Statins, inhibitors of 3-hydroxy-3-methyl glutaryl coenzyme A reductase, are potent inhibitors of cholesterol biosynthesis and have greatly improved the management of ischaemic heart disease. Recent studies suggest that direct antithrombotic and anti-inflammatory effects associated with treatment with statins may at least partly account for the reduction of cardiovascular events. In particular, statins reduce high sensitive C reactive protein (hs-CRP), tumour necrosis factor α, and metalloproteinase 9 production.¹ Recently it has been shown that statins can modify the balance of T helper subset 1 (Th 1) and 2 (Th 2) cells by inhibition of Th1 development and augmentation of Th2 development of CD4⁺ T cells.² In the present observational retrospective study we observed a relation between statin use and frequency of an unusual Th1 subset of T lymphocytes, CD4⁺CD28^null, which is often expanded in unstable angina.³

METHODS

Population

We studied 111 consecutive patients (mean (SD) age 64 (9) years; 32 women) admitted to our coronary care unit with Braunwald class IIIB unstable angina: 33 had been taking statins for at least four weeks plus standard anti-ischaemic treatment (group 1: mean age 62 (9) years; seven women); the remaining 78 patients were taking standard anti-ischaemic treatment but not statins before admission (group 2: mean (SD) age 65 (9) years; 25 women). Clinical features were recorded for both groups (table 1). All participants gave their informed consent. The ethics committee of the Catholic University of Rome approved the study.