Evaluation of C-reactive protein, a sensitive marker of inflammation, as a risk factor for stable coronary artery disease.

OBJECTIVES: Multiple lines of investigations have converged to suggest a prominent role for inflammation in coronary artery disease (CAD). The association of CRP level with active CAD is well documented. The relation, however, between levels of CRP and the presence and extent of stable CAD has seldom been studied in the developing countries. We investigated the association between serum concentration of C-reactive protein (CRP) and angiographically documented coronary artery disease (CAD) in a population of 450 individuals. DESIGN AND METHODS: Ultrasensitive immunoassay was used to measure CRP levels in 284 patients with CAD and 166 control healthy subjects. The association of CRP levels with severity of disease as indicated by > or = 50% stenosis in one vessel (n = 79), two vessels (n = 74), or three vessels (n = 131) was also investigated. RESULTS: CRP levels were greater in the patients with CAD (2.14 (0.88--3.38) vs. 1.45 (0.70--2.55) mg/L, p < 0.0001) than in the respective control subjects. Multiple logistic regression analysis showed CRP as an independent discriminating risk factor for CAD (odds ratio, 3.46, p < 0.001). Significant correlation was identified between CRP levels and severity of CAD (p < 0.0001). Prediction models that incorporated CRP in addition to other established coronary risk factors were significantly better at predicting risk than the models based on the other risk factors alone. CRP level was also an independent predictor of CAD in a subpopulation with normal levels of low density lipoprotein cholesterol (LDL-C < or = 3.4 mmol/L, p < 0.009). CONCLUSIONS: Our findings suggest that CRP has a strong association with stable CAD, as such, the measurement of CRP may improve the coronary risk assessment in Iranian CAD patients.

Effect of Tramadol (µ-opioid receptor agonist) on orthodontic tooth movements in a rat model.

OBJECTIVE: Tramadol is a synthetic analgesic of opioids which has more flexible mechanisms of action than typical opioids. Since it has been reported in previous study that typical opioids like morphine can affect the bone homeostasis, it is worthwhile to examine the effects of tramadol on tooth movement. In this study we investigated effects of tramadol on orthodontic tooth movement in rats. MATERIALS AND METHODS: 30 male wistar rats were selected and received orthodontic appliance. 3 groups were designed based on the substance that they received daily injections of during a 2-week orthodontic treatment. 1. Control group with no injection.2.Control group with normal saline injection.3. the tramadol group. After the two-week treatment period the amount of tooth movement were measured in all the groups. Also the histological analysis was performed assessing the root resorption, osteoclasts numbers and bone resorption. RESULTS: The amount of tooth movement was not significantl in the tramadol group comparing to the other groups (P>0.05).The results of 3 histological parameters (amount of root resorption, osteoclastic numbers and bone resorption) were statistically insignificant (P>0.05). CONCLUSION: Tramadol as an atypical opioid does not interfere with the process of bone remodeling and tooth movement in rat. Tramadol does not affect osteoclastic activity and bone resorption and it does not cause to change the resulted root resorption either.

Enhanced susceptibility to oxidation and diminished vitamin E content of LDL from patients with stable coronary artery disease.

BACKGROUND: Convincing evidence points to oxidative modification of LDL as an important trigger in a complex chain of events leading to atherosclerosis. We investigated the occurrence of enhanced susceptibility of LDL to oxidation and decreased vitamin E concentration in LDL as additional risk factors promoting atherosclerosis among patients with established coronary artery disease (CAD). METHODS: We examined 132 patients with angiographically confirmed CAD and compared them with 111 healthy control individuals. We measured conjugated diene production to assess susceptibility of LDL to copper-mediated oxidation. Vitamin E content of LDL was measured by HPLC. RESULTS: The mean lag time of LDL oxidation and LDL alpha-tocopherol/LDL-cholesterol ratio were lower in the patients with CAD (55 +/- 14 min and 2.4 +/- 1.0 mmol/mmol) than in the controls (63 +/- 13 min and 2.9 +/- 1.1 mmol/mmol; P <0.0001 and <0.001, respectively). Multiple stepwise regression analysis demonstrated the lag time (odds ratio, 1.96; 95% confidence interval, 1.34-2.87; P <0.0001) and concentration of vitamin E in LDL (odds ratio, 1.65; 95% confidence interval, 1.16-2.33; P <0.005) as independent determinants of CAD. Significant inverse Spearman rank correlations were found between lag time (r = -0.285; P <0.001) or concentration of vitamin E in LDL (r = -0.197; P <0.002) and severity of CAD. Lag times were not significantly correlated with serum C-reactive protein or ferritin. CONCLUSIONS: Our data suggest that a short LDL oxidation lag time and a low concentration of vitamin E in LDL might be independent coronary risk factors for stable CAD in Iranian people.

Association of increased ferritin with premature coronary stenosis in men.

BACKGROUND: Body iron status has been implicated in atherosclerotic cardiovascular disease. The main hypothesis is that high iron status is associated with increased oxidation of LDL. We investigated the potential role of ferritin as an additional risk factor promoting atherosclerosis among a young population with coronary artery disease (CAD). METHODS: Four hundred consecutive patients (218 males, 182 females) referred for diagnostic coronary angiography were examined, and risk factors for CAD, lipids, C-reactive protein (CRP), and ferritin concentrations were recorded for all participants. RESULTS: Ferritin was higher in the male patients with CAD (121 microg/L; range, 56-258 microg/L) than in the men without significant CAD (73 microg/L; range, 32-138 microg/L; P <0.002). Multiple logistic regression analysis, after adjustment for the established coronary risk factors, showed ferritin as an independent discriminating risk factor for CAD (P <0.01). Men in the highest quartile of ferritin had an odds ratio (OR) of 1.62 [95% confidence interval (95% CI), 1.12-2.42; P <0.01] compared with men in the lowest quartile of ferritin. The association between ferritin and CAD was more pronounced in male patients < or =50 years (OR = 2.65; 95% CI, 1.35-5.51; P <0.003). Ferritin was significantly higher in diabetic male patients in comparison with nondiabetic male patients [168 microg/L (range, 74-406 microg/L) vs 106 microg/L (range, 44-221 microg/L), respectively; P <0.002]. No association was observed between ferritin and CAD among the female patients. CONCLUSION: Our data suggest that increased ferritin might be an independent predictor of premature CAD in male Iranian patients.