Blood pressure (BP) is one of the most important contributing factors to pulse wave velocity (PWV), a classic measure of arterial stiffness. Although there have been many non-invasive studies to show the relation between arterial stiffness and BP, the results are controversial. The aim of this study is to evaluate the role of BP as an influencing factor on PWV using invasive method. We observed 174 normotensive and untreated hypertensive subjects using coronary angiography. Arterial stiffness was assessed through aorto-femoral PWV by foot-to-foot velocity method using fluid-filled system. And BP was measured by pressure wave at the right common femoral artery. From univariate analysis, age, diabetes mellitus (DM), hypertension, waist, waist-to-hip ratio, total cholesterol-tohigh-density lipoprotein cholesterol ratio, systolic BP (SBP), pulse pressure (PP) and mean arterial pressure (MAP) showed significant association with PWV. To avoid multiple colinearity among SBP, PP and MAP, we performed multiple regression analysis predicting PWV thrice. Age, DM and each BP were significantly and consistently correlated to PWV. In the first and third modules, compared to age, SBP and MAP were less strong predictors, respectively. However, PP was the stronger predictor than age and DM in the second module. Lastly, we simultaneously forced MAP and PP with other variables in the fourth multivariate analysis. Age, DM and PP remained significantly correlated with PWV, but the significance of MAP was lost. This is the first invasive study to suggest that PP has the strongest correlation with PWV among a variety of BP parameters.

Background— Atherosclerosis is considered to be an inflammatory disease associated with the activation of hematopoietic and immune-related organs such as the bone marrow (BM) and spleen. We evaluated the metabolic activity of those organs and of the carotid artery with 18 F-fluorodeoxyglucose positron emission tomography in patients with coronary artery disease, including acute myocardial infarction. Methods and Results— Whole-body combined 18 F-fluorodeoxyglucose positron emission tomography/computed tomography was performed in 32 patients with acute myocardial infarction, 33 patients with chronic stable angina, and 25 control subjects. The mean standard uptake value was calculated in the regions of interest in the spleen and the BM of lumbar vertebrae. The target-to-background ratio of the standard uptake values of the carotid artery and jugular vein was also calculated. In patients with acute myocardial infarction, the standard uptake values of the BM (1.67±0.16) and spleen (2.57±0.39), as well as the target-to-background ratio of the carotid artery (2.13±0.42), were significantly higher than the corresponding values of patients with angina (1.22±0.62; 2.03±0.35; 1.36±0.37; all P <0.001) and controls (0.80±0.44; 1.54±0.26; 1.22±0.22; all P <0.001), independent of traditional cardiovascular risk factors and high-sensitivity C-reactive protein. In all groups combined, the target-to-background ratio of the carotid artery was significantly associated with the standard uptake values of the BM ( r =0.535; P <0.001), spleen ( r =0.663; P <0.001), and high-sensitivity C-reactive protein ( r =0.465; P <0.001). Conclusions— The metabolic activity of the BM and spleen, as well as of the carotid artery, was highest in patients with acute myocardial infarction, intermediate in patients with angina, and lowest in control subjects. The activation of the BM and spleen was significantly associated with inflammatory activity of the carotid artery.

Objectives: Visfatin and lipocalin-2 are novel adipokines associated with insulin resistance (IR) and obesity-related metabolic disorders. We compared lipocalin-2 and visfatin concentrations between patients with coronary heart disease (CHD) and control subjects and evaluated their association with cardiovascular risk factors. Methods: We examined serum visfatin, lipocalin-2 levels, and cardiovascular risk factors in 91 subjects (49 patients with angiographically confirmed CHD versus 42 age-and gender-matched control participants). Results: Circulating lipocalin-2 levels were significantly higher in patients with CHD compared with the control subjects (82.6G38.7 ng/ml versus 43.8G27.8 ng/ml; P!0.001). However, visfatin levels were not significantly different between patients with CHD and control subjects. Serum lipocalin-2 levels were positively associated with weight (rZ0.26; PZ0.036), fasting insulin (rZ0.36; PZ0.003), and IR (rZ0.33; PZ0.007), whereas these levels showed a negative correlation with high-density lipoprotein (HDL) cholesterol (rZK0.30; PZ0.016) after adjustment for gender and body mass index. However, visfatin levels were not associated with any variables of the metabolic syndrome. The multiple regression analysis showed that lipocalin-2 levels were independently associated with HDL cholesterol and IR (R 2 Z0.199). Furthermore, the multiple logistic regression analysis showed that systolic blood pressure, IR, and lipocalin-2 levels were independently associated with CHD. Conclusions: Serum lipocalin-2 levels were significantly elevated in patients with CHD and were independently associated with CHD. The present findings suggest that the measurement of serum lipocalin-2 levels may be useful for assessing CHD risk.

The results suggest that a decrease in plasma adiponectin concentration is associated with the progression of left ventricular hypertrophy with diastolic dysfunction.

Vasoconstriction in response to Ach in the peri-stent region was less pronounced in the ZES group than the SES group at 6-month follow-up, which suggests that endothelial function associated with ZES can be more preserved than the SES.