Occurrence Of Atherosclerotic Plaques Research Articles

Common carotid intima-media thickness predicts occurrence of carotid atherosclerotic plaques: longitudinal results from the Aging Vascular Study (EVA) study.

The role of the increase in the common carotid artery (CCA) intima-media wall thickness (IMT) in the atherosclerotic process is questionable. This longitudinal study examined the predictive value of CCA-IMT measured at baseline examination (at sites free of plaques) on the occurrence of atherosclerotic plaques in the extracranial carotid arteries during 4 years of follow-up study in a sample of 1010 subjects aged 59 to 71 years. Ultrasound examinations were performed at baseline and 2 years and 4 years later. The occurrence of carotid plaques during follow-up was defined as the appearance of >/=1 plaque in previously normal carotid segments and/or the appearance of new plaques in the carotid segments that previously had plaques. Carotid plaque occurrence was observed in 185 subjects (18.3%). Age- and sex- adjusted odds ratios of carotid plaque occurrence were 2.66 (95% CI 1.58 to 4.46, P<0.001) in subjects having intermediate baseline CCA-IMT values (quartiles 2 and 3) and 3.67 (CI 2.09 to 6.44, P<0.001) in those having the highest baseline CCA-IMT values (quartile 4) compared with those having the lowest baseline CCA-IMT values (quartile 1). Multivariate adjustment for major cardiovascular risk factors did not alter the results. These findings were observed for men and women as well as for subjects with and without carotid plaques at baseline. This 4-year longitudinal study shows that CCA-IMT predicts carotid plaque occurrence in a large sample of relatively old subjects. It extends the findings obtained from cross-sectional studies and suggests that increased intima-media thickness might occur in an earlier phase of the atherosclerotic process.

Wall shear stress and early atherosclerosis: a review.

therosclerosis remains the leading cause of morbidity and mortality in the Western world [1, 2]. It is usually regarded as a systemic disease and several well-identified risk factors (i.e., hypertension, hyperlipidemia, diabetes mellitus, and cigarette smoking) have been implicated in its pathogenesis. Noninvasive imaging of atherosclerosis, such as intimal wall thickening and plaque formation, is routinely available using a variety of imaging techniques. The causes of atherosclerosis are multifactorial and knowing them could allow earlier prevention and detection of the disease. The frequent occurrence of atherosclerotic plaques in well-recognized arterial districts, together with the focal distribution of these plaques in regions of curvature, bifurcation, and branching of the vessels, suggests that fluid dynamics and vessel geometry may play a localizing role in the cause of plaque formation [3]. In vitro and in vivo models have been used to study the flow patterns in a variety of arterial territories and to look for an association between areas of preferential atherosclerotic plaque formation and blood flow hemodynamics [4‐7]. The magnitude and rate of change of blood flow close to a vessel wall, which can be expressed using the concept of wall shear stress, have been linked to the pathogenesis of atherosclerosis. Vessel segments with low wall shear stress or highly oscillatory wall shear stress appear to be at the highest risk for development of atherosclerosis. The purpose of this review is to familiarize the imager with the concepts and principles underlying wall shear stress measurements. Wall shear stress mapping may someday become part of the multifactorial, multidisciplinary approach to early atherosclerosis detection. We first review this hypothesized association between atherosclerosis and wall shear stress. We then review the use of phase-contrast velocity-encoded MR imaging and Doppler sonography to map velocity profiles in vascular structures. These hemodynamic parameters can be used to calculate how quickly the blood velocity increases when moving from the vessel wall to the center of the vessel. Estimation of wall shear stress is now possible with noninvasive imaging techniques such as MR imaging and Doppler sonography. MR imaging can be used to confirm, in vivo, what is known from in vitro hemodynamic studies and observations made at autopsy and in experimental models. Someday, this may help us better understand the importance of flow hemodynamics in the multifactorial etiology of atherosclerosis. Wall Shear Stress

Plasminogen activator inhibitor-1 and carotid intima-media thickening in patients with newly detected primary hypertension.

To investigate the correlation between ultrasonographically evaluated intima-media thickness (IMT) of common carotid artery (CCA) and cardiovascular risk factors for subjects with newly detected, uncomplicated and untreated primary hypertension. The study population consisted of 200 subjects (123 men and 77 women, aged 46+/-7.5 years). Blood pressure was measured in the clinical setting and by 24 h noninvasive ambulatory monitoring. Fasting levels of blood glucose, plasma lipids and lipoproteins, fibrinogen and plasminogen activator inhibitor (PAI)-1 were measured. Ultrasound examination included measurement of far-wall intima-media complex of CCA and morphologic evaluation of occurrence of plaques in carotid and femoral bifurcations. The prevalence of greater than normal IMT (mean IMT > or =0.80 mm) was 22%. Significant univariate correlations to the dichotomy between normal and greater than normal mean IMT were detected for age, smoking, level of LDL cholesterol, level of PAI-1 and total ultrasonographic score. Multivariate logistic regression analysis confirmed the associations between greater than normal mean IMT and plasma concentrations of LDL cholesterol and PAI-1 as well as total ultrasonographic score. Greater than normal IMT of CCA was more strictly related to other cardiovascular risk factors than it was to blood pressure and was strongly associated with the occurrence of atherosclerotic plaques in carotid and femoral arteries. The role of PAI-1 in intima-media thickening that is emerging suggests that fibrinolytic balance is an important determinant of vessel-wall homeostasis in hypertensive patients.

