Investigative methods for detecting vulnerable athero¬sclerotic plaques include intravascular ultrasonography, magnetic resonance imaging plaque thermography, and circulating markers such as CRP and cytokines may have a role in the future. Evidence is insufficient to warrant widespread screening with CRP. The measurement would be of practical value in patients with coronary artery disease and cardiovascular disease, with optimal levels of LDL cholesterol greater than 95 mg/dl (2.5 mmol/L; to convert values for LDL cholesterol to mmol per liter multiply by 0.02586).
There is little doubt that the link between inflam¬mation and clinical coronary artery disease is strong, but important gaps in our knowledge remain. The atheroma-tous plaque itself may initiate an inflammatory response. Although infection appears to accelerate the clinical course of atheroma, the contribution of infection in areas of the body outside the plaque to nonspecific inflammatory activity within the arterial wall remains obscure. Rando¬mized clinical trials using antibiotics in patients with acute coronary syndrome have not been beneficial. Further large-scale clinical trials are unnecessary. Even if the inflamma¬tion hypothesis is correct, the cost effectiveness of altering management on the basis of the results of screening for CRP needs to be determined.

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