artery and the iliac arteries is associated with a relatively low rate of recurrence (Bosch et al 1997; Tetteroo et al 1998; Dormandy and Rutherford 2000; Ahmadi et al 2001). In contrast, in the muscular conduit arteries of the femoropopliteal segment restenosis after PTA more frequently occurs (Adar et al 1989; Jeans et al 1990; Matsi et al 1994; Dormandy and Rutherford 2000). Thus, it seemed reasonable to speculate that these differences of restenosis rates may be due to differences of the extent of inflammation in response to endovascular treatment. Indeed, it could be shown that stent implantation in the muscular arteries of the femoropopliteal segment was associated with a more extensive vascular inflammatory response than stenting of the elastic iliac or carotid arteries, suggesting that the enhanced inflammatory response after femoropopliteal stenting might contribute to the higher rates of restenosis in this vessel area (Schillinger et al 2002d). Nevertheless, the predictive value of acute phase reactants remained to be demonstrated. Recently, several studies evaluated the prognostic impact of inflammatory laboratory parameters and the potential clinical relevance to predict the individual’s restenosis risk. It was consistently shown that elevated baseline values and postintervention levels of these inflammatory parameters were associated with an increased risk for restenosis after peripheral, coronary, and carotid angioplasty (Tschöpl et al 1997; Blum et al 1998; Buffon et al 1999; Schillinger et al 2001, 2002a, 2002b, 2003a, 2003b). Elevated CRP levels are an indicator of increased cardiovascular risk in healthy individuals as well as in patients with atherosclerosis (Berk et al 1990; Liuzzo et al 1994; Heinrich et al 1995; Kuller et al 1996; Mendall et al 1996; Haverkate et al 1997). Low level chronic inflammatory activity in the vascular tissue is suggested to cause a CRP elevation in patients with atherosclerosis (Mendall et al 1996), reflecting the activity of the disease. Higher peri-procedure CRP values are thus thought to indicate a higher activity of the disease and an increased susceptibility for hypertrophic vascular remodeling and excessive neointima formation after percutaneous angioplasty. However, it remains indeterminate whether acute phase reactants are only indicators of an increased risk for restenosis or causally contribute to its occurrence. One mechanism of a causal role could be the activation of the complement system, local vascular inflammatory reactions, and subsequent tissue damage (Torzewski et al 1998). Furthermore, CRP at concentrations known to predict adverse vascular events decreases nitric Vascular Health and Risk Management 2005:1(1) Inflammation and restenosis oxide synthesis and inhibits angiogenesis (Verma et al 2002); both factors are markedly involved in the pathogenesis of vascular disease. The crucial question remains, whether acute phase reactants like CRP will be clinically useful to predict the individual’s risk for restenosis. Currently, clear cut-off levels of CRP indicating an increased restenosis risk are lacking, and routine application of these inflammatory parameters therefore seems not to be justified. Inflammatory and antiinflammatory genes: involvement in restenosis? Recent research has focused on the potential implications of genetic variability on the pathophysiology of vascular disease (Jukema et al 2000; Kastrati et al 2000; Bauters et al 2001; Roguin et al 2001). Traditional risk factors for recurrent lumen narrowing after percutaneous angioplasty – like local hemodynamics or technical success – account for only a minor proportion of the restenosis risk, and genetic predisposition seems to markedly influence the individual’s susceptibility for this process (Exner et al 2001). In particular, genes encoding for inflammatory or anti- inflammatory proteins are suggested to play a pivotal role in the pathophysiology of lesion recurrence. Several candidate genes have been investigated so far. Briefly, genetic variability may be found in most of the genes encoding for the inflammatory parameters mentioned above: interleukins, selectins, CAMs etc. Variable expression of almost all of these factors may influence the extent of vascular inflammation in response to percutaneous angioplasty, and thus the occurrence of restenosis. However, results of most observational studies demonstrating an association between a genetic characteristic and the restenosis risk have to be interpreted cautiously – type II errors or false positive findings are likely to occur in small patient series. Exemplary, two specific gene polymorphisms may be discussed that are potentially involved in the patho- physiology of restenosis in the peripheral vessel area: the heme oxygenase 1 (HO-1) genotype, as an antiinflammatory factor; and the interleukin 6 (IL-6) genotype, as an inflammatory polymorphism. Heme oxygenase-1 (HO-1) is a novel vascular protective factor with potent antiinflammatory and antioxidant effects and the ability to inhibit the proliferation of smooth muscle cells (Maines 1988; Tenhunen et al 1989; Duckers et al 2001; Ishikawa et al 2001; Tulis et al 2001). Development of restenosis in large 75