Obesity and Cardiovascular Disease: An Obesity Medicine Association (OMA) Clinical Practice Statement (CPS) 2026

Figures

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  Fig. 1. Obesity, Epidemiology, and Cardiovascular Disease (CVD). Global obesity rates have climbed sharply, doubling in 73 countries since 1980 and contributing to millions of deaths each year—most from cardiovascular disease. In the United States, over 40% of adults have obesity, independently accelerating cardiovascular risk beyond traditional metabolic complications. Commercial, social, and environmental forces are major drivers of this epidemic and its downstream CVD burden. Meaningful reductions in obesity-related cardiovascular disease require a comprehensive, equity-focused, system-level, team-based approach. Sustained weight reduction lowers CVD risk, and the most effective and equitable outcomes arise from coordinated, optimized, multidisciplinary care. Although a higher body mass index (BMI) correlates with cardiovascular risk at the population level, increased visceral adipose tissue accumulation is a more accurate indicator of pathogenic adipose tissue distribution and a stronger predictor of individual cardiometabolic complications and cardiovascular disease risk.

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  Fig. 2. Obesity, Sick Fat Disease (Adiposopathy), Fat Mass Disease, and Cardiovascular Disease (CVD). Obesity promotes CVD through two complementary mechanisms: the mechanical effects of excess fat mass (“fat mass disease”) and the metabolic–inflammatory dysfunction of adipose tissue (“sick fat disease”). Fat mass disease increases cardiac workload and impairs cardiopulmonary function, contributing to left-ventricular hypertrophy, diastolic dysfunction, sleep apnea, and reduced physical activity. Adiposopathy (“sick fat disease”) arises when hypertrophic, dysfunctional adipocytes trigger hormonal and immune disturbances that elevate glucose, blood pressure, atherogenic lipids, and thrombosis risk, collectively accelerating the risk of CVD.

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  Fig. 3. Obesity, “Ectopic Fat” (e.g., Visceral, Cardiac, Hepatic, Muscle, Pancreas, Kidney) and Cardiovascular Disease (CVD). Obesity leads to CVD not simply through excess body weight, but through limits in adipose tissue expandability in peripheral subcutaneous adipose tissue (SAT), triggering both adiposopathy (i.e., resulting in adipocyte and adipose tissue endocrinopathies and immunopathies/inflammation) and energy overflow. During limitations in SAT energy storage, free fatty acids spill into the circulation and deposit as ectopic fat in visceral adipose tissue depots and within organs such as the liver, muscle, heart, and pancreas. In addition to adiposopathic immunopathies and endocrinopathies, the “ectopic fat” infiltrations of non-adipose tissue organs may result in lipotoxicity, insulin resistance, worsening cardiometabolic risk factors, and ultimately, CVD (i.e., atherosclerosis and myocardial damage).

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  Fig. 4. Obesity, Diabetes Mellitus, and Cardiovascular Disease (CVD). “Sick fat” (adiposopathy) is anatomically manifest by adipocyte hypertrophy and visceral adipose tissue accumulation. The accumulation of visceral adiposity can be considered a marker of global fat dysfunction and immune/endocrine dysregulation. The resultant insulin resistance and beta cell dysfunction can lead to hyperglycemia, with type 2 diabetes mellitus being a major CVD risk factor. Clinically meaningful weight reduction can reverse aspects of adiposopathy, improve conditions like obstructive sleep apnea that worsen glycemic control, and in some cases even facilitate diabetes remission. Effective treatment of patients with obesity and type 2 diabetes mellitus combines healthful nutrition, regular physical activity, behavioral strategies, and evidence-based therapies (e.g., obesity medications and bariatric procedures) to reduce excess body fat and lower cardiometabolic risk.

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  Fig. 5. Obesity, Hypertension, and Cardiovascular Disease (CVD). Increased body fat is the leading contributor to high blood pressure, driven both by the physical effects of excess body fat (e.g., compression of the kidneys and sleep apnea) which activate the renin–angiotensin–aldosterone system, and by dysfunctional adipose tissue that increases hormone and immune activity. Among the adiposopathic consequences of obesity leading to hypertension include increased sympathetic nervous system activity because of insulin resistance, hyperinsulinemia, and hyperleptinemia. Accurate measurement of blood pressure requires consistent technique, including proper cuff size and awareness of “white-coat syndrome” elevation. Treatment of obesity and hypertension is best focused on weight reduction through healthful nutrition such as the Dietary Approaches to Stop Hypertension and Mediterranean eating patterns, regular physical activity, behavior modification, obesity medications, and bariatric procedures, with improvements in blood pressure generally proportional to the degree of weight reduction.

