dinoprost and Carotid-Artery-Diseases

It remains unclear whether atherosclerosis in one vascular bed progresses in parallel with that in other vascular beds. We investigated serial changes in vessel wall areas (VWAs) in various vessels over 2 years of follow-up. Vessel wall areas in the thoracic descending aorta (TDA), common carotid artery (CCA), right (RCA), and left main trunk (LMT) of coronary artery were determined in 52 patients with coronary artery disease (CAD) using 64-slice multidetector computed tomography. Plasma levels of high-sensitivity CRP (hs-CRP) and matrix metalloproteinase (MMP)-9, as well as urinary 8-iso-prostaglandin F2α (PGF2α) were determined at the baseline. After the follow-up period, plaque progression in a specific vessel did not parallel that of other vessels, although changes in TDA-VWAs were weakly correlated with those of LMT-VWAs. Basal levels of hs-CRP, MMP-9, and PGF2α did not predict progression or regression of VWAs in any vessels. Multivariate analyses showed that LDL-cholesterol < 100 mg/dl and use of statin emerged as predictors of regressing VWAs in TDA (p < 0.05 and p < 0.05, respectively) and LMT (p < 0.05 and p = 0.13, respectively). Changes in soft plaques over 2 years paralleled those of VWAs in both coronary arteries. In conclusion, the progression or regression of atherosclerotic plaques is inhomogeneous among the vascular beds of patients with CAD.

Topics: Aged; Aorta, Thoracic; Aortic Diseases; Aortography; Atherosclerosis; Biomarkers; C-Reactive Protein; Carotid Artery Diseases; Carotid Artery, Common; Cholesterol, LDL; Coronary Angiography; Coronary Artery Disease; Dinoprost; Disease Progression; Female; Follow-Up Studies; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Japan; Logistic Models; Male; Matrix Metalloproteinase 9; Middle Aged; Time Factors; Tomography, X-Ray Computed

In order to characterize whether different degrees of adipose tissue storage may be associated with markers of early atherosclerosis, we evaluated oxidant-antioxidant status and inflammatory markers and determined carotid intima-media thickness (cIMT) in healthy constitutional lean and obese pre-pubertal children.. Eighty healthy pre-pubertal lean and obese children were recruited and compared with 40 age, gender, and pubertal stage-matched normal controls. Anthropometric measurements, oxidant (urinary isoprostanes (PGF-2alpha), lag phase, and malondialdehyde (MDA)) and antioxidant status (vitamin E), inflammatory markers (high sensitive C-reactive protein (hs-CRP)), and insulin sensitivity (fasting glucose-insulin ratio, homeostasis model assessment of insulin resistance (HOMA-IR)) were investigated. Furthermore, cIMT was measured by high-resolution ultrasound.. hs-CRP was not different between lean and control subjects (P=0.45), while higher values were found in obese compared with lean and control children (P<0.001 and P<0.001 respectively). PGF-2alpha and MDA were higher while lag phase shorter in lean and obese subjects compared with controls (lean P<0.001; P<0.001; P<0.001 and obese P<0.001; P<0.001; P<0.001 respectively), while no differences were documented between lean and obese subjects (P=0.78, P=0.019, and P=0.53 respectively). Compared with controls, cIMT was increased in lean and in obese subjects (P=0.001; P=0.004), while no differences were documented between obese and lean subjects (P=0.1). In a multiple stepwise linear regression analysis, cIMT was related with PGF-2alpha (beta=0.641, P<0.001) and HOMA-IR (beta=0.307; P<0.001).. Pre-pubertal lean and obese children present increased oxidative stress and impaired inflammation and insulin sensitivity, which in turn seem to result in similar impaired endothelial dysfunction and early signs of atherosclerosis, already in childhood.

