Carotid Artery Hypertrophy and Atherosclerosis

Central blood pressure (BP) has been shown to predict cardiovascular disease clinical outcomes better than brachial BP in studies that demonstrate expected pulse pressure (PP) amplification. The likely underlying mechanism for this observation is a closer relation of central BP to preclinical cardiac and vascular disease because of its more accurate representation of loading conditions on the heart and coronary and cerebral vessels. Over the past 2 decades, proof of concept for this hypothesis has been provided by many cross-sectional analyses. Furthermore, several longitudinal studies in hypertensive patients have provided preliminary evidence to suggest that changes in central BP by pharmacological therapy are more important than decreases in brachial BP in altering cardiac and vascular hypertrophy associated with hypertension. This review will describe studies that have compared central and peripheral BP to intermediate cardiovascular phenotypes (target organ damage). Although end-diastolic BP is nearly identical throughout the arterial tree, it has been recognized for 50 years that systolic BP varies, at times strikingly, among arterial segments because of the phenomenon of arterial PP amplification. As a result, direct arterial pressure measurements with solid-state or fluid-filled catheters have shown that brachial and radial systolic BP is variably higher than concurrently measured central aortic systolic BP. Accordingly, the common practice of using conventional sphygmomanometric measurements of brachial BP as pressure load imposed on the heart and on central circulation (including coronary and cerebrovascular arterial trees) may be erroneous. The most commonly used measures of preclinical hypertensive target organ damage, left ventricular (LV) mass and common carotid artery (CCA) geometry, can both be readily and accurately measured using noninvasive techniques, most commonly by the use of ultrasound. Noninvasive central BP has been most commonly derived using either carotid or radial artery applanation tonometry and invasively validated generalized transfer functions.