Possible effects of lipoprotein-associated phospholipase A2 single-nucleotide polymorphisms on cardiovascular risk in patients with preeclampsia.

PURPOSE: Lipoprotein lipase-associated phospholipase A2 (Lp-PLA2) is a vascular inflammatory marker associated with cardiovascular diseases (CVD). Women with preeclampsia (PE) have elevated vascular inflammation and at higher CVD risk in the later life. We hypothesize that vascular inflammation related genetic variations increase the risk for developing future cardiovascular disease in women with PE. To test this hypothesis, we studied PLA2G7 gene polymorphisms, Lp-PLA2 mass, activity, index, and other cardiovascular risk factors in women with preeclampsia. METHODS: A total of 200 pregnant women were included into the study. We stratified the PE group: early (28.7 ± 3.0 weeks) and late onset (36.0 ± 1.4 weeks). Serum Lp-PLA2 mass in the early PE and the late PE group were significantly higher than the control group (p = .000). Lp-PLA2 index, Hs-C-reactive protein (CRP), serum amyloid A (SAA), calprotectin, and PTX3 levels were higher in early and late PE (p = .000). Single-nucleotide mutations of PLA2G7 rs1805017 (r = -0.228, p < .05) and rs9381475 (r = 0.216, p < .05) were correlated with LpPLA2 mass for the early PE group. Logistic regression analysis showed that LP-PA2 mass an independent risk factor for early PE with rs1805017 and rs9381475 carriers. CONCLUSIONS: Lp-PLA2 genetic variability with vascular inflammatory markers might contribute the incidence of future cardiovascular events.

Nontraditional risk factors in carotid artery disease.

Carotid atherosclerosis (AS) is one of the main risk factors for ischemic stroke. Our aim is to evaluate the nontraditional biochemical markers in asymptomatic and symptomatic patients with carotid artery plaque. This study was conducted on 55 patients: 43 with symptomatic and 12 with asymptomatic carotid artery disease. Lipoprotein (a) (Lp(a)), homocysteine, adiponectin, nitric oxide (NO), and tumor necrosis factor alpha (TNF-alpha) levels were measured in the plasma. The mean of total cholesterol, triglyceride, and homocysteine levels was significantly elevated in the symptomatic group as compared with the asymptomatic group (P = .03). In the asymptomatic group, adiponectin and NO levels showed elevations as compared with the symptomatic group but this increase was not significant (P > .05). Lipoprotein (a) and TNF-alpha levels acted inversely with adiponectin and NO. There was an insignificant decline in Lp(a) and TNF-alpha levels in the asymptomatic group as compared with the symptomatic group (P > .05).

The role of adiponectin in atherosclerosis and thrombosis.

Obesity is a major risk factor for morbidity and mortality from cardiovascular causes. Adiponectin has been identified recently as one of the adipocytokines with important metabolic effects. It can suppress atherogenesis by inhibiting the adherence of monocytes, reducing their phagocytic activity, and suppressing the accumulation of modified lipoproteins in the vascular wall. In addition, as adiponectin decrease endothelial damage and stimulates production of NO from vascular endothelial cells, hypoadiponectinemia may be partially contribute to thrombus formation.

Evaluation of fibronectin, vitronectin, and leptin levels in coronary artery disease: impacts on thrombosis and thrombolysis.

In this study, the levels of fibronectin, vitronectin, leptin, tissue plasminogen activator (t-PA), and lipid parameters were investigated in patients with coronary artery disease (CAD) and control group. The average plasma fibronectin levels in CAD patients group were significantly higher compared with the control group (p=0.006). Moreover, in patients with triple-vessel disease, plasma fibronectin levels were found to be significantly higher than those in the control group (p<0.05). Plasma vitronectin levels in patients with CAD were found to be significantly higher than those in the control group (p=0.000). In addition, in patients with double vessel disease plasma vitronectin levels were significantly higher than no vessel disease and control group, triple vessel disease was significantly higher as compared with no vessel disease, single vessel disease, and control group (p<0.05). We could not find any significant differences in t-PA values between CAD patients and control group. On the other hand, the average leptin levels in the group of patients were higher than those in the control group but there were no statistically significant differences found between them (p>0.05) because of high SD values. There was strong (+) correlation between fibronectin, vitronectin, and severity of disease [vitronectin/severity of disease, r = 0.5074 (p = 0.000), fibronectin/severity of disease, r = 0.2971 (p = 0.007)]. In conclusion, we can say that fibronectin and vitronectin have become greatly important in pathogenesis of coronary artery disease. High leptin levels may be contribute to platelet aggregation in patients with coronary artery disease. But, elevated serum levels of leptin cannot be useful diagnostic and monitoring markers in patients with coronary artery disease.

Plasma vitronectin levels in patients with coronary atherosclerosis are increased and correlate with extent of disease.

BACKGROUND: Acute thrombosis after atherosclerotic plaques disruption is a major complication of primary atherosclerosis, leading to acute ischemic syndromes and atherosclerotic progression. Vitronectin (VN) is multifunctional glycoprotein in blood and in the extracellular matrix. It binds glycosaminoglycans, collagen, plasminogen and urokinase receptor. VN stabilizes the inhibitory confirmation of plasminogen activation inhibitor-1 (PAI-1). Vitronectin may control the clearance of vascular thrombi by binding and stabilizing PAI-1, a key regulator of fibrinolysis. Therefore, VN is generally regarded as a cofactor for PAI-1 activity. On the other hand vitronectin binds to platelet glycoproteins may mediate platelet adhesion and aggregation at sites of vascular injury. Previous studies showed that anti-VN antibodies inhibit platelet aggregation in vitro, suggesting that vitronectin contributes to platelet accumulation at sites of vascular injury. In this study; we investigated the levels of plasma vitronectin in patients with Coronary Artery Disease (CAD) and control group. METHODS: The patient group was divided into four subgroups: patients with no, single, double and triple vessel disease according to their angiography results. ELISA procedure (Technoclone) was used to determine the plasma vitronectin levels. RESULTS: Plasma vitronectin levels in patient with CAD (% 125.87 +/- 58.38) were found to be significantly higher than control group (% 89.47 +/- 25.3) (p:0.000). In addition, in patients with double vessel disease (% 146.03 +/- 71.69) plasma vitronectin levels were significantly higher than no vessel disease (% 87.84 +/- 22.30) and control group, triple vessel disease (% 160.81 +/- 57.02) significantly higher as compare with no, single vessel disease (% 111.68 +/- 45.34) and control group (p < 0.05). There was no correlation between vitronectin and lipid parameters. CONCLUSION: These findings suggested that vitronectin is a marker of CAD. Elevated levels may indicate its role in the genesis and/or progression of CAD or may be the results of a compensatory mechanism.