Inflammation has a key role in coronary atherosclerotic disease (CAD), as it contributes to the development, progression, instability and rupture of the atherosclerotic plaque. The long-term treatment and continuous suppression of inflammation is a therapeutic goal for patients with increased cardiovascular risk and chronic CAD syndromes. In contrast, in acute myocardial infarction (MI), the presence of inflammation is necessary for smooth healing, tissue neovascularization, and limitation of left ventricular remodeling, rendering a "controlled amount" of inflammation desirable in this context. As a result, the use of nonselective, broad-spectrum anti-inflammatory drugs does not offer any beneficial effect and may turn out to be harmful. Nevertheless, the possibility that modification of a usual inflammatory response in MI with selective anti-inflammatory agents cannot be excluded. Conversely, an excessive, uncontrolled, and prolonged inflammatory response after an acute MI may result in extensive irreversible myocardial damage and should be timely recognized and treated, preferably with a selective anti-inflammatory agent. In the present review we highlight the key role of inflammation in chronic and acute CAD, discuss the underlying pathophysiology, and present the results of representative experimental and clinical studies evaluating the pharmaceutical modification of the inflammatory response in this context.