In his review of inflammation, atherosclerosis, and coronary artery disease, Hansson (April 21 issue)¹ focuses on T cells, macrophages, and mast cells as the cellular components of the immune system that play a key role in ischemic heart disease. However, he omits a possible role for neutrophils.

Thrombocytopenia is a common hematologic disorder in persons infected with the human immunodeficiency virus (HIV).¹ Although often asymptomatic, the thrombocytopenia in these patients may be associated with a variety of bleeding abnormalities. Corticosteroids, intravenous immune globulin, and interferon can improve HIV-associated thrombocytopenia, although the responses are not sustained after the cessation of treatment.¹ Several studies have shown increases in platelet counts in HIV-infected patients with thrombocytopenia who were treated with zidovudine,^1,2 but these responses were not sustained. Maness et al. reported a similar effect of indinavir,³ but their report did not include data on the viral load.

Sabatine et al. (May 4 issue)¹ report the results of the Further Cardiovascular Outcomes Research with PCSK9 Inhibition in Subjects with Elevated Risk (FOURIER) trial. The addition of evolocumab to standard therapy was associated with an absolute risk reduction of 2 percentage points in both the primary and secondary end points after a median duration of follow-up of 26 months.