Abstract:
Obesity is a major risk factor for the development and progression of heart failure (HF). It is present in approximately 70% of patients with heart failure with preserved ejection fraction (HFpEF) when assessed using body mass index
(BMI), with an even higher prevalence when evaluated based on visceral adipose tissue accumulation around internal organs. Obesity contributes to HF through multiple pathophysiological mechanisms, including increased cardiac workload, metabolic dysregulation, and systemic inflammation. Excess adipose tissue leads to elevated circulating blood volume and cardiac output, which, over time, can result in left ventricular hypertrophy and subsequent systolic or diastolic dysfunction. Furthermore, obesity is frequently associated with comorbid conditions such as hypertension, diabetes mellitus, and dyslipidemia, all of which further elevate the risk of HF. Implementing strategies aimed at weight reduction, including dietary modifications, behavioral interventions, physical activity, bariatric surgery, and pharmacologic therapy, may be beneficial for both the prevention and treatment of HF, particularly HFpEF. Currently, several clinical trials are investigating the efficacy of pharmacological agents such as semaglutide and tirzepatide in managing HFpEF in patients with concomitant obesity. Preliminary findings from these studies suggest favourable outcomes, particularly in terms of weight reduction and improvements in cardiovascular outcome. This pharmacological approach holds significant promise for enhancing both the quality of life and clinical outcomes in individuals with HF and obesity. In patients with established HF, obesity exhibits a paradoxical effect. Several studies have suggested that individuals with overweight or mild obesity (BMI 27–35 kg/m²) may experience better survival rates and improved cardiovascular outcomes compared to those with normal or low body weight, a phenomenon termed the "obesity paradox." However, it is crucial to recognize that this paradox is primarily observed when obesity is defined by BMI. When obesity is assessed based on adipose tissue type and distribution—particularly visceral fat and its localization around internal organs—the paradoxical relationship is no longer evident. Notably, severe obesity is associated with worse clinical outcomes, including increased hospitalization rates, reduced exercise tolerance, and diminished quality of life. The diagnosis of HF in obese individuals presents a clinical challenge due to overlapping symptoms, such as dyspnea and fatigue, which are common to both conditions. Furthermore, imaging modalities such as echocardiography and biomarkers like N-terminal pro–B-type natriuretic peptide (NT-proBNP) may be less reliable in obese patients due to altered hemodynamics and adipose tissue interference. The management of HF in obese individuals involves a multifaceted approach, incorporating lifestyle modifications, pharmacologic therapy, and, in some cases, bariatric surgery. Weight reduction through dietary interventions and physical activity has been demonstrated to improve symptomatology, decrease hospitalization rates, and enhance overall cardiac function. Given the increasing global prevalence of obesity, addressing its impact on HF remains a critical aspect of contemporary cardiovascular disease management.
