The triggering mechanism of unstable angina is the transient interruption of myocardial perfusion due to a thrombus, superimposed to a fissured atherosclerotic coronary plaque. An inflammatory process that precedes endothelial rupture has recently been identified, and may play a triggering role and/or perpetuate the previously described phenomena, thus altering the adhesiveness of the endothelium for leukocytes or platelets, and stimulating the procoagulant and vasoconstrictive actions of the endothelium. The existence of this inflammatory mechanism is based on histological, hematological and humoral evidence, including the presence of high levels of PCR, a plasma protein that increases its concentration more than 25% during the inflammatory phenomenon. Several studies of unstable angina have shown an increase in the serum concentration of inflammation markers, such as PCR and amiloid A and an association between baseline PCR levels and the future prognosis. Summarizing, the increase in the level of PCR is an independent predictor of adverse evolution in patients with unstable angina or non-Q wave myocardial infarction. In addition, the prognostic value of persistently high PCR levels may be greater than that of a temporary increase. An additive prognostic value of PCR and troponins has also been observed. Although clinical evaluation is essential for risk assessment, humoral markers such as PCR, may be useful as a complement to the information provided by conventional tests.