Sarcopenic obesity (SO), defined as the coexistence of excess fat mass and reduced skeletal muscle mass and strength, is an emerging cardiovascular risk factor, particularly in older adults. This review summarizes recent findings on the diagnosis, prevalence, health impacts, and treatment of SO. Growing evidence suggests that SO exacerbates cardiometabolic risk and adverse health outcomes beyond either condition alone, but the heterogeneity in diagnostic criteria and the observational nature of most studies prevent a causal relationship assessment. A recent consensus definition from the European Society for Clinical Nutrition and Metabolism and the European Association for the Study of Obesity provides standardized criteria for SO diagnosis. SO is characterized by the interplay of obesity and age-related changes, which contribute to cardiovascular disease (CVD) through inflammatory, metabolic, and hormonal mechanisms. SO is associated with increased CVD risk, including hypertension, dyslipidemia, diabetes, and metabolic syndrome. However, the "obesity paradox" suggests that older individuals with established CVD classified as overweight or obese may have better prognoses, raising questions about the relationship between obesity and sarcopenia. The pathophysiology of SO involves metabolic, endocrine, hormonal, and neuromuscular changes that lead to impaired muscle protein synthesis, increased muscle breakdown, and progressive loss of muscle mass and function. SO shares common etiological mechanisms with CVD, including pro-inflammatory adipokines, oxidative stress, and mitochondrial dysfunction. These factors contribute to insulin resistance, hyperglycemia, and hyperinsulinemia, which can lead to vascular remodeling, endothelial dysfunction, and hypertension. SO is diagnosed using standardized criteria, including body composition analysis and muscle function testing. The ESPEN/EASO consensus definition aims to standardize SO diagnosis and improve prevalence estimates. Epidemiological studies show that SO prevalence varies widely, with higher rates in certain regions and populations. Clinical data indicate that SO is associated with increased CVD risk, including CVD events, CAD, stroke, and heart failure. SO is also linked to higher all-cause mortality. However, the association between SO and metabolic syndrome is less consistent. Treatment for SO focuses on lifestyle interventions, including diet, exercise, and resistance training, with emerging pharmacologic therapies showing promise. Future research should focus on using the ESPEN/EASO consensus definition to improve risk prediction and treatment strategies for SO. The review highlights the importance of body composition analysis and phenotyping in understanding SO and its impact on cardiovascular health.Sarcopenic obesity (SO), defined as the coexistence of excess fat mass and reduced skeletal muscle mass and strength, is an emerging cardiovascular risk factor, particularly in older adults. This review summarizes recent findings on the diagnosis, prevalence, health impacts, and treatment of SO. Growing evidence suggests that SO exacerbates cardiometabolic risk and adverse health outcomes beyond either condition alone, but the heterogeneity in diagnostic criteria and the observational nature of most studies prevent a causal relationship assessment. A recent consensus definition from the European Society for Clinical Nutrition and Metabolism and the European Association for the Study of Obesity provides standardized criteria for SO diagnosis. SO is characterized by the interplay of obesity and age-related changes, which contribute to cardiovascular disease (CVD) through inflammatory, metabolic, and hormonal mechanisms. SO is associated with increased CVD risk, including hypertension, dyslipidemia, diabetes, and metabolic syndrome. However, the "obesity paradox" suggests that older individuals with established CVD classified as overweight or obese may have better prognoses, raising questions about the relationship between obesity and sarcopenia. The pathophysiology of SO involves metabolic, endocrine, hormonal, and neuromuscular changes that lead to impaired muscle protein synthesis, increased muscle breakdown, and progressive loss of muscle mass and function. SO shares common etiological mechanisms with CVD, including pro-inflammatory adipokines, oxidative stress, and mitochondrial dysfunction. These factors contribute to insulin resistance, hyperglycemia, and hyperinsulinemia, which can lead to vascular remodeling, endothelial dysfunction, and hypertension. SO is diagnosed using standardized criteria, including body composition analysis and muscle function testing. The ESPEN/EASO consensus definition aims to standardize SO diagnosis and improve prevalence estimates. Epidemiological studies show that SO prevalence varies widely, with higher rates in certain regions and populations. Clinical data indicate that SO is associated with increased CVD risk, including CVD events, CAD, stroke, and heart failure. SO is also linked to higher all-cause mortality. However, the association between SO and metabolic syndrome is less consistent. Treatment for SO focuses on lifestyle interventions, including diet, exercise, and resistance training, with emerging pharmacologic therapies showing promise. Future research should focus on using the ESPEN/EASO consensus definition to improve risk prediction and treatment strategies for SO. The review highlights the importance of body composition analysis and phenotyping in understanding SO and its impact on cardiovascular health.