Inflammation
Could Lp(a) explain COVID-19 clotting complications? A Dutch-led team proposes IL-6-driven Lp(a) surges as a testable hypothesis (Curr Atheroscler Rep 2020)
Original title: Lipoprotein(a) and Its Potential Association with Thrombosis and Inflammation in COVID-19: a Testable Hypothesis
This review by Moriarty, Gorby, Stroes, Kastelein, Davidson and Tsimikas proposes that elevated Lp(a), through its antifibrinolytic apolipoprotein(a) component and pro-inflammatory oxidised phospholipid content, could contribute to the arterial and venous thrombosis complications increasingly reported in COVID-19 patients. Since the LPA gene contains an interleukin-6 (IL-6) response element, a cytokine storm from COVID-19 infection could trigger an acute-phase increase in Lp(a), potentially destabilising quiescent atherosclerotic plaques and precipitating myocardial infarction or stroke in patients with baseline elevated Lp(a) or an infection-triggered rise. The authors propose testing this hypothesis through Lp(a) registries in COVID-19 patients, studies of IL-6 antagonists, and consideration of systematic Lp(a) testing, prophylactic anticoagulation, and Lp(a)-lowering therapies such as apheresis in high-risk infected inpatients.
Original abstract
Purpose Of Review: The COVID-19 pandemic has infected over > 11 million as of today people worldwide and is associated with significant cardiovascular manifestations, particularly in subjects with preexisting comorbidities and cardiovascular risk factors. Recently, a predisposition for arterial and venous thromboses has been reported in COVID-19 infection. We hypothesize that besides conventional risk factors, subjects with elevated lipoprotein(a) (Lp(a)) may have a particularly high risk of developing cardiovascular complications.
Recent Findings: The Lp(a) molecule has the propensity for inhibiting endogenous fibrinolysis through its apolipoprotein(a) component and for enhancing proinflammatory effects such as through its content of oxidized phospholipids. The LPA gene contains an interleukin-6 (IL-6) response element that may induce an acute phase-type increase in Lp(a) levels following a cytokine storm from COVID-19. Thus, subjects with either baseline elevated Lp(a) or those who have an increase following COVID-19 infection, or both, may be at very high risk of developing thromboses. Elevated Lp(a) may also lead to acute destabilization of preexisting but quiescent atherosclerotic plaques, which might induce acute myocardial infarction and stroke. Ongoing studies with IL-6 antagonists may be informative in understanding this relationship, and registries are being initiated to measure Lp(a) in subjects infected with COVID-19. If indeed an association is suggestive of being causal, consideration can be given to systematic testing of Lp(a) and prophylactic systemic anticoagulation in infected inpatients. Therapeutic lipid apheresis and pharmacotherapy for the reduction of Lp(a) levels may minimize thrombogenic potential and proinflammatory effects. We propose studies to test the hypothesis that Lp(a) may contribute to cardiovascular complications of COVID-19.
Dutch researchinflammationthrombosis
Summary written by lp-a.org from the published abstract; figures as published. Page updated 18 August 2026. Methods.