Wall volume increased more when the largest lipid cluster was loc

Wall volume increased more when the largest lipid cluster was located close to the lumen. The volume of lipid increased when fewer lipid clusters were present at baseline. The volume of calcium increased with greater volume of lipid at baseline. A similar multivariate analysis was used to evaluate the impact of various vascular risk factors (statin use, smoking, hypertension, and diabetes) on carotid imaging features. The volume of calcium increased more in patients on statins (coefficient 4.79, 1.73

to 7.86, P = .002) (Supp Fig 6). The volume of lipid increased more in older patients (coefficient 0.36, 0.21 to 0.50, P < .001) and in patients who smoked (coefficient 8.89, 6.82 to 10.95, P < .001) Palbociclib price (Supp Fig 7). This study of patients undergoing emergent CT evaluation for symptoms of acute ischemic stroke shows that there are a number of imaging markers that significantly predict the evolution of CT imaging features of carotid artery atherosclerotic disease over a 1-year period. Wall volume increased more when the largest lipid cluster

was located close to the lumen. The volume of lipid increased more when fewer lipid clusters were present at baseline. The volume of selleck products calcium increased with greater volume of lipid at baseline. Moreover, our results indicate that in our study population, certain risk factors—age, smoking, hyperlipidemia/statin use—have a significant impact on the evolution of CT patterns of carotid disease. Older patients and patients who smoked had a greater increase in the volume of lipid over 1 year. Patients who were on statins had a greater increase in the volume of calcium. Smoking and hyperlipidemia are well-known risk factors for the progression of atherosclerotic disease and clinical events related to that disease.[11, 12, 14-17, 22-27] However, the exact mechanisms behind their influence on the progression of this disease are not entirely clear. Our results provide some possible additional insight into

these mechanisms. The patients who smoked had a greater increase in the number of lipid clusters over 1 year. High Morin Hydrate lipid content is one aspect of plaque morphology that is characteristic of the “vulnerable plaque.”[2-5] So, smoking may increase the lipid content of plaques, increasing plaque vulnerability and the risk for future clinical events of stroke or TIA. Statin use rather than hyperlipidemia per se was looked at in this study. The volume of calcium increased more in patients using statins. So, the protective value in statins may partly lie in their propensity to increase calcification of atherosclerotic plaques, thus increasing plaque stability and decreasing clinical events.

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