Topics: Antioxidants; Biomarkers; Body Weight; C-Reactive Protein; Carotid Arteries; Carotid Artery Diseases; Child; Chronic Disease; Dinoprost; Female; Humans; Inflammation; Insulin Resistance; Male; Malondialdehyde; Obesity; Oxidants; Regression Analysis; Severity of Illness Index; Tunica Intima; Ultrasonography; Vitamin E

Obesity in children appears to be associated with increased risk of cardiovascular and metabolic diseases later in life. Early development of insulin resistance and impaired oxidant-antioxidant status may lead to endothelial dysfunction and increased carotid intima media thickness (IMT) even in childhood. The aim of this study was to measure IMT and the relationship between IMT, insulin resistance and oxidant status in obese pre-pubertal children. In 53 obese pre-pubertal children (27M/26F, mean age 8+/-2 years), anthropometric measurements and inflammatory markers (hs-CRP and PGF-2 alpha), were evaluated compared with 41 healthy pre-pubertal subjects (21M/20F, mean age 7+/-2 years). OGTT was performed and insulin resistance (IR) indices (HOMA-IR, WBISI, G/I and QUICKI) were calculated in all patients. High-resolution ultrasound techniques were used to evaluate IMT. Obese children had higher levels of PGF-2 alpha and hs-CRP compared to healthy subjects (p=0.001 and p=0.005). Furthermore, fasting insulin levels and HOMA-IR were higher in obese children than in controls (p=0.001 and p=0.001) while WBISI was significantly lower (p=0.002). In addition, obeses had an increased IMT (p=0.001). In obese children there was a significant correlation between IMT and indices of IR (HOMA-IR: beta=-1.233, p=0.002; WBISI: beta=-0.921, p=0.008; G/I: beta=-0.811, p=0.003) and between IMT and PGF-2 alpha (beta=0.505, p=0.004). After categorizing subjects according to tertiles of body mass index (BMI) (or=26.23 kg/m(2)) and to waist circumference (WC) (or=79.04 cm), no influence of BMI or WC on IMT were found in the three groups. In conclusion, early changes in glucose metabolism and an alteration of oxidant-antioxidant status may be present in obese pre-pubertal children; this could lead to increase IMT and early cardiovascular disease.

Topics: Biomarkers; Blood Glucose; C-Reactive Protein; Carotid Artery Diseases; Child; Comorbidity; Dinoprost; Female; Humans; Insulin; Insulin Resistance; Male; Obesity; Oxidative Stress; Risk Factors; Tunica Intima; Tunica Media; Ultrasonography

Topics: Arteriosclerosis; Carotid Artery Diseases; Coronary Artery Disease; Dinoprost; Humans; Lipid Peroxidation; Logistic Models; Lupus Erythematosus, Systemic; Oxidative Stress; Tumor Necrosis Factor-alpha

Oxidized low-density lipoprotein (Ox-LDL)is implicated in the pathogenesis of atherosclerosis. Circulating oxidation-specific epitopes on plasma Ox-LDL has been linked with coronary artery disease, but its determinants and its association with early development of atherosclerosis in familial combined hyperlipidemia (FCHL) has not been very well studied. This study aimed to investigate the determinants of the circulating Ox-LDL and the association between Ox-LDL and carotid intima-media thickness (IMT) in asymptomatic members of FCHL families.. Ox-LDL, susceptibility of LDL to oxidation in vitro, plasma 8-isoprostane and antioxidants, lipids and lipoproteins, LDL particle size, and carotid IMT were measured in 150 asymptomatic FCHL family members. Affected FCHL family members had reduced LDL particle size and lag time for LDL oxidation, increased plasma levels of Ox-LDL, increased plasma urate and alpha-tocopherol, and a trend for the increase of 8-isoprostane as compared with nonaffected FCHL. Ox-LDL was independently associated with serum LDL cholesterol, apoB, and 8-isoprostane in multivariate analysis but only univariately correlated with LDL particle size and lag time for LDL oxidation. In addition, Ox-LDL was significantly associated with carotid mean IMT independently of other clinical and biochemical variables in a multivariate model.. Serum LDL cholesterol, apoB levels, and 8-isoprostane were the most important determinants of Ox-LDL. Ox-LDL is independently associated with carotid IMT in asymptomatic FCHL family members and can be used as a marker of early atherosclerosis in FCHL.

