Serum MCP-1 and VEGF levels are not affected by inhibition of the renin-angiotensin system in patients with acute myocardial infarction.
Monocyte chemoattractant protein-1 (MCP-1) and vascular endothelial growth factor (VEGF) stimulate angiogenesis in ischemic tissues, and both of their expression are stimulated by angiotensin II. We measured the serum concentrations of MCP-1 and VEGF in patients with acute myocardial infarction (AMI) and investigated the effects of an early administration of angiotensin-converting enzyme inhibitor (ACEI) and angiotensin II type 1 receptor blocker (ARB) on their levels. Thirty-six patients with AMI were divided randomly into 3 therapeutic groups; the ACEI perindopril, the ARB candesartan and control (without perindopril and candesartan), and the drugs were administered within 36 hours after the onset of AMI. Peripheral blood mononuclear cells (PBMC) obtained from the patients were incubated for 24 hours. The levels of MCP-1 and VEGF in the serum and the supernatant of PBMC were measured by ELISA. The serum MCP-1 and VEGF levels in AMI patients at the time of admission were not significantly different from those in healthy control subjects, but both MCP-1 and VEGF levels in the patients were increased significantly after 7 days. There was no significant difference in the serum MCP-1 and VEGF levels among the 3 therapeutic groups. The production of MCP-1 and VEGF by PBMC was also increased in AMI patients compared with healthy control subjects, and there was also no difference in their production among the 3 therapeutic groups. In conclusion, circulating MCP-1 and VEGF levels and their production by PBMC are elevated during the course of AMI, and early administration of ACEI and ARB does not affect their levels.
Division of Cardiovascular Medicine, Jichi Medical School, Tochigi, Japan.
Yoshiaki
Y
Murakami
Kenji
K
Kurosaki
Keiji
K
Matsui
Kazuyuki
K
Shimada
Uichi
U
Ikeda
D000368:Aged; D000369:Aged, 80 and over; D047228:Angiotensin II Type 1 Receptor Blockers; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D001562:Benzimidazoles / Q000494:pharmacology; D001713:Biphenyl Compounds; D018932:Chemokine CCL2 / Q000096:biosynthesis / Q000097:blood*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000378:metabolism; D009203:Myocardial Infarction / Q000378:metabolism* / Q000503:physiopathology*; D020913:Perindopril / Q000494:pharmacology; D012084:Renin-Angiotensin System / Q000187:drug effects* / Q000502:physiology; D013777:Tetrazoles / Q000494:pharmacology; D042461:Vascular Endothelial Growth Factor A / Q000096:biosynthesis / Q000097:blood*
D047228:Angiotensin II Type 1 Receptor Blockers; D000806:Angiotensin-Converting Enzyme Inhibitors; D001562:Benzimidazoles; D001713:Biphenyl Compounds; D018932:Chemokine CCL2; D013777:Tetrazoles; D042461:Vascular Endothelial Growth Factor A; C081643:candesartan; D020913:Perindopril