mean age: 66-years-old; including 22 males). An ICE catheter utilizing a 9 MHz frequency was inserted into the LA via the atrial septum, and placed at the LA-PV junction. Circumferential ablation was performed in the LA outside of the PV ostium, encircling both the superior and inferior ostia together under ICE imaging.Results: The anatomy of the LA to the PVs and catheter sites were clearly identified by the ICE during the procedure, which enabled a precise and safe catheter manipulation with minimal fluoroscopy. Further, the wall thickness of the PV and LA, and position of the esophagus could be obtained by ICE, facilitating care in adjusting the power and/or duration of the current delivery.Conclusion: ICE imaging of the LA-PV junction permitted real time monitoring of the target sites for PVI during the ablation procedure, and was considered a useful technique for performing PVI.

Cardiopulmonary arrest due to persistent coronary spasm in a young woman: Are we properly diagnosing vasospastic angina?

Coronary spasm is a risk factor for acute myocardial infarction and sudden cardiac death. This is a case of a young female patient with cardiopulmonary arrest induced by coronary spasm on arrival at our hospital. There has been no case that prolonged spontaneous attack was confirmed in multi-vessels. This case demonstrates that persistent coronary spasm is lethal and an important cause of cardiopulmonary arrest even in young people. It is extremely important to detect patients with coronary spasm before the ischemic events associated with cardiopulmonary arrest occur.

A Case With Apical Hypertrophic Cardiomyopathy, Multiple Coronary Artery–Left Ventricular Fistulae, and a Morphological Structure Mimicking Left Ventricular Noncompaction Statue of Cerberus or Double-Headed Eagle?

Multiple coronary fistulae that drain into the left ventricle are rarely associated with apical hypertrophic cardiomyopathy.1 On the other hand, associations of left ventricular noncompaction (LVNC) and multiple coronary fistulae or hypertrophic cardiomyopathy have previously been reported in several cases.2,3 We report here a unique case of apical hypertrophy of the left ventricle, multiple coronary–left ventricular fistulae, and a morphological structure of the left ventricular myocardium mimicking LVNC. A 59-year-old man was admitted to our hospital for fever and rapidly progressing dyspnea that had persisted for 10 days. He had been diagnosed with apical hypertrophic cardiomyopathy in his 30s, although he had no regular medical checkups and was asymptomatic. On admission, the patient had mild wheezes audible in the midportion of the right lung and a diastolic murmur heard at the Erb and the cardiac apical area. Chest x-ray and computed tomography revealed cardiac enlargement with increased pulmonary vasculature, granular shadows in the lower areas of both lungs, and increased density of the right middle lung area. These findings suggested failure of the left side of the heart with pneumonia. A 12-lead electrocardiogram (ECG) …