Obesity is a major contributor to heart failure (HF), particularly heart failure with preserved ejection fraction (HFpEF). Obesity leads to structural and functional changes in the cardiovascular system, including left ventricular (LV) remodelling, epicardial fat accumulation, endothelial dysfunction, and coronary microvascular dysfunction. These changes increase the risk of HF, atrial fibrillation, sudden cardiac death, and other cardiovascular diseases. Obesity is associated with metabolic and inflammatory disorders, such as insulin resistance, oxidative stress, and chronic low-grade inflammation, which further exacerbate cardiovascular disease. Obesity is classified based on body mass index (BMI), with BMI ≥ 30 kg/m² defined as obesity. The global prevalence of obesity has increased significantly over the past decades, and it is now a major public health issue. Obesity is closely linked to other cardiovascular risk factors, such as hypertension, diabetes, and dyslipidaemia, which contribute to the development of HF. Obesity also increases the risk of obstructive sleep apnoea (OSAS), which is an independent risk factor for cardiovascular diseases, including HF. Obesity is associated with a higher prevalence of HFpEF compared to HF with reduced ejection fraction (HFrEF). The pathogenesis of HFpEF in obesity involves multiple mechanisms, including LV remodelling, epicardial fat accumulation, and coronary microvascular disease (CMVD). CMVD is a key contributor to HFpEF and is characterized by impaired coronary flow reserve (CFR), reduced coronary blood flow, and increased vascular resistance. Cardiovascular imaging techniques, such as echocardiography, cardiac MRI, and PET/CT, are essential for diagnosing and managing HF in obese patients. These techniques help assess LV function, epicardial fat, and coronary microvascular disease. Echocardiography is the most widely used and cost-effective method for evaluating LV remodelling and function in obese patients. The treatment of HF in obese patients is challenging, particularly in those with preserved ejection fraction (HFpEF). Weight loss is a critical therapeutic intervention, and various strategies, including bariatric surgery, GLP-1 receptor agonists, and SGLT2 inhibitors, have shown promise in reducing body weight and improving HF outcomes. SGLT2 inhibitors have been shown to reduce the risk of cardiovascular death and hospitalization for HF in both diabetic and non-diabetic patients. They also reduce epicardial fat accumulation and improve coronary microvascular function. In conclusion, obesity is a significant contributor to the development and progression of HF, particularly HFpEF. Effective management of obesity is essential for improving outcomes in patients with HF. Weight loss, along with targeted therapies such as SGLT2 inhibitors, plays a crucial role in the treatment of HF in obese patients.Obesity is a major contributor to heart failure (HF), particularly heart failure with preserved ejection fraction (HFpEF). Obesity leads to structural and functional changes in the cardiovascular system, including left ventricular (LV) remodelling, epicardial fat accumulation, endothelial dysfunction, and coronary microvascular dysfunction. These changes increase the risk of HF, atrial fibrillation, sudden cardiac death, and other cardiovascular diseases. Obesity is associated with metabolic and inflammatory disorders, such as insulin resistance, oxidative stress, and chronic low-grade inflammation, which further exacerbate cardiovascular disease. Obesity is classified based on body mass index (BMI), with BMI ≥ 30 kg/m² defined as obesity. The global prevalence of obesity has increased significantly over the past decades, and it is now a major public health issue. Obesity is closely linked to other cardiovascular risk factors, such as hypertension, diabetes, and dyslipidaemia, which contribute to the development of HF. Obesity also increases the risk of obstructive sleep apnoea (OSAS), which is an independent risk factor for cardiovascular diseases, including HF. Obesity is associated with a higher prevalence of HFpEF compared to HF with reduced ejection fraction (HFrEF). The pathogenesis of HFpEF in obesity involves multiple mechanisms, including LV remodelling, epicardial fat accumulation, and coronary microvascular disease (CMVD). CMVD is a key contributor to HFpEF and is characterized by impaired coronary flow reserve (CFR), reduced coronary blood flow, and increased vascular resistance. Cardiovascular imaging techniques, such as echocardiography, cardiac MRI, and PET/CT, are essential for diagnosing and managing HF in obese patients. These techniques help assess LV function, epicardial fat, and coronary microvascular disease. Echocardiography is the most widely used and cost-effective method for evaluating LV remodelling and function in obese patients. The treatment of HF in obese patients is challenging, particularly in those with preserved ejection fraction (HFpEF). Weight loss is a critical therapeutic intervention, and various strategies, including bariatric surgery, GLP-1 receptor agonists, and SGLT2 inhibitors, have shown promise in reducing body weight and improving HF outcomes. SGLT2 inhibitors have been shown to reduce the risk of cardiovascular death and hospitalization for HF in both diabetic and non-diabetic patients. They also reduce epicardial fat accumulation and improve coronary microvascular function. In conclusion, obesity is a significant contributor to the development and progression of HF, particularly HFpEF. Effective management of obesity is essential for improving outcomes in patients with HF. Weight loss, along with targeted therapies such as SGLT2 inhibitors, plays a crucial role in the treatment of HF in obese patients.