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  Fig. 6. Obesity, Dyslipidemia, and Cardiovascular Disease (CVD). Obesity is a chronic, relapsing disease that in addition to adverse fat mass consequences, may result in dysfunctional adipose tissue, which in turn, promotes a harmful lipid pattern known as “adiposopathic dyslipidemia.” This pattern features high triglycerides, low high-density lipoprotein cholesterol (HDL-C), and increased atherogenic particles such as small dense low-density lipoprotein (LDL) and apolipoprotein B. While weight-reduction strategies improve triglycerides and high-density lipoprotein cholesterol, achieving optimal low-density lipoprotein cholesterol (LDL-C) control often requires substantial weight reduction coupled with evidence-based cholesterol-lowering therapies such as statins.

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  Fig. 7. Obesity, Metabolic Syndrome, and Cardiovascular Disease (CVD). Adiposopathy, or “sick fat,” explains how obesity leads to metabolic syndrome and CVD by transforming adipose tissue into a dysfunctional endocrine and immune organ that drives high glucose, high blood pressure, and atherogenic lipid abnormalities. In many individuals, this adipose-tissue dysfunction—not genetics alone—is the primary cause of the clustered risk factors that define metabolic syndrome. Metabolic syndrome is diagnosed when three or more are present: abdominal obesity, elevated fasting glucose, elevated blood pressure, high triglycerides, or reduced high-density lipoprotein cholesterol. Increased low density lipoprotein cholesterol is not a diagnostic component of the metabolic syndrome.

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  Fig. 8. Obesity, Thrombosis, and Cardiovascular Disease (CVD). Obesity promotes a prothrombotic state through the mechanical effects of excess fat (“fat mass disease”), which cause vascular compression and venous stasis. Obesity may also facilitate thrombosis through the metabolic–inflammatory effects of dysfunctional adipose tissue (“sick fat disease”), which may lead to increased inflammation, endothelial injury, and increased tendency for blood clotting. In addition to deep vein thrombosis, pulmonary embolism, and chronic venous insufficiency, clinicians may also encounter obesity-related lymphedema and the distinct familial condition of lipedema. Although weight-reduction strategies are beneficial, they are often not sufficient to fully address venous, lymphatic, or lipedemic disorders.

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  Fig. 9a. Obesity, Obstructive Sleep Apnea (OSA), and Cardiovascular Disease (CVD). Obesity drives obstructive sleep apnea (OSA) through anatomical airway narrowing and excess pharyngeal and tongue fat. As many as 70% of individuals with obesity may develop OSA. The relationship is bidirectional: OSA disrupts sleep and alters appetite-regulating hormones, promoting weight gain and further worsening airway obstruction. Untreated OSA increases cardiovascular and metabolic risks, while weight reduction, lifestyle changes, obesity medications, and bariatric procedures can reduce OSA severity.

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  Fig. 9b. Some obesity medications have approved Food and Drug Administration (FDA) indicated uses to treat adverse health outcomes that go beyond improvement in obesity alone. Optimal medical management acknowledges that the priority is not to just treat the weight of the patient, but to also improve the health outcomes of the patient. Not only is tirzepatide indicated to treat overweight and/or obesity, but tirzepatide also has an explicit FDA indication to treat moderate to severe obstructive sleep apnea (OSA) in adults with obesity. Similarly, in addition to an indicated use to treat overweight and/or obesity, semaglutide has FDA indicated uses to reduce the risk of major adverse cardiovascular events and as a treatment for noncirrhotic metabolic dysfunction associated steatohepatitis.

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  Fig. 10. Obesity and Cardiovascular Structural Changes. Obesity contributes to CVD not only through excess body fat but also through the specific location of adipose tissue and its direct structural effects on the heart and blood vessels. Epicardial and perivascular adipose tissue can release inflammatory signals and toxic lipids directly into the heart and coronary arteries, promoting hypertrophy, steatosis, and fibrosis through an “outside-to-inside” mechanism. At the same time, circulating inflammatory factors and atherogenic lipoproteins can injure coronary arteries from the lumen outward, creating an “inside-to-outside” assault that accelerates arterial stiffness and atherosclerosis.

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  Fig. 11. Obesity and Heart Failure. Obesity initially creates a high-output state with normal-to-low vascular resistance: the expanded fat mass raises metabolic demand, which increases blood volume, preload, and sympathetic activity. Over time, sustained sympathetic tone and arterial stiffening raise afterload, so the combined volume and pressure load produces left-ventricular hypertrophy and a central pathway to heart failure with preserved ejection fraction (HFpEF). Excess epicardial adipose tissue adds a second injury by restraining the heart within the pericardium and infiltrating the myocardium with inflammatory and fibrotic signaling, further impairing diastolic filling and worsening HFpEF.