How Obesity is Linked with Venous Thromboembolism and Myocardial Injury in COVID-19 Patients

A study shows that higher obesity classification is linked to enhanced inflammation and is a risk factor for blood clots and heart damage in patients with COVID-19. The results were published in Obesity Research & Clinical Practice.

Obese patients with COVID are at higher risk of going on a ventilator and dying from the respiratory disease. COVID-19, as the researchers noted, has been associated with both macrovascular and microvascular thromboses, likely through inflammation-induced endothelial cell damage. More severe COVID and higher mortality among obese patients might be attributable to the population’s higher risk of thrombosis, as obesity is known to be associated with endotheliopathy and platelet activation. The researchers wrote: “We aimed to elucidate the association between obesity and thrombosis through investigating the rates of venous thromboembolism (VTE) and myocardial injury, a marker of microvascular thrombosis, among patients with COVID-19.”

In this retrospective cohort study, researchers assessed 609  hospitalized with COVID-19 at a single institution. The population was categorized based on obesity class. Overall, 58% of patients were not obese, 18% were patients with class I obesity, 12% were patients with class II obesity, and 12% were patients with class III obesity. The key endpoints were defined as venous thromboembolism (VTE) and myocardial injury, a marker of microvascular thrombosis in COVID-19.

According to the results of the study, patients with class I and III obesity had markedly higher risk-adjusted odds of VTE compared to patients without obesity (OR=2.54, 95% CI, 1.05–6.14 for class I obesity; and OR = 3.95, 95% CI: 1.40–11.14 for class III obesity). The researchers observed that patients with class III obesity had notably higher risk-adjusted myocardial injury odds than their non-obese counterparts (OR= 2.15, 95% CI, 1.12–4.12). Both VTE and myocardial injury were significantly associated with greater risk-adjusted odds of mortality, the researchers noted.

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In terms of limitations, the researchers noted the underestimation of VTE events, as imaging was not conducted for every patient. Also, they wrote that “there may be differences in characteristics between those receiving and not receiving imaging within each BMI category.”

They added that “[this study] demonstrates that greater risk of macrovascular and microvascular thromboses may contribute to the elevated morbidity and mortality in patients with obesity and COVID-19.”

“Obesity increases the risk of thrombosis by low-grade inflammation and oxidative damage, leading to endothelial injury and increased platelet activation. There is growing evidence that a hyper-inflammatory state in COVID-19 also induces endothelial dysfunction and can activate tissue factor leading to platelet upregulation. Hence, higher obesity class may enhance inflammation and be an additive risk factor for thrombosis in patients with COVID-19,” the researchers wrote in conclusion.