Stiffness In Coronary Artery Disease Patients Research Articles

Lipoprotein-associated phospholipase A2 levels, endothelial dysfunction and arterial stiffness in patients with stable coronary artery disease

Abstract Background Lipoprotein-associated Phospholipase A2 (Lp-PLA2), has inflammatory and atherogenic actions in the vascular wall. We investigate the impact of high Lp-PLA2 levels on endothelial function and arterial stiffness on patients with coronary artery disease (CAD). Methods We enrolled 374 consecutive patients with stable CAD (mean age 61±11 years). Endothelial function was evaluated by flow-mediated dilation (FMD) and reflected waves with augmentation index (AIx) of the central aortic pressure. Serum levels of Lp-PLA2 were measured with ELISA. Results In the studied population the median values of Lp-PLA2 levels was 125 (96–152) μg/L. There was no difference between subjects with Lp-PLA2 levels above and below 125μg/L concerning classical risk factors for CAD. Importantly, subjects with Lp-PLA2 values ≥125μg/L had significantly impaired FMD (4.44±2.19% vs. 4.89±2.07%, p=0.04) and AIx values (25.21±8.70% vs. 23.06±9.47%, p=0.03), compared to participants with lower Lp-PLA2 serum levels. A linear regression analysis revealed that Lp-PLA2 ≥125μg/L negatively relates to impaired FMD [b=−0.54 (95% CI: −1.05 to −0.02), p=0.04] and AIx values [b=2.14 (95% CI: 0.18–4.01), p=0.03] independently of cofounders. Conclusions Elevated Lp-PLA2 relates to endothelial dysfunction and arterial stiffness in CAD patients. These findings highlight the significant role of Lp-PlA2 in the process of atherosclerosis. Funding Acknowledgement Type of funding source: None

Arterial stiffness in patients with coronary artery disease: relation with in-stent restenosis following percutaneous coronary intervention.

BackgroundCoronary artery disease (CAD) is one of the most important issues in modern medicine due to its high mortality and prevalence. An early detection and prevention can reduce morbidity and mortality. Arterial stiffness is a potent and independent predictor of CAD. We aimed to investigate the arterial stiffness in CAD patients undergoing the coronary angiography. Also, we investigated a possible correlation between arterial stiffness and in-stent restenosis (ISR), an important limitation of percutaneous coronary intervention (PCI).MethodsThe study included 160 patients undergoing coronary angiography, treated either with PCI or with CABG. The pulse wave velocity (PWV) and augmentation index (AIx) were measured by the Arteriograph.ResultsPWV in the CAD group (12.24 ± 2.78 m/s) was significantly higher compared to the control group (8.27 ± 1.89 m/s). PWV in ISR and left main (LM) stenosis group (14.03 ± 3.15 and 13.89 ± 2.95 m/s) was significantly higher compared to the control and CAD groups. Peripheral and central AIx were significantly higher in CAD group (1.38 ± 30.63 % and 38.35 ± 15.52 %) than in control group (−11.35 ± 26.74 % and 26.91 ± 10.62 %). Patients with LM stenosis have significantly higher values of peripheral and central AIx (23.37 ± 23.77 % and 49.71 ± 12.02 %) than the CAD and ISR group.ConclusionsThe study confirmed a positive correlation between arterial stiffness measures, PWV and AIx, and CAD. Also, this study showed the correlation between PWV and ISR which can help to select more appropriate stent.Electronic supplementary materialThe online version of this article (doi:10.1186/s12872-016-0305-4) contains supplementary material, which is available to authorized users.

Association of serum leptin levels with central arterial stiffness in coronary artery disease patients.

BackgroundSerum adipokines have roles in the development of arterial stiffness. Our aim was to investigate the relationship of leptin and the surrogate marker carotid-femoral pulse wave velocity (cfPWV) in coronary artery disease (CAD) patients.MethodsFasting blood samples were obtained from 105 CAD patients. cfPWV was measured with the SphygmoCor system. A cfPWV > 10 m/s was defined as high arterial stiffness, and ≤ 10 m/s as low arterial stiffness.ResultsThirty-seven patients (35.2 %) had high arterial stiffness, and had a higher percentage of diabetes (P = 0.001), hypertension (P = 0.010), older age (P = 0.001), and higher systolic blood pressure (SBP) (P < 0.001), diastolic blood pressure (DBP) (P = 0.021), pulse pressure (P = 0.014), and serum leptin level (P = 0.002) compared to patients with low arterial stiffness. Serum leptin levels correlated with the number of angiographically documented stenotic coronary artery vessels (P < 0.001). After adjusting for factors significantly associated with arterial stiffness, multivariate logistic regression analysis showed that leptin (odds ratio = 1.026, 95 % confidence interval: 1.002–1.051, P = 0.037) was a significant independent predictor of arterial stiffness.ConclusionsIncreasing serum concentration of leptin correlated positively with the total number of stenotic coronary arteries, and serum leptin level may predict the development of arterial stiffness in CAD patients.

