Search

Higher intakes of fish and n-3 polyunsaturated fatty acids (n-3PUFAs: eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)) are associated with a reduced risk of coronary artery disease (CAD). We investigated the relationships between fish-derived n-3PUFAs and prevalence of CAD, and to assess the association of n-3PUFAs with atherosclerosis-related markers in an urban area. This study was designed as a hospital-based cross-sectional study on 649 consecutive outpatients who had undergone regular examinations between April 2009 and October 2009. After adjustments for the coronary risk factors in a multilogistic regression analysis of variables for which a significant difference was identified between the group of patients with a prevalence of CAD and the group with no prevalence of CAD, the multivariable odds ratio (95 % confidence interval) was 0.394 (0.205/0.760; P = 0.005) for the highest (92.4-373.5 μg/ml) versus lowest (6.2-40.0 μg/ml) quartile of serum EPA values and 0.433 (0.228/0.824; P = 0.011) for the highest (160.7-451.8 μg/ml) versus lowest (35.7-100.7 μg/ml) quartile of serum DHA values. Multivariate regression analyses after adjustment for risk factors showed that higher serum EPA and DHA levels were independent variables of a higher level of serum apolipoprotein A-1, a major compound of high-density lipoprotein. However, the results suggested that there might be conflicting effects of EPA and DHA in regard of the serum levels of other lipid markers. This cross-sectional study suggests that higher serum levels of n-3PUFAs were associated with a lower prevalence of CAD and an increase in serum apolipoprotein A-1 level, even in an urban area. [ABSTRACT FROM AUTHOR]

The purpose of this study was to clarify the relation between differential leukocyte counts and inhibition of the development of coronary atherosclerosis in patients with coronary artery disease. A 6-month prospective study was conducted in 84 patients treated with pravastatin. Plaque volume, as assessed by volumetric analysis using intravascular ultrasound, decreased significantly by 12.6% (p <0.0001 vs baseline) after treatment; furthermore, a corresponding decrease of total leukocyte count (8.9%, p <0.01 vs baseline) was seen. Change in plaque volume was correlated with changes in monocyte (r = 0.35, p = 0.002) and lymphocyte (r = 0.25, p = 0.03) counts but not with changes in neutrophil, eosinophil, or basophil counts. In a multivariate regression analysis with changes in serum lipids, traditional risk factors, and medications as covariates, the decrease in monocyte count was identified as an independent predictor of coronary plaque regression (beta coefficient 0.313, 95% confidence interval 0.089 to 0.353, p = 0.0014). No correlation was found between change in monocyte count and changes in any other lipid levels. This study demonstrated that monocyte count was the only leukocyte type significantly and independently associated with coronary atherosclerotic regression, even after adjustment for changes in any lipid levels. In conclusion, the decrease in monocyte count as a nonlipid-lowering effect of statins may be used as a novel marker of coronary atherosclerotic regression. [Copyright &y& Elsevier]

Abstract: Background: Focal vasospasm is reportedly involved in a high incidence of acute coronary syndrome (ACS) as compared with diffuse vasospasm. No adequate studies have been conducted on the mechanism underlying the higher incidence of ACS involving focal vasospasm than of those involving diffuse vasospasm in patients with coronary spastic angina. Methods and results: Blood samples were collected from the aortic root (Ao) and the coronary sinus (CS) before provoking left coronary vasospasm using intracoronary administration of acetylcholine. After relief of vasospasm, volumetric analyses of vasospastic lesions were evaluated with 3-dimensional intravasucular ultrasound in 64 patients. The percent plaque volume was more prominent in focal (n =31) than in diffuse vasospasm (n =33) (40.9±9.4 vs. 23.3±9.2%, p <0.0001). The Cs-Ao difference of malondialdehyde-modified low-density lipoprotein (MDA-LDL) level, as a marker of atherothrombosis, in focal vasospasm increased significantly as compared with diffuse vasospasm (6.9±6.7 vs. 1.2±5.7 U/L, p =0.001). In a multiple-logistic regression analysis with the traditional risk factors, the Cs-Ao difference of MDA-LDL level was a variable differing independently between the 2 types of vasospasm. Conclusions: Higher MDA-LDL levels were observed in the coronary circulation in patients with focal vasospasm than in those with diffuse vasospasm. Under these conditions, the dramatically increased percent plaque volume in cases with focal vasoconstriction may play an important role in the development of acute coronary events. [Copyright &y& Elsevier]

Abstract: Epidemiological studies have demonstrated that the peripheral blood leukocyte count could be used as a marker of the progression of atherosclerosis. Few data exist regarding the relationship between inhibition of the progression of coronary atherosclerosis and the anti-inflammatory effects of statins, especially the drugs’ effects on the leukocyte count in patients with coronary artery disease. A 6-month prospective study was, therefore, conducted in 50 patients treated with pravastatin. The plaque volume, as assessed by volumetric analysis using intravascular ultrasound, reduced significantly by 14% (p <0.0001, vs. baseline) following the treatment, furthermore, a corresponding decrease of the leukocyte count (8.9%, p <0.01, vs. baseline) was also seen. No correlation was found between the change in the leukocyte count and any of the changes in the lipid levels; changes in either of these are known to be associated with the rate of progression of atherosclerosis. A multivariate regression analysis using other traditional risk factors and medications as covariates revealed that the decrease in the leukocyte count was an independent predictor of inhibition of the progression of coronary atherosclerosis. In conclusion, a reduction of the leukocyte count as one of the non-lipid-lowering effects of pravastatin may be a novel marker of regression of coronary atherosclerosis. [Copyright &y& Elsevier]

