Pathogenesis of cardiovascular disease in HIV infection

Abstract

Purpose of review: Cardiovascular disease (CVD) is one of the most common causes of death in HIV-infected adults. Understanding the pathogenesis of cardiovascular disease in the setting of HIV infection is essential for the development of appropriate management strategies.

Recent findings: Antiretroviral therapy with most protease inhibitors and thymidine nucleoside analogue reverse transcriptase inhibitors has been linked to dyslipidaemia and insulin resistance. The adverse glycaemic effects of longer term, current generation protease inhibitors, however, appear relatively modest. Nevertheless, about half of the risk associated with antiretroviral therapy remains unexplained by lipid abnormalities. More recently, HIV has been associated with increased risk of cardiovascular disease. HIV nef inhibits HDL efflux from macrophages and so may directly lower HDL cholesterol levels. Untreated HIV infection is also associated with increased levels of D-dimer, a pro-inflammatory and pro-thrombotic marker of cardiovascular disease, and HIV has direct effects on vascular tissue in vitro that remains of uncertain clinical significance.

Summary: Antiretroviral therapy without metabolic effects that suppresses HIV effectively is likely to be associated with the lowest risk of cardiovascular disease.