Purpose of review
Current antiretroviral therapies have dramatically changed the disease course of HIV infection. Although antiretroviral therapy is effective at decreasing viral replication and preserving CD4+ T-cell numbers, low-level immune activation and inflammation persist in virally suppressed HIV-infected patients. This chronic immune activation/inflammation may contribute to an increased risk for venous and arterial thrombosis.
Several markers of coagulation and inflammation are increased in HIV-infected patients. The Strategies for the Management of Antiretroviral Therapy study reported that plasma D-dimer levels, a marker of fibrinolysis, independently predicted morbidity in HIV-infected patients. Increased plasma and cell surface levels of the procoagulant tissue factor have also been reported in patients with HIV disease. Fibrinogen, von Willebrand factor, and P-selectin are likewise increased in plasma samples of HIV-infected patients; all of these markers suggest HIV-infection results in a procoagulant state. Treatment with antiretroviral therapy reduces, but does not always normalize, levels of biomarkers associated with inflammation and coagulation in HIV+ patients.
HIV-infected patients are at greater risk for both venous and arterial thrombosis. Chronic immune activation and inflammation in these patients appears to contribute to coagulation risk. Antiretroviral therapy reduces viral replication, immune activation, and markers of coagulation, but these indices do not always return to normal, even after several years of viremic control.