Objective: This study aimed to estimate the pooled level of self-care behaviour among heart failure patients in Ethiopia.
Design: Systematic review and meta-analysis.
Data Source: PubMed/MEDLINE, HINARI, Web of Sciences, Scopus, Google Scholar, Science Direct, African journals online and University repositories were searched from 1 January 2000 to 1 November 2023.
Eligibility Criteria: We include studies that examined self-care behaviour among heart failure patients, studies that report factors associated with self-care behaviour and observational studies (cross-sectional, case-control and cohort) with full text available.
Data Extraction And Synthesis: The data were extracted with Microsoft Excel and analysed by using STATA V.11 software. The weighted inverse variance random-effects model at 95% CI was used to estimate the pooled level of self-care behaviour and its associated factors among heart failure patients. Tests of heterogeneity, test of publication bias and subgroup analyses were also employed.
Results: Thirteen cross-sectional studies with 4321 study participants were included; and the pooled level of good self-care behaviour among heart failure patients in Ethiopia was found to be 38.3% (95% CI 31.46 to 45.13). Only 68.8% of heart failure patients were knowledgeable about heart failure. Knowledge about heart failure (Adjusted Odds Ratio (AOR)=3.39; 95% CI 2.42 to 4.74) and absence of comorbidity (AOR=2.69; 95% CI 1.35 to 5.37) were significantly associated with good self-care behaviour among heart failure patients in Ethiopia.
Conclusion: The majority of heart failure patients in Ethiopia did not adhere to the recommended self-care behaviours. Nearly one-third of heart failure patients were not knowledgeable about heart failure. Knowledge about heart failure and the absence of comorbidities were significantly associated with good self-care behaviour. Therefore, efforts should be devoted to increasing knowledge and preventing comorbidities among heart failure patients.
Prospero Registration Number: CRD42023394373.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10729130 | PMC |
http://dx.doi.org/10.1136/bmjopen-2023-071960 | DOI Listing |
N Engl J Med
January 2025
From Duke University School of Medicine, Durham, NC; and Duke Clinical Research Institute, Durham, NC.
Am J Respir Crit Care Med
January 2025
University of Minnesota, Medicine, Minneapolis, Minnesota, United States.
Chronic Obstr Pulm Dis
January 2024
Division of Pulmonary and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States.
Background: The impact of iron deficiency on COPD morbidity independent of anemia status is unknown. Understanding the association between iron deficiency, anemia status, and risk of hospitalization in COPD may inform an approach to these comorbidities.
Study Design And Methods: Adults ≥40 years from the Johns Hopkins COPD Precision Medicine Center of Excellence data repository with an outpatient iron profile and 1 year of subsequent follow-up time were included in the study.
Proc Natl Acad Sci U S A
February 2025
Department of Molecular Microbiology, Washington University in St. Louis, School of Medicine, St. Louis, MO 63130.
bradyzoites reside in tissue cysts that undergo cycles of expansion, rupture, and release to foster chronic infection. The glycosylated cyst wall acts as a protective barrier, although the processes responsible for formation, remodeling, and turnover are not understood. Herein, we identify a noncanonical chitinase-like enzyme TgCLP1 that localizes to micronemes and is targeted to the cyst wall after secretion.
View Article and Find Full Text PDFPLoS One
January 2025
Precision Laboratory of Vascular Medicine, Shanxi Cardiovascular Hospital Affiliated Shanxi Medical University, Taiyuan, PR China.
Background: Myocardial ischemia-reperfusion injury (MIRI) is an important complication in the treatment of heart failure, and its treatment has not made satisfactory progress. Nitroxyl (HNO) showed protective effects on the heart failure, however, the effect and underlying mechanism of HNO on MIRI remain largely unclear.
Methods: MIRI model in this study was established to induce H9C2 cell injury through hypoxia/reoxygenation (H/R) in vitro.
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