Silent myocardial ischemia may be related to inflammatory response.

Silent myocardial ischemia (SMI) is a common phenomenon in patients with coronary artery diseases, which frequently occurs at rest, during daily life activities or after physical or emotional exertion. Although individual differences in pain threshold may partially explain the variability in pain perception, the mechanisms responsible for SMI are not well understood. A defective warning mechanism was proposed by some investigators as the reason for the absence of pain, stressing that sensibility to pain differs from patient to patient. A central nervous system as well as peripheral nerve endings alteration was also posited. There is increasing evidence that the development of atherosclerosis is associated with inflammation, and increased levels of inflammatory markers have been documented in various settings of coronary artery disease. Patients with chronic and stable coronary artery disease have clear evidence of a low-grade inflammation, which is independent of traditional cardiovascular risk factors. A systemic inflammatory response to coronary angioplasty has also been reported after balloon angioplasty and after stent implantation. More recently, intriguing observations have shown that there is a particular biochemical pattern of inflammatory system activation (an increased production of inflammatory cytokines) that explains the lack of anginal symptoms in patients with silent myocardial ischemia. That is, pain perception may result from microenviromental balance between proinflammatory and anti-inflammatory cytokines.