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We present the case of a 59-year-old woman diagnosed with Mycobacterium shinjukuense infection using mass spectrometry of bronchioalveolar lavage fluid. We initiated treatment with clarithromycin, rifampicin, and ethambutol based on the results of drug susceptibility testing, which improved lung opacities. Most previous cases were treated with the standard regimen for Mycobacterium tuberculosis. However, our regimen may provide a therapeutic option for this rare nontuberculous Mycobacterium infection. [ABSTRACT FROM AUTHOR]

Background The association between social factors and the long-term prognosis of acute heart failure (AHF) remains unclear. Methods and results One thousand fifty-one AHF patients were screened, and 915 were enrolled. Four hundred forty-two AHF patients ≥75 years of age (the elderly cohort) were also included in a sub-analysis. Participants who fulfilled one of the three marital status-, offspring-, and living status-related criteria were considered socially vulnerable. On this basis they were classified into the socially vulnerable ( n = 396) and non-socially vulnerable ( n = 519) groups in the overall cohort, and the socially vulnerable ( n = 219) and non-socially vulnerable ( n = 223) groups in the elderly cohort. Kaplan–Meier curves showed that the survival rate of the socially vulnerable group was significantly poorer than that of the non-socially vulnerable group in the overall ( p = 0.049) and elderly ( p = 0.004) cohorts. A multivariate Cox regression model revealed that social vulnerability was an independent predictor of 1000-day mortality in the overall [hazard ratio (HR): 1.340, 95% confidence interval (CI): 1.003–1.043, p = 0.048] and elderly cohort (HR: 1.531, 95% CI: 1.027–2.280, p = 0.036). Regarding the components of social vulnerability, the marital status was an independent factor in the elderly cohort (HR: 1.500, 95% CI 1.043–2.157, p = 0.029). Conclusion Social vulnerability was independently associated with long-term outcomes in AHF patients, especially in the elderly cohort. Organization of the social structure of AHF patients might be able to improve their prognosis. [ABSTRACT FROM AUTHOR]

Background The gender differences in the prognosis of Asian patients with acute heart failure (AHF) remain to be elucidated. Methods and results One thousand fifty AHF patients were enrolled. The patients were assigned to a female group ( n = 354) and a male group ( n = 696). A Kaplan–Meier curve showed that the cardiovascular survival rate of the female group was significantly lower than that of the male group ( p = 0.005). A multivariate Cox regression model identified female gender [hazard ratio (HR): 1.381, 95% CI: 1.018–1.872] as an independent predictor of 730-day cardiovascular death. In subgroup analysis by age, in patients over 79 years, female gender significantly increased the cardiovascular death (HR: 1.715, 95% CI: 1.088–2.074, p < 0.001) with a significant interaction ( p -value for interaction < 0.001). The prognosis, including cardiovascular death, was significantly poorer among elderly female patients (≥79 years) than among elderly male patients ( p = 0.019). The multivariate Cox regression model identified female gender as an independent predictor of 730-day cardiovascular death in patients who were older than 79 years of age (HR, 1.943; 95% CI, 1.192–3.167). Conclusions Female gender was associated with poor prognosis in AHF patients. In particular, old age (≥79 years) was associated with adverse outcomes in female patients with AHF. [ABSTRACT FROM AUTHOR]

The prevalence of atrial fibrillation (AF) has been increasing in aging societies. The prognostic impact of AF associated with worsening heart failure (HF) remains obscure. We analyzed 1170 acute heart failure (AHF) patients who required intensive care. Patients were assigned to two groups according to the prevalence of AF: no episode of AF (n = 940) and pre-existing AF (Group-1, n = 230). Patients with no episode of AF (n = 940) were further divided into two groups according to presence of new-onset of AF after admission (Group-2a, n = 258) or not (Group-2b, n = 682). Kaplan-Meier curve analysis showed that prognosis, including all-cause mortality and HF-events within 1000 days, was significantly poorer in the Group-1 compared to the Group-2b. However, a multivariate Cox regression model showed that the Group-1 was not an independent predictor of 1000-day mortality and HF-events. Furthermore, Kaplan-Meier curve analysis showed that prognosis, including all-cause mortality and HF-events within 1000 days, was significantly poorer in the Group-2a than in the Group-2b. A multivariate Cox regression model revealed that the Group-2a was an independent predictor of 1000-day mortality (HR: 1.403, 95% CI: 1.018–1.934) and HF-events (HR: 1.352, 95% CI: 1.071–1.708). A multivariate logistic regression model showed that only age (≥75 years old) was independently associated with new-onset of AF after admission (odds ratio: 1.556, 95% CI: 1.130–2.143). New-onset AF associated with worsening HF increases with age and is independently-associated with adverse outcome in patients with AHF. • The prognostic impact of AF associated with worsening heart failure (HF) is not obscured. • A multivariate Cox regression model showed that the pre-AF was not an independent predictor of 1000-day mortality and HF event. • A multivariate Cox regression model revealed that the new-onset AF group was an independent predictor of 1000-day mortality. • A multivariate logistic regression model showed that only age was independently associated with new onset of AF after admission. [ABSTRACT FROM AUTHOR]

Idiopathic pulmonary fibrosis (IPF) is a lethal lung disease with a poor prognosis. Fibroblast proliferation amplifies extracellular matrix deposition and increases angiogenesis. Vascular endothelial growth factor (VEGF) is one of the most potent angiogenic factors. VEGF interacts with VEGF receptors (VEGFR1 and VEGFR2). A previous study showed that VEGFR1 tyrosine kinase (TK) signaling induced blood flow recovery mediated by bone marrow (BM)-derived stem cells. We hypothesized that VEGFR1-TK signaling might be related to pulmonary fibrosis. Six-week-old male C57Bl/6 wild-type (WT) mice and VEGFR1 TK knockout mice (TKKO mice) were treated with a single intratracheal injection of bleomycin (BLM; 0.1 μg in 50 μl saline) or vehicle (saline; 50 μl). Lung fibrosis was evaluated by histology, real-time PCR and ELISA for pro-fibrotic factors, and assessment of lung mechanics. The fibrotic area in the lung and the lung elastance were significantly reduced in TKKO mice (P < 0.01). The expression of the fibrosis-related factors type I collagen, S100A4, and transforming growth factor (TGF)-β was also significantly reduced in TKKO mice on day 21 after BLM injection. TKKO mice also had significantly lower levels of stromal cell-derived factor (SDF)-1 in the lungs and plasma on days 14 and 21 after BLM treatment (P < 0.05). Moreover, the expression of C-X-C chemokine receptor type 7 (CXCR7) and CXCR4, the receptors for SDF-1, was also suppressed in TKKO mice. Immunohistochemical analysis showed that treatment with a CXCR4 antibody decreased the accumulation of VEGFR1+ cells in the lung in WT mice but not in TKKO mice. These results suggest that VEGFR1 TK signaling promotes BLM-induced pulmonary fibrosis by activating the SDF-1/CXCR4 axis in infiltrating VEGFR1+ cells. [ABSTRACT FROM AUTHOR]