Abstract: Relationship between angiographic morphology and high-sensitivity C-reactive protein (hs-CRP) levels is not fully understood. The serum levels of hs-CRP levels were higher in focal than in diffuse vasospasm in patients with coronary spastic angina. Intravascular ultrasound showed greater plaque volume at the site of vasospasm in the focal vasospasm, in the absence of significant angiographic stenosis, whereas diffuse intimal thickening throughout the coronary arteries was observed in the diffuse vasospasm. The distinct differences in the hs-CRP levels may be closely associated with coronary plaque appearances. [ABSTRACT FROM AUTHOR]

The cholesterol-esterifying enzyme, lecithin-cholesterol acyltransferase (LCAT), is believed to play a key role in reverse cholesterol transport. However, recent investigations have demonstrated that higher LCAT activity levels increase the formation of triglyceride (TG)-rich lipoproteins (TRLs) and atherogenesis. We hypothesized that higher LCAT activity measured as a serum cholesterol esterification rate by the endogenous substrate method might increase the formation of TRLs and thereby alter low-density lipoprotein (LDL) heterogeneity. The estimated LDL particle size [relative LDL migration (LDL-Rm)] was measured by polyacrylamide gel electrophoresis with the LipoPhor system (Joko, Tokyo, Japan) in 538 consecutive patients with at least risk factor for atherosclerosis. Multivariate regression analysis after adjustments for traditional risk factors identified elevated TRL-related marker (TG, remnant-like particle cholesterol, apolipoprotein C-II, and apolipoprotein C-III) levels as independent predictors of smaller-sized LDL particle size, both in the overall subject population and in the subset of patients with serum LDL cholesterol levels of <100 mg/dL. Area under the receiver operating characteristic curve of the LCAT activity (0.79; sensitivity 60 %; specificity 84.8 %) was observed for the evaluation of the indicators of an LDL-Rm value of ≥0.40, which suggests the presence of large amounts of small-dense LDL. The results lend support to the hypothesis that increased LCAT activity may be associated with increased formation of TRLs, leading to a reduction in LDL particle size. Therefore, to reduce the risk of atherosclerotic cardiovascular disease, it may be of importance to pay attention not only to a quantitative change in the serum LDL-C, but also to the LCAT activity which is possibly associated with LDL heterogeneity. [ABSTRACT FROM AUTHOR]

Recently, investigation may have focused on modification of apolipoprotein A-I (apoA-I) associated with anti-inflammatory effect for the potential prevention of cardiovascular events. The purpose of this study was to evaluate the effects of atorvastatin and pitavastatin on serum apoA-I levels and to investigate the role of apoA-I in the anti-inflammatory effect of statin. We conducted a 6-month, prospective, randomized, open-label study in which we assigned hypercholesterolemic patients to a pitavastatin group ( n = 52; 2 mg/day) or an atorvastatin group ( n = 52; 10 mg/day) to investigate the effects of these two statins on the serum apoA-I levels and serum high-sensitivity C-reactive protein (hs-CRP) levels. There were no significant differences between the two groups in the changes in the low-density lipoprotein cholesterol, high-density lipoprotein cholesterol (HDL-C), or hs-CRP levels, but the change in apoA-I in the pitavastatin group was significantly greater than in the atorvastatin group (5.3 vs. 1.4 %; p = 0.0001). A stepwise regression analysis revealed that the percent change in (Δ) serum apoA-I level was an independent predictor of the Δ serum hs-CRP (standard correlation coefficient = −0.198; p = 0.047). However, there was a significant negative correlation between the Δ apoA-I levels and Δ hs-CRP levels in the pitavastatin group ( r = −0.283, p = 0.042), but not the atorvastatin group ( r = −0.133, p = 0.356). The results suggest that the contribution of apoA-I to the reduction in serum hs-CRP levels by these two statins may be different. A decrease in hs-CRP level accompanied by an increase in apoA-I level may be involved in the pleiotropic effects of pitavastatin. [ABSTRACT FROM AUTHOR]

Monocytes and high-density lipoprotein cholesterol (HDL-C) play important roles in the process of coronary atherosclerosis. We hypothesized that a reasonable predictive model of coronary plaque regression might be constructed using the change in the peripheral monocyte count and the serum HDL-C level. The plaque volume, as assessed by volumetric intravascular ultrasound, was measured at the baseline and after 6 months of pravastatin therapy in 114 patients with coronary artery disease. After 6 months of pravastatin therapy, a significant decrease of the plaque volume by 9.9% ( p < 0.0001, vs. baseline) was observed; furthermore, a corresponding increase of the serum HDL-C level and decrease of the peripheral blood monocyte count were also seen (12.5%, p < 0.01 and −7.3%, p < 0.0001). In a multivariate regression analysis using the serum lipids and traditional risk factors as the covariates, the increase in the serum HDL-C ( β −0.56, p < 0.0001) and the decrease in monocyte count ( β 0.23, p = 0.03) were identified as independent predictors of the plaque regression. A model for the prediction of plaque regression according to whether the achieved the change in (Δ) monocyte count and ΔHDL-C were above or below the median values was prepared. Among the four groups, the group with ΔHDL-C ≥8.8% and Δmonocyte count ≤−8.6% showed the largest plaque regression (−20.4%), and the group with ΔHDL-C <8.8% and Δmonocyte count >−8.6% showed the increase of the plaque volume (2.6%). In view of the inflammatory nature of atherosclerosis, the model constructed using the two predictors may be a useful model for the prediction of plaque regression. [ABSTRACT FROM AUTHOR]

Abstract: We experienced a case of vasospastic angina showing resolution of vasospasm in the acetylcholine provocation test corresponding to regression of coronary atherosclerotic plaque following treatment with a combination of benidipine and pravastatin. [Copyright &y& Elsevier]