Obesity is one of the most important modifiable risk factors for cardiovascular disease (CVD). Excess body fat, particularly visceral adiposity, contributes to the development of hypertension, dyslipidemia, insulin resistance, systemic inflammation, endothelial dysfunction, and atherosclerosis. Together, these pathophysiological mechanisms substantially increase the risk of myocardial infarction, stroke, heart failure, atrial fibrillation, and premature cardiovascular death.

Obesity and Hypertension

Individuals with obesity have approximately a 1.5- to 2-fold higher risk of developing arterial hypertension compared with individuals of normal body weight. Consequently, all major international hypertension guidelines recommend weight reduction as a cornerstone of non-pharmacological blood pressure management in overweight and obese patients.

Clinical studies consistently demonstrate that weight loss lowers blood pressure. On average, a reduction of 1 kg of body weight is associated with an approximate decrease of 1 mmHg in both systolic and diastolic blood pressure, although the magnitude of blood pressure reduction varies among individuals. Sustained weight loss also improves vascular function, reduces sympathetic nervous system activity, decreases activation of the renin-angiotensin-aldosterone system, and enhances insulin sensitivity.

Weight Gain and Cardiovascular Mortality

Long-term weight gain is associated with a progressive increase in cardiovascular morbidity and mortality. Epidemiological studies have shown that adults who gain 4–10% of their body weight after the age of 20 have approximately a 1.6-fold increased risk of cardiovascular death over long-term follow-up. More substantial weight gain of approximately 35% is associated with an almost threefold increase in cardiovascular mortality risk.

The relationship between body mass index (BMI) and mortality has often been described as J-shaped or U-shaped, indicating that both severe underweight and severe obesity are associated with increased mortality. Data from the Systolic Blood Pressure Intervention Trial (SPRINT) demonstrated that higher BMI was associated with an increased risk of all-cause mortality and stroke, particularly in individuals with additional cardiovascular risk factors.

Stroke Risk

Several large population-based studies have demonstrated that obesity significantly increases the risk of ischemic stroke.

The Copenhagen City Heart Study reported that individuals with obesity had approximately a 40% higher risk of stroke than those with normal body weight (Hazard Ratio [HR] ≈ 1.4). Similar findings were observed in the Copenhagen General Population Study, although the magnitude of risk was somewhat smaller (HR ≈ 1.1). Numerous international cohort studies and meta-analyses have confirmed that both increasing BMI and central obesity independently contribute to stroke risk.

Visceral (Central) Obesity

Current evidence indicates that visceral adiposity is a substantially stronger predictor of cardiovascular disease than BMI alone. BMI provides a simple estimate of body weight relative to height but does not distinguish between fat mass, lean body mass, or fat distribution.

Individuals with a normal BMI may nevertheless have excessive visceral fat accumulation—a condition sometimes referred to as normal-weight obesity—which is associated with a markedly elevated risk of cardiovascular disease and metabolic dysfunction.

For this reason, current international guidelines recommend assessing waist circumference in addition to BMI as an indicator of central obesity and cardiovascular risk.

Commonly used waist circumference thresholds indicating increased cardiometabolic risk are:

• Men: ≥94 cm (substantially increased risk ≥102 cm)
• Women: ≥80 cm (substantially increased risk ≥88 cm)

Central obesity approximately doubles to triples the risk of cardiovascular disease independently of BMI and is closely associated with insulin resistance, chronic inflammation, hypertension, dyslipidemia, and type 2 diabetes mellitus.

Metabolically Healthy Obesity

A subset of individuals with obesity exhibit relatively preserved metabolic health despite an elevated BMI. This phenotype is commonly referred to as metabolically healthy obesity (MHO) and is characterized by lower visceral fat accumulation, greater insulin sensitivity, and fewer cardiometabolic abnormalities.

However, recent longitudinal studies indicate that metabolically healthy obesity is often a transient condition. Many individuals with MHO eventually develop metabolic syndrome, type 2 diabetes, or cardiovascular disease over time. Consequently, obesity should not be considered benign solely because metabolic abnormalities are initially absent.

Clinical Implications

Reducing excess body weight—particularly visceral fat—is among the most effective strategies for lowering cardiovascular risk. Lifestyle interventions that combine calorie restriction, regular physical activity, behavioral modification, and adequate sleep can significantly improve blood pressure, lipid profiles, glucose metabolism, systemic inflammation, and overall cardiovascular health.

For individuals with severe obesity, pharmacological treatment with modern anti-obesity medications or bariatric surgery can produce substantial and sustained reductions in cardiovascular risk and may lower the