Impact of a Home Telehealth Program After a Hospitalized COPD Exacerbation: A Propensity Score Analysis

Introduction: Currently there is lack of data regarding the impact of a home telehealth program on readmissions and mortality rate after a COPD exacerbation-related hospitalization. Objective: To demonstrate if a tele-monitoring system after a COPD exacerbation admission could have a favorable effect in 1-year readmissions and mortality in a real-world setting. Methods: This is an observational study where we compared an intervention group of COPD patients treated after hospitalization that conveyed a telehealth program with a followance period of 1 year with a control group of patients evaluated during one year before the intervention began. A propensity-score analyses was developed to control for confounders. The main clinical outcome was 1-year all-cause mortality or COPD-related readmission. Results: The analysis comprised 351 telemonitoring patients and 495 patients in the control group. The intervention resulted in less mortality or readmission after 12 months (35.2% vs. 45.2%; hazard ratio [HR] 0.71 [95% CI=0.56–0.91]; p=0.007). This benefit was maintained after the propensity score analysis (HR=0.66 [95% CI=0.51–0.84]). This benefit, which was seen from the first month of the study and during its whole duration, is maintained when mortality (HR=0.54; 95% CI=[0.36–0.82]) or readmission (subdistribution hazard ratio [SHR] 0.66; 95% CI=[0.50–0.86]) are analyzed separately. Conclusion: Telemonitoring after a severe COPD exacerbation is associated with less mortality or readmissions at 12 months in a real world clinical setting. (AU)

Impact of a Home Telehealth Program After a Hospitalized COPD Exacerbation: A Propensity Score Analysis.

INTRODUCTION: Currently there is lack of data regarding the impact of a home telehealth program on readmissions and mortality rate after a COPD exacerbation-related hospitalization. OBJECTIVE: To demonstrate if a tele-monitoring system after a COPD exacerbation admission could have a favorable effect in 1-year readmissions and mortality in a real-world setting. METHODS: This is an observational study where we compared an intervention group of COPD patients treated after hospitalization that conveyed a telehealth program with a followance period of 1 year with a control group of patients evaluated during one year before the intervention began. A propensity-score analyses was developed to control for confounders. The main clinical outcome was 1-year all-cause mortality or COPD-related readmission. RESULTS: The analysis comprised 351 telemonitoring patients and 495 patients in the control group. The intervention resulted in less mortality or readmission after 12 months (35.2% vs. 45.2%; hazard ratio [HR] 0.71 [95% CI=0.56-0.91]; p=0.007). This benefit was maintained after the propensity score analysis (HR=0.66 [95% CI=0.51-0.84]). This benefit, which was seen from the first month of the study and during its whole duration, is maintained when mortality (HR=0.54; 95% CI=[0.36-0.82]) or readmission (subdistribution hazard ratio [SHR] 0.66; 95% CI=[0.50-0.86]) are analyzed separately. CONCLUSION: Telemonitoring after a severe COPD exacerbation is associated with less mortality or readmissions at 12 months in a real world clinical setting.

Expression of myostatin in human hematopoietic cells unveils novel autocrine/paracrine actions for the hormone.

Myostatin is a member of the transforming growth factor ß (TGFß) superfamily that has a well-established role as a mediator of muscle growth and development. However, myostatin is now emerging as a pleiotropic hormone with multiple actions in the regulation of the metabolism as well as several aspects of both cardiac and smooth muscle cells physiology. In addition, myostatin is also expressed in several nonmuscular cells where its physiological role remains to be elucidated in most cases. In this report, we have shown that both myostatin and its receptor system are expressed in blood cells and in hematopoietic cell lines. Furthermore, myostatin treatment promotes differentiation of both HL60 and K562 cells through a mechanism that involves activation of extracellular signal-regulated kinases 1/2 and p38-mitogen-activated protein kinase, thus leading to the possibility that myostatin may be a paracrine/autocrine factor involved in the control of haematopoiesis. In addition, the presence of myostatin expression in immune cells could envisage a novel role for the hormone in the pathogenesis of inflammatory diseases.