Topics: Adult; Antioxidants; Biomarkers; Carotid Arteries; Carotid Artery Diseases; Dinoprost; Disease Susceptibility; Female; Finland; Humans; Hyperlipidemia, Familial Combined; Lipids; Lipoproteins; Lipoproteins, LDL; Male; Particle Size; Tunica Intima; Tunica Media; Ultrasonography

To study the effects of in vivo transluminal balloon angioplasty (TBA) on the structure and function of the arterial wall, a canine model of hemorrhagic cerebral vasospasm of the high cervical internal carotid artery (ICA) was used. This model was also used to determine whether TBA performed before clot placement could prevent the development of vasospasm.. Twelve dogs underwent surgical exposure of both distal-cervical ICAs, followed by baseline angiography. One randomly selected ICA in each dog was then subjected to in vivo TBA and repeated angiography. Both distal ICAs were then surrounded with blood clots held by silicone elastomer sheaths. Seven days later angiography was repeated, and all animals were killed. The ICAs in four animals were perfusion-fixed in situ for morphological analysis by electron microscopy, and the arteries in the remaining eight animals were removed and immediately immersed in oxygenated Krebs' solution. Contractile responses of isolated arterial rings from each ICA were recorded after treatment with KCl, noradrenaline, serotonin, and prostaglandin F2 alpha, while relaxations in response to the calcium ionophore A23187 and papaverine were recorded after tonic contraction to noradrenaline had been established. The morphology and pharmacological responses of ICAs that had been exposed to blood with or without prior TBA were compared with data obtained from control arterial segments of intact, more proximal regions of the ICAs from each animal.. TBA resulted in immediate angiographic enlargement of the ICA lumen that was still evident 7 days later despite the placement of clotted blood around the artery. Scanning and transmission electron microscopy demonstrated flattening of the intima and internal elastic lamina in these dilated arteries, associated with patchy losses of endothelial cells. In contrast, ICAs that had been exposed to clotted blood but had not undergone prior TBA developed consistent angiographic and morphological vasospasm. In comparison with control vessels and nondilated vasospastic vessels, vessels dilated with TBA and then exposed to clotted blood showed significantly diminished responses to all compounds tested, with the exception of prostaglandin F2 alpha.. These results indicate that in vivo TBA results in a degree of functional impairment of vascular smooth muscle that persists for at least 7 days. This result is consistent with previous observations of the acute effects of TBA in isolated arteries. Furthermore, these results support the hypothesis that normal smooth muscle function is required for the development of vasospasm. Finally, these results indicate that TBA performed before the onset of vasospasm prevents its development.

Topics: Angiography; Angioplasty, Balloon; Animals; Blood Coagulation; Calcimycin; Carotid Artery Diseases; Carotid Artery, Internal; Dinoprost; Dogs; In Vitro Techniques; Ionophores; Ischemic Attack, Transient; Muscle, Smooth, Vascular; Norepinephrine; Papaverine; Potassium Chloride; Serotonin; Vasoconstrictor Agents; Vasodilator Agents

Cisternal and lumbar cerebrospinal fluid obtained some days following a subarachnoid haemorrhage contains abnormally large quantities of various prostanoids; some may be partly the result of abnormal production by the cerebral arteries. The extra-arterial and intra-arterial production of 6 oxo PGF1 alpha (prostacyclin metabolite), PGE2, PGF2 alpha and TXB2 were measured in perfused rabbit common carotid arteries taken both from normal rabbits and from rabbits in which the arteries had been ensheathed by blood clot in vivo for 7 days using two techniques. Prostaglandin production by control arteries was highest during the first hour of perfusion but declined or increased marginally (PGE2) during the succeeding three hours. Arteries exposed to a periarterial haematoma for 7 days produced prostaglandins at a high rate throughout the 4 hours of study, and there was a progressive and marked increase in PGE2 production. The disproportionate increase in the cerebral vasoconstrictor PGE2 may reflect the inflammatory response which occurred in the adventitia of the vessels. Increased prostanoid production by cerebral arteries probably does contribute to the increased levels in CSF after subarachnoid haemorrhage.

Topics: 6-Ketoprostaglandin F1 alpha; Animals; Carotid Arteries; Carotid Artery Diseases; Dinoprost; Dinoprostone; Eicosanoic Acids; Endothelium; Hematoma; Indomethacin; Prostaglandins E; Prostaglandins F; Rabbits; Subarachnoid Hemorrhage; Thromboxane B2; Vasoconstriction