ABSTRACT
<p><b>BACKGROUND</b>Atrial AutoCapture™ (ACap™) was a new technological development that confirmed atrial capture by analyzing evoked response (ER) with a new method - paced depolarization integral ER detection - and optimized energy output to changes in the stimulation threshold. The purpose of this study was to evaluate the clinical performance of ACap™ function.</p><p><b>METHODS</b>This was a prospective, observational, nonrandomized two-center study. Between November 2008 and August 2014, 102 patients were enrolled from two different institutions. Data were collected by case report forms at enrollment, hospital discharge, and in-office follow-ups scheduled at 1, 2, 3, 6, and 12 months postimplantation.</p><p><b>RESULTS</b>Ambulatory ACap™ function started to become available for 20.6% of patients at 1 day, then progressed to 30.4% at 7 days, 38.6% at 1 month, 41.6% at 2 months, 47.5% at 3 months, 53.5% at 6 months, and 63.4% at 1 year. The cause of the unsuccessful attempts to perform ACap™ threshold was ER/polarization <2:1. Availability for SD, BND, and HOCM indications had shown better results than AVB indication. For SD indication cases, feasibility was significantly better for SD with paroxysmal atrial fibrillation (pAF) than SD without pAF (78.4% vs. 35.0% at 1 year, n = 71, P< 0.001). At each stage of the clinical follow-ups, there had been a strict correlation between ACap™ measurements and those conducted manually with P 0.001 (n = 299).</p><p><b>CONCLUSIONS</b>It has been concluded that ACap™ function was safe and effective to confirm atrial threshold and reduce energy output automatically. ACap™ function is unavailable for some patients at early stages of the implantation; however, availability has been progressively increasing during follow-up.</p>
ABSTRACT
<p><b>OBJECTIVE</b>To report the clinical features and the prognosis, the methods of diagnosis and treatment, and the early detection of the pulmonary toxicity induced by amiodarone.</p><p><b>METHOD</b>The clinical course, the findings of X-ray and CT and the results of treatment were summarized and analyzed in six patients with amiodarone-induced pulmonary toxicity.</p><p><b>RESULTS</b>Five males, one female, aged 62 - 69 (66.0 +/- 2.4) years. Amiodarone was used because of paroxysmal atrial fibrillation in five patients and ventricular arrhythmia in one. The loading dose was 7 g and the maintaining dose was 0.2 g/d or less. Pulmonary toxicity was recognized at the times in 0.5 - 4.0 (2.1 +/- 1.3) years after amiodarone therapy. Dyspnea occurred, crack rales were audible in both lower parts of the lungs, and the chest X-ray showed grid-like changes in case one. No symptom was found in the others. Their diagnosis was made according to the pulmonary intestinal changes by high-resolution computerized tomography when the lung marking was increased or deranged by chest X-ray during the regular follow-up. Pulmonary function examination showed that the restrictive ventilation and the CO diffusing capacity decreased in case one, while the CO diffusing capacity was normal in the others. The decreased obstructive ventilation capacity was found in case six. Amiodarone was discontinued in all the cases after the diagnosis of induced pulmonary toxicity. One patient was treated with corticosteroid, three with azithromycin, and the another two patients were not treated with drug. During 0.1 - 5.0 year period of follow-up the symptoms were markedly attenuated in case one, and no new symptoms and radiography findings were found in the others.</p><p><b>CONCLUSIONS</b>Pulmonary toxicity is a serious adverse effect of amiodarone. The typical feature is pulmonary intestinal fibrosis and thick pulmonary intestine in the early stage. Corticosteroid treatment seems effective. It would be helpful for early diagnosis to take chest X-ray examination regularly and CT examination in suspicions cases during the therapy. The prognosis may be good in the early diagnosed cases.</p>