Elevation of matrix metalloproteinases and interleukin-6 in the culprit coronary artery of myocardial infarction.

BACKGROUND: Interleukin-6 (IL-6) and metalloproteinases (MMPs) are involved in the instability of vulnerable plaque associated with the induction of acute myocardial infarction (AMI). We examined the regional changes of cytokines, MMPs and adhesion molecules in patients with AMI to elucidate how these factors are involved in the onset of AMI. MATERIALS AND METHODS: One hundred and twenty-two patients with AMI were included. Blood was aspirated from the culprit coronary artery with a thrombectomy catheter, and was also sampled from peripheral veins during the coronary intervention. Control samples were obtained from the peripheral blood of age-matched patients. RESULTS: The serum levels of IL-6 (P < 0.05), tumour necrosis factor-alpha (P < 0.005), MMP-1 (P < 0.001), MMP-13 (P < 0.001), soluble intercellular adhesion molecule-1 (P < 0.005), and soluble vascular cellular adhesion molecule-1 (P < 0.05) in peripheral blood were significantly higher in the AMI group than in the controls. Aspirated serum contained significantly higher levels of IL-6 (P < 0.001), MMP-1 (P < 0.001), and MMP-13 (P < 0.05) compared to the peripheral blood of AMI. Serum IL-6 levels were significantly higher in the aspirated than in the peripheral blood in the patients hospitalized within 6 h and 6-12 h, but were similar in the aspirated and peripheral blood of the patients hospitalized 12-24 h after the onset of AMI. There were no differences between the aspirated serum and peripheral blood in the levels of interleukin-1beta and MMP-2. CONCLUSIONS: The levels of MMP-1, MMP-13 and IL-6 were higher in the culprit coronary artery than in the peripheral blood. These factors appear to be involved in the early stage of AMI.

[Serum inorganic fluoride concentrations and their urinary excretion during and after sevoflurane, isoflurane, or enflurane anesthesia in man].

Serum inorganic fluoride concentrations and their urinary excretion were examined during and after sevoflurane, isoflurane, or enflurane anesthesia in man. Duration of anesthesia was 3 hours in sevoflurane and enflurane groups (S3 group: n = 10, E3 group: n = 5), and 3 or 5 hours in isoflurane groups (I3 group: n = 5, I5 group: n = 5). Serum inorganic fluoride concentration of the S3 and E3 groups increased immediately following induction, and reached the maximum concentration of 21.8 +/- 9.3 (M +/- SD) mumol.l-1 (S3), 13.6 +/- 6.2 mumol.l-1 (E3) at 1 hour after anesthesia. Serum inorganic fluoride decreased after the peak concentrations, and returned to the pre-anesthesia level at 96 hours (S3) and 144 hours (E3) after anesthesia. On the other hand, serum inorganic fluoride of the I3 and I5 groups scarcely changed from the pre-anesthesia level, and maximum concentrations of these two groups were one tenth of the S3 group. Urinary excretion of inorganic fluoride of the S3 and E3 group began to increase from 2 hours after anesthesia, and showed plateau of 60-90 mmol.h-1 from 12 hours to 24 hours after anesthesia. The change of serum inorganic fluoride sharply contrasted with urinary excretion. Our results suggest that fluoride excretion is largely carried out by the kidney. Therefore sevoflurane or enflurane anesthesia should be avoided in patients with renal dysfunction.

Postprandial changes in LDL phenotypes in patients with myocardial infarction.

BACKGROUND: Low-density lipoprotein (LDL) particle size is strongly affected by both fasting and postprandial triglyceride levels. We report here that the LDL phenotype shifts toward the smaller phenotype during oral fat tolerance tests (OFTTs) in some patients with myocardial infarction (MI); a condition closely associated with postprandial increases of triglyceride and remnant-like particles (RLPs). METHODS: Oral fat tolerance tests were performed on 63 MI patients with fasting serum triglyceride levels of less than 2.25 mmol L-1 (= 200 mg dL-1). Remnant-like particles and other serum lipids were compared among patients characterized by three LDL phenotypes based on nondenaturing gradient gel electrophoresis: pattern A (large LDLs, peak LDL particle size > or = 260 A), pattern I (intermediate-sized LDLs, LDL size > 255 A, < 260 A), and pattern B (small, dense LDLs, LDL size < or = 255 A). RESULTS: The LDL size decreased significantly in patients with the highest tertile of areas under the incremental curves (AUICs) of triglycerides above the fasting levels. The LDL phenotype shifted toward the smaller phenotype after a fat load in three of eight patients with pattern A and in seven of 35 patients with pattern I. The AUICs of triglyceride-rich lipoproteins were significantly higher in these patients than in the patients exhibiting little change in LDL size, whereas the fasting metabolic parameters were similar among the patients of the same LDL phenotype in the fasting state. CONCLUSION: These results suggest that alimentary lipaemia plays an important role in the remodeling of LDL particles into the more atherogenic small, dense LDLs in patients with MI.