patients undergoing coronary angiography, an intracardiac inflammatory response has been observed in patients with unstable angina that appears to be a result of low-grade myocardial necrosis. The ruptured plaque does not appear to contribute to the acute phase response.
It must be emphasized, however, that an inflammatory response may be mounted by the body in the absence of infection by bacteria or other microorganisms. A nonspe¬cific inflammatory response may be caused by several natural mechanisms mounted by the body as a protective measure. The mechanisms (pathogenesis) that underlie the formation and progression of atheromatous lesions and the rupture that finally causes obstruction of blood flow require considerable further research. The excellent research and investigative work on coronary artery disease carried out in many centers worldwide over the past 30 years have not resulted in a major breakthrough.

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