Intravenous amiodarone suppressed the electrical storm and decreased the QT and Tp-e dispersions in patients treated by using CRT with a defibrillator.

Introduction Given that few studies investigated the efficacy of catheter ablation (CA) in patients with paroxysmal atrial fibrillation (AF) and atrial septal defect (ASD), this study evaluated its effectiveness in patients with paroxysmal AF and ASD. Methods and Results Of the 216 patients who underwent ASD device closure at two hospitals, 36 patients had paroxysmal AF. After April 2012, CA for AF was performed before ASD device closure (ASD‐CA group; n = 20). The ASD‐CA group had a significantly higher AF‐free survival rate after ASD device closure compared to patients without CA for AF before ASD device closure (ASD‐non‐CA group; n = 16) (ASD‐CA group: 2 patients vs. ASD‐non‐CA group: 9 patients; follow‐up period: 4.2 ± 2.5 years; log‐rank p = .01). In addition, the AF‐free survival rates were similar between the ASD‐CA group and 80 paroxysmal AF patients who underwent CA without any detectable structural heart disease (non‐SHD‐CA group). The two groups were matched by propensity scores for age, sex, and left atrium dimension (ASD‐CA group: 2 patients vs. non‐SHD‐CA group: 5 patients; follow‐up period: 3.3 ± 1.8 years; log‐rank p = .28). Conclusion CA for AF before ASD device closure might be an effective treatment option for patients with paroxysmal AF and ASD.

Cardiac involvement in muscular dystrophy (MD) is known to cause heart failure (HF). However, little is known about the differences in electrocardiographic and echocardiographic findings between MD patients with and without the experience of hospitalization for HF. We retrospectively identified 95 MD patients (mean age at diagnosis of MD 41.1 ± 18.7 years; males 64.2%), including nine (9.4%) patients who were hospitalized for HF (the HF group) and 86 (90.6%) patients who were not (the non-HF group) during the follow-up period (16.7 ± 12.2 years). The HF group had a significantly wider QRS duration (126.0 ± 37.6 vs. 98.1 ± 16.7 ms, p < 0.001) and QTc interval (454.6 ± 50.5 vs. 409.5 ± 23.6 ms, p < 0.001) at the time of HF hospitalization than the non-HF group. The HF group also had a significantly lower left ventricular (LV) ejection fraction (35.4 ± 19.2 vs. 62.5 ± 11.3%, p < 0.001) and significantly larger diastolic LV dimension (64 ± 2 vs. 45 ± 1 mm, p < 0.001) and left atrial diameter (38 ± 12 vs. 29 ± 6 mm, p = 0.003) at the time of HF hospitalization than the non-HF group. In the HF group, the QRS duration was significantly wider at the time of HF hospitalization than at the initial electrocardiogram before the development of HF (129.8 ± 30.7 vs. 119.0 ± 33.3 ms, p = 0.018). This study suggests that HF occurs in MD patients with electrocardiographic and echocardiographic abnormalities. Early recognition of abnormal findings during a regular electrocardiographic or echocardiographic follow-up may be useful for identifying cardiac involvement in MD.

A 60-year-old woman presented with ST-elevation myocardial infarction due to extrinsic compression of the left main coronary artery (LMCA) caused by a dilated pulmonary artery (PA) with idiopathic pulmonary hypertension and was successfully treated with intravascular ultrasound-and optical coherence tomographyguided stenting. Continuous subcutaneous epoprostenol infusion therapy was initiated immediately after the procedure and increased aggressively. Imaging modalities were extremely useful in making the diagnosis and providing follow-up of LMCA compression syndrome in this case. Over the one-year observation period, a sufficient hemodynamic improvement was obtained, without exacerbation of the PA dilatation, resulting in the absence of compression of the LMCA.

Although a previous randomized study showed that the use of atrial natriuretic peptide (carperitide) improved the long-term prognosis of patients with heart failure, its effect on short-term prognosis remains unclear. We retrospectively identified patients who were admitted to our tertiary-care center with acute decompensated heart failure (ADHF) between April 2009 and December 2013.We divided the eligible patients into two groups: patients who started receiving carperitide on the day of admission (carperitide group) and those who did not receive carperitide during hospitalization (control group). We compared the in-hospital mortality between the two groups using propensity scores derived from 40 baseline variables. We identified 879 eligible patients (mean age, 75.2 years; male, 56.7%), including 336 (38.2%) in the carperitide group and 543 (61.8%) in the control group. One-to-one propensity score matching created 177 pairs. Although the unmatched analysis found a significantly lower in-hospital mortality in the carperitide group than in the control group (3.3% vs. 7.9%, respectively, p = 0.005), the propensity score-matched analysis found no significant difference in in-hospital mortality between the two groups [4.0% vs. 5.1%, p = 0.609; risk difference, -1.1%, 95% confidence interval (CI), -5.5-3.2%]. Logistic regression analysis with adjustment for propensity scores also found no significant association between carperitide use and in-hospital mortality (adjusted odds ratio, 0.61; 95% CI, 0.29 to 1.28; p = 0.605). The present retrospective study showed that carperitide use as the initial treatment was not significantly associated with lower in-hospital mortality in patients with ADHF.