Endothelin and cardiovascular remodelling in end-stage renal disease.

Plasma endothelin (ET) is elevated in end-stage renal disease (ESRD), but the origin and consequences of this increase remain unclear. In the present study we analysed the relationships between plasma ET levels and cardiovascular alterations in ESRD. Common carotid artery (CCA) intima-media thickness (IMT) and diameter, atherosclerotic plaque occurrence, and left ventricular (LV) geometry and function were determined by ultrasound imaging in 76 haemodialysis patients and in 57 age-, sex-, and blood pressure-matched controls. Arterial stiffness was evaluated via carotid-femoral pulse wave velocity (CF-PWV), forearm post-ischaemic vasodilation was measured by venous plethysmography, and plasma ET levels were determined using a specific immunoenzymoassay. Compared with controls, ESRD patients had elevated plasma ET levels (1.6 +/- 1.4 vs 4.6 +/- 3.8 pg/ml; P < 0.001), increased LV mass (P < 0.001), increased CCA-IMT (P < 0.001), a higher prevalence of atherosclerotic plaques (P < 0.001) and increased CF-PWV (P < 0.01). Plasma ET levels correlated positively with LV outflow velocity integral (r = 0.57; P < 0.0001), stroke index (P < 0.01), and baseline forearm blood flow (P < 0.001) which were all significantly higher in ESRD patients than in controls (P < 0.01). After adjustment for age, blood pressure, haemoglobin levels, gender and body dimensions, plasma ET levels were significantly correlated to LV mass (r = 0.46; P < 0.001), CCA-IMT and CCA intima-media cross-sectional area (r = 0.41; P < 0.001), and CF-PWV (P < 0.05). Post-ischaemic forearm vasodilation was decreased in ESRD (85 +/- 31 vs 119 +/- 28%; P < 0.001) and there was a negative correlation between post-ischaemic flow recovery and ET levels (r = -0.49; P < 0.001). In ESRD patients, plasma ET levels were positively and independently correlated with the prevalence of CCA atherosclerotic plaque (P < 0.01). These results indicate that the increased plasma ET levels in ESRD patients are associated with left ventricular hypertrophy and arterial intima-media thickening, suggesting that increased ET concentrations in ESRD patients may be of pathophysiological significance in the process of cardiovascular remodelling.

The influence of the angle of confluence on the flow in a vertebro-basilar junction model

In earlier work, it was demonstrated that the flow in models of the vertebro-basilar junction is highly three-dimensional and the geometry exerts a strong influence on the hemodynamics. The morphology of the vertebro-basilar junction is very variable amongst individuals. In a study of 85 human vertebro-basilar junctions, the angle between the vertebral arteries varied between 10 and 160°. To determine how the flow is influenced by this geometrical parameter, the flow is studied both experimentally, with laser Doppler velocimetry, and numerically, with a finite element package. A series of junction models is used with a range of confluence angles (45, 85 and 125°). It appears that the angle of confluence has a strong influence on the structure and strength of the secondary flow field. The secondary velocities persist far downstream. Further-more, near the apex, a region with low velocities is present. The larger the confluence angle is, the larger this region is, and even backflow may occur. In addition, the occurrence of atherosclerotic plaques in 85 human vertebrobasilar junctions is studied. Only one preferential location was found: the apex, the other plaques seem to be randomly distributed. The magnitude of the confluence angle of junctions with sharp-edged apices has a significant influence ( p = 0.006) on the occurrence of a plaque at the apex. Apparently, a large confluence angle is a geometrical risk factor for atherosclerosis.

Atherosclerotic carotid disease in asymptomatic individuals: An histological study of 53 cases.

The carotid bifurcation was studied histologically in 53 consecutive autopsies from persons over 65 years of age who were asymptomatic for carotid artery disease and showed no carotid related brain infarcts. The autopsy material is considered to be representative for the population in Oslo. The area stenosis was determined morphometrically in histological sections and the cases were examined for the occurrence of atherosclerotic plaques, calcifications, plaque hemorrhages, ulcerations, and mural thrombi. About one half of the cases had more than 50% stenosis. There was increasing frequency of plaque hemorrhages, ulcerations and mural thrombi with increasing stenosis. When the stenosis exceeded 60%, most cases had small recent and old plaque hemorrhages and one half had ulcerations and mural thrombi. In addition, numerous healed ulcerations and organized thrombi were seen. It is concluded that plaque complications are frequent in cases with stenosis and that most of them apparently heal without giving rise to symptoms. The presence of such lesions in asymptomatic cases must therefore be interpreted with caution.