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Abstract Background Coronary artery calcium (CAC) improves cardiovascular event prediction. Visceral adipose tissue (VAT) is a cardiometabolic risk factor that may directly or through its related comorbidities determine the obesity-related risk. A clinical VAT estimator could allow an efficient evaluation of obesity-related risk. We aimed to analyze the effect of VAT and its related cardiometabolic risk factors on CAC progression. Methods CAC was quantified at baseline and after 5 years by computed tomography (CT), determining its progression. VAT and pericardial fat were measured by CT and estimated by a clinical surrogate (METS-VF). Considered cardiometabolic risk factors were: peripheral insulin resistance (IR), HOMA-IR, adipose tissue IR (ADIPO-IR), and adiponectin. Factors independently associated to CAC progression were analyzed by adjusted Cox proportional hazard models, including statin use and ASCVD risk score as covariates. We performed interaction and mediation models to propose possible pathways for CAC progression. Results The study included 862 adults (53 ± 9 years, 53% women), incidence CAC progression rate: 30.2 (95% CI 25.3–35.8)/1000 person-years. VAT (HR: 1.004, 95% CI 1.001–1.007, p

Background: Coronary artery calcium (CAC) improves cardiovascular event prediction. Visceral adipose tissue (VAT) is a cardiometabolic risk factor that may directly or through its related comorbidities determine the obesity-related risk. A clinical VAT estimator could allow an efficient evaluation of obesity-related risk. We aimed to analyze the effect of VAT and its related cardiometabolic risk factors on CAC progression. Methods: CAC was quantified at baseline and after 5 years by computed tomography (CT), determining its progression. VAT and pericardial fat were measured by CT and estimated by a clinical surrogate (METS-VF). Considered cardiometabolic risk factors were: peripheral insulin resistance (IR), HOMA-IR, adipose tissue IR (ADIPO-IR), and adiponectin. Factors independently associated to CAC progression were analyzed by adjusted Cox proportional hazard models, including statin use and ASCVD risk score as covariates. We performed interaction and mediation models to propose possible pathways for CAC progression. Results: The study included 862 adults (53 ± 9 years, 53% women), incidence CAC progression rate: 30.2 (95% CI 25.3–35.8)/1000 person-years. VAT (HR: 1.004, 95% CI 1.001–1.007, p < 0.01) and METS-VF (HR: 1.001, 95% CI 1.0–1.001, p < 0.05) independently predicted CAC progression. VAT-associated CAC progression risk was evident among low-risk ASCVD subjects, and attenuated among medium–high-risk subjects, suggesting that traditional risk factors overcome adiposity in the latter. VAT mediates 51.8% (95% CI 44.5–58.8%) of the effect attributable to IR together with adipose tissue dysfunction on CAC progression. Conclusions: This study supports the hypothesis that VAT is a mediator of the risk conferred by subcutaneous adipose tissue dysfunction. METS-VF is an efficient clinical surrogate that could facilitate the identification of at-risk adiposity subjects in daily clinical practice. [ABSTRACT FROM AUTHOR]

Obesity is a significant risk factor for the development of cardiovascular diseases. This review addresses the complex interaction between obesity and cardiovascular risk, highlighting dysfunctional adiposity as a crucial precursor in the metabolic renal cardiovascular continuum. The underlying pathophysiological mechanisms are reviewed, emphasizing the importance of risk identification and proper stratification, as well as the various available treatment strategies, including pharmacological and non-pharmacological interventions that have proven to reduce cardiovascular risk. Practical tools and evidence-based strategies are provided to enhance clinical management and cardiovascular health outcomes in this particularly vulnerable patient population.