fimasartan and Inflammation

The renin-angiotensin system plays an important role in promoting atherosclerotic plaque inflammation, which may be inhibited by angiotension-II receptor blockers.. We investigated the effects of fimasartan and amlodipine therapy on carotid atherosclerotic plaque inflammation using. Fifty patients with acute coronary syndrome (ACS) and at least one lesion with. The two groups had similar baseline characteristics. At the 6-month follow-up, index vessel and aorta MDS TBR significantly decreased in both groups. However, the percent change in index vessel MDS TBR was similar between the two groups (-9.33 ± 14.2% vs -7.73 ± 19.1%, respectively, P = 0.9). No significant difference was found for the percent change in the whole vessel TBR for the index vessel between the two groups, with similar findings for changes in MDS TBR or whole vessel TBR for the aorta. Total cholesterol, low-density lipoprotein cholesterol levels, and blood pressure improved to a similar degree in both groups.. Fimasartan and amlodipine reduce carotid atherosclerotic plaque inflammation similarly in patients with ACS, offering the same level of effectiveness.

Topics: Amlodipine; Biphenyl Compounds; Calcium Channel Blockers; Carotid Arteries; Carotid Artery Diseases; Dose-Response Relationship, Drug; Female; Follow-Up Studies; Humans; Inflammation; Male; Middle Aged; Plaque, Atherosclerotic; Positron-Emission Tomography; Prospective Studies; Pyrimidines; Tetrazoles; Treatment Outcome

The beneficial effects of angiotensin II type 1 receptor blockers (ARBs) on atherosclerosis have been demonstrated in numerous studies. We investigated the effects of fimasartan on reducing neointimal formation and systemic inflammation after carotid artery (CA) injury in Apolipoprotein E knockout (ApoE KO) mice.. ApoE KO mice were randomly allocated to Group I (without CA injury), Group II (without CA injury + Fimasartan), Group III (CA injury), and Group IV (CA injury + Fimasartan). Fimasartan was orally administered everyday starting 3 days before iatrogenic left CA injury.. At 28 days, neointimal hyperplasia and the inflammatory cytokines including TNFα, IL-6, ICAM, and MMP-9 in the peripheral blood were significantly reduced in Groups II and IV compared to Groups I and III, respectively. All fimasartan-administered groups revealed significant increases of CD4. This study suggests fimasartan could be an efficient strategy for reduction of atherosclerotic progression, with a decrease in immune response and systemic inflammation.

Topics: Angiotensin Receptor Antagonists; Animals; Apolipoproteins E; Biphenyl Compounds; Carotid Artery Injuries; Inflammation; Interleukin-6; Male; Matrix Metalloproteinase 9; Mice; Mice, Knockout; Neointima; Pyrimidines; T-Lymphocytes, Regulatory; Tetrazoles; Tumor Necrosis Factor-alpha