During the last decade, several studies have documented the unfavorable effects of inflammation on cardiovascular function and its role in the pathophysiology of atherosclerotic disease. The interplay between inflammation and arterial system is multifaceted. On the one hand, the arterial endothelium contributes to the initiation and the perpetuation of inflammation. On the other hand, the inflammatory cascade affects adversely the endothelium-dependent processes and the mechanical properties of the arteries. These effects give rise to impaired vasomotion, arterial stiffening and increased wave reflections and thus result in an unfavorable hemodynamic loading of the heart. Chronic inflammatory diseases (such as rheumatoid arthritis, and others) as well as acute inflammatory stimuli (such as acute infections) may adversely influence the arterial performance. Moreover, systemic subclinical low-grade inflammation, as expressed by high blood levels of inflammatory markers/mediators, is a common denominator of most cardiovascular risk factors (hypertension, diabetes, etc.) and importantly, it is closely related to impaired arterial elastic properties. In addition, vasculogenic erectile dysfunction, which comprises an alternative phenotype of arterial dysfunction and an emerging cardiovascular risk predictor, is accompanied by low-grade inflammatory activation. Among the several inflammatory markers/mediators, C-reactive protein level has been consistently associated with indices of arterial function in several populations. However, data regarding a possible direct etiological role of CRP in arterial dysfunction and atherosclerosis, if any, are yet inconclusive. Current evidence suggests that anti-inflammatory strategies benefit arterial function in several clinical settings. Further research is needed to elucidate whether inflammation may comprise a worthwhile treatment target regarding the cardiovascular system.