This Article Full Text Full Text (PDF) All Versions of this Article: 34/10/2372    most recent 01.STR.0000091394.42752.D5v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Meschia, J. F. Articles by Gerber, T. C. Search for Related Content PubMed PubMed Citation Articles by Meschia, J. F. Articles by Gerber, T. C.

(Stroke. 2003;34:2372.)
© 2003 American Heart Association, Inc.

Original Contributions

Editorial Comment—Vascular Thickness and Calcification as Markers of Atherosclerotic Burden

Department of Neurology
Division of Internal Medicine and Cardiovascular Diseases and Department of Radiology, Mayo Clinic, Jacksonville, Florida

An extract of the first 250 words of the full text is provided, because this article has no abstract.

The study by Hollander et al¹ provides an uncommon opportunity to directly compare the predictive value of various noninvasive tests of atherosclerotic burden for stroke in community dwellers. The study included a cohort of 7000 stroke-free subjects. Slightly more than half of the subjects had a complete set of measures of carotid plaque, carotid intima-media thickness (IMT), ankle-arm index, and aortic calcification. Study participants were followed up for a mean of 6.1 years. On the basis of point estimates, measures of carotid IMT and aortic calcifications were stronger determinants of stroke than measures of carotid plaque and ankle-arm index. Carotid IMT, the most potent risk factor assessed in the study, imparted a relative risk of stroke of 2.23 for values in the highest tertile. Ankle-arm index, the least potent risk factor, imparted a relative risk of stroke of 1.55 for values in the lowest tertile.

Investigators also found that carotid IMT and aortic calcifications were independent risk factors. Statistical independence suggests that different pathophysiological processes may cause IMT and vascular calcifications and that these markers are not simply measures of atherosclerotic burden induced by so-called classic risk factors. B-mode ultrasonographic measurement of IMT of the extracranial carotid arteries assesses at least 2 responses of the blood vessel wall to cardiovascular risk factors. Intimal thickening resulting from cellular accumulation and matrix deposition can be seen in normal aging of the vascular system, even in the absence of atherosclerotic plaque.² Medial thickening caused by smooth muscle cell hypertrophy is closely related to . . . [Full Text of this Article]