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    • Therefore the patient was diagnosed with BIP and steroid the

    2019-06-25

    Therefore, the patient was diagnosed with BIP, and steroid therapy with oral prednisolone at 40mg/day (0.5mg/kg/day) was initiated. The patient responded well to steroid therapy. After several weeks, his respiratory condition improved to Hugh–Jones class I. Since the imaging findings improved and the KL-6 level declined to 469U/mL (Fig. 2), we gradually reduced the dose of prednisolone. On the 43rd day of admission, the patient was discharged. Prednisolone was tapered gradually on an outpatient basis, and withdrawn in March 2013. Although the infiltrative shadow persisted on chest radiography and CT, his elevated serum KL-6 level had reduced and his respiratory function had improved. The patient did not have a recurrence of IP.
    Discussion There are 2 probably interdependent mechanisms involved in drug-induced IP: (1) direct, dose-dependent toxicity, and (2) an immune-mediated reaction. In the present case, we speculated that the mechanism of BIP might involve an immune reaction rather than pulmonary cytotoxicity for 3 reasons. The first was that IP was induced at a low dose of bepridil (100mg/day). In our case, the dose of bepridil was lower than that reported in previous reports (range: 100–400mg, median: 145mg). The second was the strong positive DLST result for bepridil, although the sensitivity of the DLST for diagnosis of BIP was reported to be low (Table 1). The third was that cytotoxic pulmonary injury due to drugs is often steroid-resistant, whereas our patient responded well to steroid therapy.
    Limitations
    Conclusions
    Conflict of interest
    Introduction Twelve-lead electrocardiography (ECG) in patients with Wolff–Parkinson–White (WPW) syndrome demonstrates typical delta waves and a short PQ interval, suggesting the presence of a manifest accessory pathway (AP), the so-called manifest WPW syndrome. Approximately 30–50% of patients with APs do not have delta waves because they TCS PIM-1 1 have only a retrograde electrical connection [1–4]. In contrast, several studies have reported left ventricular (LV) dysfunction in patients with manifest WPW syndrome without supraventricular tachycardia, and the LV dysfunction is primarily associated with a remarkable dyssynchrony caused by a septal AP [5–10].
    Case report In a 12-lead ECG, the PR interval was not short (138ms), and no typical delta waves were detected by the auto-analysis (Fig. 1A). Chest radiography did not indicate any cardiac enlargement. The plasma brain natriuretic peptide level was <5pg/mL. Fig. 2A shows the results of M-mode transthoracic echocardiography. The LV ejection fraction (LVEF) measured by the bi-plane Simpson׳s method was 43%. The LV diameter was slightly dilated, and the LV diastolic and systolic diameters (LVDd and LVDs) were 56mm and 45mm, respectively. However, no LV wall thinning was noted (the interventricular septum and posterior wall thickness were 0.82cm and 1.19cm, respectively). Remarkable LV dyssynchrony was observed between the septal and lateral walls. There were no abnormalities of tricuspid valve attachment such as an Ebstein׳s anomaly. Three quadripolar electrode catheters were placed in the high right atrium (HRA), in the right ventricle, and at the bundle of His via the femoral vein. During right ventricular pacing, the earliest atrial activation was recorded at HRA 1–2, on the lateral side of the right atrium (Fig. 2). We diagnosed the patient with WPW syndrome type B and performed an RFCA of the AP in consecutive sessions. The catheters placed in the HRA and at the bundle of His were extracted. We placed a decapolar electrode catheter around the lateral side of the tricuspid valve annulus and used an 8-mm-tip ablation catheter, placed with a steerable introducer, to map the ablation site of the right lateral AP. The shortest atrioventricular (A-V) interval was observed above the ablation catheter on the lateral annulus of the tricuspid valve. During right ventricular pacing, retrograde conduction via the AP was blocked 2.8s into RFCA application (Fig. 3A). After RFCA was completed, both the antegrade and retrograde conduction via the AP had disappeared. The QRS during the sinus rhythm became narrow.