Atherosclerosis, and its associated complications, are a major cause of morbidity and mortality, and it is now recognised as a chronic inflammatory disorder. Progression of inflammation depends on the balance between recruitment of inflammatory cells and their subsequent removal from a site of inflammation. Apoptosis, or programmed cell death, is a fundamental process governing cell survival and is a major determinant of the resolution of the inflammatory response. Apoptotic cells are instantly recognised for non-inflammatory clearance by phagocytes (e.g. macrophages) and removed from the vicinity of inflammation without the release of their pro-inflammatory cell contents. Nitric oxide (NO) plays an important role in many biological processes and has several anti-atherogenic properties including vasodilatation, inhibition of platelet activation and aggregation, and the regulation of apoptosis in a variety of cell types involved in atherogenesis. A critical early event during atherogenesis is injury to the endothelium. The ensuing damage results in endothelial dysfunction, including a reduction in the capacity of the endothelium to generate NO. Decreased NO bioavailability is likely to influence many cellular processes occurring within atherosclerotic lesions, including apoptosis. Modulation of apoptosis is a novel target for therapeutic intervention in the treatment of chronic inflammatory disorders, such as atherosclerosis. This modulation may help limit or resolve inflammation without the concomitant recruitment of subsequent inflammatory cells, thereby reducing the potential for further tissue damage. NO is a possible candidate for manipulation of atherosclerotic processes due to both its powerful anti-atherogenic characteristics and ability to affect apoptosis. This review highlights the role of apoptosis in atherosclerosis and discusses the therapeutic potential of NO to limit and/or resolve vascular inflammation.