International journal of cardiology · 2026
Severe obesity and in-hospital outcomes in acute myocardial infarction: Insights into the role of systemic inflammation.
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Cosentino Nicola, Velato Letizia, Bonomi Alice, Morocutti Chiara, Trombara Filippo, Genovese Stefano, Molinari Chiara, Lucci Claudia, Grazi Marco, Assanelli Emilio, Sorrentino Sabato, Pontone Gianluca, Marenzi Giancarlo
Аннотация
BACKGROUND: Obese patients often show better short-term outcomes in cardiovascular disease, but the impact of severe obesity on acute myocardial infarction (AMI) outcomes is unclear. This study explored the relationship between severe obesity and in-hospital outcomes in AMI, with a focus on inflammation, as measured by high-sensitivity C-reactive protein (hs-CRP).
METHODS: We performed a retrospective analysis of 3887 AMI patients admitted to a tertiary cardiac center from 2010 to 2025. Patients were stratified by body mass index (BMI). The primary endpoint was a composite of in-hospital mortality, acute heart failure, and acute kidney injury.
RESULTS: The primary endpoint incidence was similar across BMI groups up to BMI <35 kg/m2, then significantly increased in patients with BMI ≥35 kg/m2 (20% vs. 31%; p = 0.002). Severe obesity (BMI >35 kg/m2; n = 158) was associated with a two-fold increased risk of adverse outcomes (OR 2.21, 95%CI 1.04-2.97). After adjusting for admission hs-CRP, the predictive value of severe obesity was lost, while hs-CRP remained a strong independent predictor (OR 1.02, 95%CI 1.01-1.03 for every two-unit increase). Patients with severe obesity and elevated hs-CRP (≥2 mg/dL) had the highest event rate (35%). Path analysis showed that 63% of severe obesity's effect on adverse outcomes was mediated by inflammation.
CONCLUSIONS: Our findings show that severe obesity is a significant risk factor for adverse in-hospital outcomes in AMI, challenging the "obesity paradox." This increased risk is largely mediated by systemic inflammation.
METHODS: We performed a retrospective analysis of 3887 AMI patients admitted to a tertiary cardiac center from 2010 to 2025. Patients were stratified by body mass index (BMI). The primary endpoint was a composite of in-hospital mortality, acute heart failure, and acute kidney injury.
RESULTS: The primary endpoint incidence was similar across BMI groups up to BMI <35 kg/m2, then significantly increased in patients with BMI ≥35 kg/m2 (20% vs. 31%; p = 0.002). Severe obesity (BMI >35 kg/m2; n = 158) was associated with a two-fold increased risk of adverse outcomes (OR 2.21, 95%CI 1.04-2.97). After adjusting for admission hs-CRP, the predictive value of severe obesity was lost, while hs-CRP remained a strong independent predictor (OR 1.02, 95%CI 1.01-1.03 for every two-unit increase). Patients with severe obesity and elevated hs-CRP (≥2 mg/dL) had the highest event rate (35%). Path analysis showed that 63% of severe obesity's effect on adverse outcomes was mediated by inflammation.
CONCLUSIONS: Our findings show that severe obesity is a significant risk factor for adverse in-hospital outcomes in AMI, challenging the "obesity paradox." This increased risk is largely mediated by systemic inflammation.