Obesity a Risk Factor for Severe COVID-19 Infection: Multiple Potential Mechanisms.

By N. Sattar, I. McInnes, J. McMurray. Circulation, 2020

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Circulation. 2020;142:4–6. DOI: 10.1161/CIRCULATIONAHA.120.047659 4 Naveed Sattar , MD Iain B. McInnes, MD John J.V. McMurray, MD T he coronavirus disease 2019 (COVID-19) pandemic has led to worldwide research efforts to identify people at greatest risk of developing critical illness and dying. Initial data pointed toward older individuals being particularly vulnerable, as well as those with diabetes mellitus or cardiovascular (including hypertension), respiratory, or kidney disease. These problems are often concentrated in certain racial groups (eg, African Americans and Asians), which also appear to be more prone to worse COVID-19 outcomes.1 Increasing numbers of reports have linked obesity to more severe COVID-19 illness and death.1–3 In a French study, the risk for invasive mechanical ventilation in patients with COVID-19 infection admitted to the intensive treatment unit was more than 7-fold higher for those with body mass index (BMI) >35 compared with BMI <25 kg/m2.2 Among individuals with COVID-19 who were <60 years of age in New York City, those with a BMI between 30 to 34 kg/m2 and >35 kg/m2 were 1.8 times and 3.6 times more likely to be admitted to critical care, respectively, than individuals with a BMI <30 kg/m2.3 We suggest obesity or excess ectopic fat deposition may be a unifying risk factor for severe COVID-19 infection, reducing protective cardiorespiratory reserve as well as potentiating the immune dysregulation that appears, at least in part, to mediate the progression to critical illness and organ failure in a proportion of patients with COVID-19 (Figure). Whether obesity is an independent risk factor for susceptibility to infection requires further research. From a cardiovascular perspective, trial and genetic evidence conclusively show that obesity (and excess fat mass) are causally related to hypertension, diabetes mellitus, coronary heart disease, stroke, atrial fibrillation, renal disease, and heart failure. Obesity potentiates multiple cardiovascular risk factors, the premature development of cardiovascular disease, and adverse cardiorenal outcomes. There is also a metabolic concern. In individuals with diabetes mellitus, or at high risk of diabetes mellitus, obesity and excess ectopic fat lead to impairment of insulin resistance and reduced β-cell function. Both the latter limit ability to evoke an appropriate metabolic response on immunologic challenge, leading some patients with diabetes mellitus to require substantial amounts of insulin during severe infections. Overall, the integrated regulation of metabolism required for the complex cellular interactions, and for effective host defense, is lost, leading to functional immunologic deficit. COVID-19 may also directly disrupt pancreatic β-cell function through an interaction with angiotensin-converting enzyme 2. Furthermore, obesity enhances thrombosis, which is relevant given the association between severe COVID-19 and prothrombotic disseminated intravascular coagulation and high rates of venous thromboembolism. Beyond cardiometabolic and thrombotic consequences, obesity has detrimental effects on lung function, diminishing forced expiratory volume and forced vital capacity (Figure). Higher relative fat mass is also linked to such adverse changes, perhaps relevant to emerging reports of greater critical illness from COVID-19 in © 2020 American Heart Association, Inc. ON MY MIND

Subfields: Clinical Psychology, Infectious Diseases, Neurology

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