Relationships between use of statins and arterial stiffness in normotensive and hypertensive patients with coronary artery disease

Background Statins improve arterial stiffness in patients with coronary artery disease (CAD). Hypertension is a predominant contributor of arterial stiffening. However, the influence of hypertension on the effect of statins for improving arterial stiffness in CAD patients has seldom been investigated. Therefore, in this study, we investigated the relationships between statin use and arterial stiffness in normotensive and hypertensive CAD patients. Methods Brachial-ankle pulse wave velocity (ba-PWV) was measured in 437 patients, including 220 hypertensive CAD patients (121 used statins, 99 did not) and 217 normotensive CAD patients (105 used statins, 112 did not). The normotensive and hypertensive CAD patients were matched according to age, sex, and body mass index (BMI). Results In the normotensive and hypertensive CAD patients, lipid profiles were significantly improved in the statin group compared with the non-statin group. No significant differences in the administered statins (i.e., atorvastatin, simvastatin, rosuvastatin, and pravastatin) and statin therapy duration were found between normotensive and hypertensive CAD patients (all P&gt;0.05). No significant correlation of ba-PWV and statin therapy duration was found in all CAD patients, normotensive CAD patients, or hypertensive CAD patients (all P&gt;0.05). ba-PWV in the statin group was significantly lower than that in the non-statin group in normotensive CAD patients ((1331.68±167.52) cm/s vs. (1468.61±244.54) cm/s, P=0.002) but not in hypertensive CAD patients (P&gt;0.05). In multiple linear regression analyses, statin therapy was significantly associated with ba-PWV after adjusting for confounding variables in normotensive CAD patients (P=0.018) but not in hypertensive CAD patients (P&gt;0.05). Conclusions Statins may significantly improve arterial stiffness in CAD patients, and hypertension may probably influence the effectiveness of statin therapy in improving arterial stiffness in this population. Further studies are required to investigate the effect of statins on arterial stiffness in normotensive and hypertensive CAD patients.

Abstract 365: The Impact of CYP2C19*2 Polymorphism on Endothelial Function and Arterial Stiffness in Patients with Coronary Artery Disease Receiving Clopidogrel

Background: The role of CYP2C19*2 polymorphism in clopidogrel response and cardiovascular prognosis has come under question in recent studies. Measurement of endothelial function and arterial stiffness are well validated in large population studies as strong predictors of adverse cardiovascular outcomes. We examined the impact of CYP2C19*2 polymorphism on endothelial function and arterial stiffness in coronary artery disease (CAD) patients. Methods: The study included 245 patients with stable CAD, receiving clopidogrel regimen (75mg/d). CYP2C19*2 genotyping was performed by real-time polymerase chain reaction. CAD patients were divided in two groups. Group A consisted of patients homozygous for the wild type and group B consisted of patients carrying at least one CYP2C19*2 loss-of-function allele. Endothelial function was evaluated by flow-mediated dilatation (FMD). Carotid-femoral pulse wave velocity (PWV) was measured as an index of aortic stiffness. Results: Group A included 153 patients (62.4%) and group B 92 patients (37.6%). There was no statistically significant difference between the two groups in age (62±10 vs. 60±12 years, p=0.12), male sex (90% vs. 91%, p=0.65) and the presence of dyslipidemia (74% vs. 70%, p=0.57), diabetes mellitus (27% vs. 27%, p=0.97) and arterial hypertension (80% vs. 81%, p=0.74). Importantly, there was no difference in FMD (4.82±2.17% vs. 4.92±2.47%, p=0.74) and PWV values (9.08±2.02m/sec vs. 8.89±2.49m/sec, p=0.55) between the two groups. Conclusion: CYP2C19*2 polymorphism is not associated with endothelial function and arterial stiffness in CAD patients receiving clopidogrel. These findings are consisted with the absence of an effect of the CYP2C19*2 loss-of-function alleles on cardiovascular risk among CAD patients treated with clopidogrel, as it is documented in recent large trials.

Assessment of arterial stiffness affected by atorvastatin in coronary artery disease using pulse wave velocity

Several studies have shown arterial stiffness changes associated with coronary artery disease (CAD). Recently, statins were reported to improve arterial stiffness. The aim of the study was to evaluate the effect of atorvastatin on arterial stiffness in CAD patients using pulse wave velocity (PWV). We evaluated 63 patients with hyperlipemia and CAD. Forty-three patients were given 10mg atorvastatin daily and 20 patients were assigned to a low-fat diet. Carotid-femoral PWV (PWV-CF), carotid-radial PWV (PWV-CR) and carotid-distal PWV (PWV-CD) were measured in all patients. Compared with baseline, PWV-CF, PWV-CR and PWV-CD decreased after therapy in the atorvastatin group (13.22+/-3.39 & 11.85+/-2.87; 11.85+/-2.72 & 10.73+/-2.31; and 11.04+/-1.99 & 10.15+/-1.75, P < 0.05). There was no difference in the control group (13.29+/-2.89 & 13.93+/-2.89; 11.52+/-2.25 & 12.31+/-2.22; and 10.46+/-1.86 & 11.15+/-1.85, P > 0.05). After treatment, values of total cholesterol, triglyceride and low density lipoprotein (LDL) cholesterol were reduced in the 2 groups (P < 0.05). The study demonstrated that atorvastatin can improve arterial stiffness in CAD patients independent of its lipid-lowering properties.