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Weight bias and stigma have limited the awareness of the systemic consequences related to obesity. As the narrative evolves, obesity is emerging as a driver and enhancer of many pathological conditions. Among these, the risk of venous thromboembolism (VTE) is a critical concern linked to obesity, ranking as the third most common cardiovascular condition. Obesity is recognized as a multifactorial risk factor for VTE, influenced by genetic, demographic, behavioral, and socio-economic conditions. Despite established links, the exact incidence of obesity related VTE in the general population remains largely unknown. The complexity of distinguishing between provoked and unprovoked VTE, coupled with gaps in obesity definition and assessment still complicates a tailored risk assessment of VTE risk. Obesity reactivity, hypercoagulability, and endothelial dysfunction are driven by the so-called ‘adiposopathy’. This state of chronic inflammation and metabolic disturbance amplifies thrombin generation and alters endothelial function, promoting a pro-thrombotic environment. Additionally, the inflammation-induced clot formation—also referred to as ‘immunothrombosis’ further exacerbates VTE risk in people living with obesity. Furthermore, current evidence highlights significant gaps in the management of obesity related VTE, particularly concerning prophylaxis and treatment efficacy of anticoagulants in people living with obesity. This review underscores the need for tailored therapeutic approaches and well-designed clinical trials to address the unique challenges posed by obesity in VTE prevention and management. Advanced research and innovative strategies are imperative to improve outcomes and reduce the burden of VTE in people living with obesity.
Weight bias and stigma have limited the awareness of the systemic consequences related to obesity. As the narrative evolves, obesity is emerging as a driver and enhancer of many pathological conditions. Among these, the risk of venous thromboembolism (VTE) is a critical concern linked to obesity, ranking as the third most common cardiovascular condition. Obesity is recognized as a multifactorial risk factor for VTE, influenced by genetic, demographic, behavioral, and socio-economic conditions. Despite established links, the exact incidence of obesity related VTE in the general population remains largely unknown. The complexity of distinguishing between provoked and unprovoked VTE, coupled with gaps in obesity definition and assessment still complicates a tailored risk assessment of VTE risk. Obesity reactivity, hypercoagulability, and endothelial dysfunction are driven by the so-called ‘adiposopathy’. This state of chronic inflammation and metabolic disturbance amplifies thrombin generation and alters endothelial function, promoting a pro-thrombotic environment. Additionally, the inflammation-induced clot formation—also referred to as ‘immunothrombosis’ further exacerbates VTE risk in people living with obesity. Furthermore, current evidence highlights significant gaps in the management of obesity related VTE, particularly concerning prophylaxis and treatment efficacy of anticoagulants in people living with obesity. This review underscores the need for tailored therapeutic approaches and well-designed clinical trials to address the unique challenges posed by obesity in VTE prevention and management. Advanced research and innovative strategies are imperative to improve outcomes and reduce the burden of VTE in people living with obesity.
Study Objectives Obstructive sleep apnea (OSA) is characterized by disordered breathing during sleep and is associated with major cardiovascular complications. Glucagon-like peptide 1 receptor agonists (GLP-1RA) as an important treatment for obesity and diabetes mellitus show promising therapeutic prospect in OSA. We conducted a meta-analysis to evaluate the effect of GLP-1RA intervention in OSA individuals. Methods We searched the PubMed and Web of Science databases (published until July 1, 2024), The included studies evaluated the GLP-1RA in OSA individuals and the efficacy outcomes measured by apnea-hypopnea index (AHI). Results Six studies with a total of 1067 participants enrolled. GLP-1RA significantly decreased AHI with an estimated treatment difference of−9.48 events per hour (95% CI, −12.56 to −6.40, I2=92%). The change in weight was -10.99kg and BMI was –1.60kg/m2. The mean difference in SBP was -4.81mmHg and in DBP was –0.32 mmHg. Tirzepatide significantly reduced AHI more than liraglutide with an estimated treatment difference of -21.86 events per hour (95% CI, -25.93 to-17.79) vs -5.10 events per hour (95% CI, -6.95 to-3.26). Obese individuals experienced a more significant decrease in AHI with an estimated treatment difference of−12.93 events per hour vs -4.31 events per hour. The application of CPAP and the duration of follow-up did not affect the therapeutic effect. Conclusion GLP-1RA could significantly reduce the severity of OSA, and also lead to weight loss and lower blood pressure. Further high-quality RCTs are needed to explore different GLP-1RA treatments and durations in OSA, and identify patient subgroups that may benefit the most.
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