Why the study?
Does TLR-4 expression differ in plaque debris of patients with acute coronary syndrome compared to stable angina?
Does TLR-4 expression differ in plaque debris of patients with acute coronary syndrome compared to stable angina?
TLR-4 is upregulated in the plaque debris of patients with acute coronary syndrome compared to stable angina, suggesting its role in plaque instability and atherogenesis.
TLR-4 expression in plaque debris may signal instability in ACS; leaves open its value as a therapeutic target pending prospective validation.
Atherosclerosis is a disease characterized by inflammation in the arterial wall. Atherogenesis is dependent on the innate immune response involving activation of Toll-like receptors (TLRs) and the expression of inflammatory proteins, those may lead to acute coronary syndrome (ACS). We investigated the expression level of TLR-4 in ACS, as compared with TLR-2 and patients with stable angina. Fifty-eight consecutive patients who underwent primary percutaneous coronary intervention (PCI, n = 29) because of ACS and elective PCI (n = 29) because of stable angina using a filter-device distal protection device system were prospectively analyzed. mRNA levels of TLR-2 and TLR-4 in debris containing various inflammatory tissues entrapped in the filter device were altogether analyzed using real-time PCR. There were no significant differences in age, sex distribution, between stable angina and ACS groups. TLR-4 expression levels were higher in patients with ACS than in patients with stable angina. TLR-4 might play a more important role than TLR-2 in atherogenesis, especially in ACS.
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Satoh et al. (2014) studied this question.
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