Published online before print January 14, 2008, doi: 10.1161/HYPERTENSIONAHA.107.098830
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(Hypertension. 2008;51:177.)
© 2008 American Heart Association, Inc.
Editorial Commentaries |
Vascular Stiffness and the "Chicken-or-the-Egg" Question
From the Division of Preventive Medicine (S.P.G.), Department of Medicine, and Department of Epidemiology (D.K.A.), University of Alabama at Birmingham.
Correspondence to Stephen P. Glasser, Division of Preventive Medicine, Department of Medicine, University of Alabama at Birmingham, 1717 11th Ave S, Birmingham, AL 35216. E-mail sglasser{at}uab.edu
Although the incidence of hypertension approaches 90% for people over the age of 70 years, the etiology of hypertension remains elusive for the vast majority. The complications of long-standing hypertension are well known and relate to arterial disease with clinical manifestations in the heart, brain, and kidney. However, the paradigm of elevated blood pressure resulting in vasculopathy continues to be challenged. Rather than hypertension resulting in altered vascular structure and function, it seems that changes in vascular integrity (structure) precede and may be causal in the development of elevated blood pressure with resultant hypertension that ultimately leads to clinical events (Figure). Alterations in cardiovascular structure and function that have been shown to precede the finding of elevated blood pressure include the occurrence of left ventricular hypertrophy in children and young adults of hypertensive parents1 (although one cannot rule out the role of blood pressure in causing cardiovascular remodeling in studies where only resting, occasional measurements of blood pressure are made), diastolic filling abnormalities in normotensive individuals predisposed to hypertension,2 endothelial dysfunction as a precursor to the finding of hypertension,3 and increased arterial stiffness in normotensive subjects predisposed to develop hypertension.4 Recently it has been reported that, in confirmed prehypertensive subjects, intimal-medial thickness is increased in the common carotid artery when compared with subjects who remain normotensive.5 In addition, Lackland6 has demonstrated an association between low birth weight and the subsequent development of hypertension, with the greatest risk of hypertension occurring among those with low birth weight and accelerated "catch-up weight."
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In an Atherosclerosis Risk in Communities analysis, incident hypertension was predicted when subjects were in the highest quartile of arterial stiffness. In that study, 6992 subjects (men and women age 45 to 64 years), who were normotensive at baseline, had carotid artery ultrasound–assessed arterial elasticity measured at baseline and were then evaluated for the development of hypertension at 3 years (defined as a blood pressure 
160/95 mm Hg or requiring antihypertensive therapy). For each 1 SD decrease in elasticity, there was a 15% increase in developing hypertension.7 In an analysis of the Minnesota Children’s Blood Pressure Study, 10- to 14 -year–old normotensive school children were surveyed in 1977 to 1978, and a selected sample was followed for incident hypertension. Of the 1207 students followed, 179 had arterial compliance measured by a noninvasive pulse contour analysis technique. Systolic blood pressure was inversely related to large artery compliance before and after adjustment for cardiovascular risk factors (gender, weight, height, insulin sensitivity, high-density lipoprotein and low-density lipoprotein cholesterol).8
Using a variety of techniques, it has been shown that alterations in vascular structure and function also occur with diabetes mellitus. McVeigh et al9 demonstrated that vascular compliance was significantly reduced in diabetic subjects regardless of the presence or absence of physical complications of the disease. However, as is true for hypertension, although it was once thought that the vascular changes in diabetic subjects were the result of associated atherosclerosis, Oxlund et al10 demonstrated that alterations in arterial compliance were not correlated with the degree of atherosclerosis and that diabetic subjects develop alterations in arterial connective tissue independent of the presence of atherosclerosis. In another Atherosclerosis Risk in Communities analysis, the association of arterial stiffness with glucose tolerance and serum insulin concentrations was evaluated in 4701 subjects who were prediabetic.11 Their findings were compatible with the view that the prediabetic state is associated with increased arterial stiffness and that the stiffness was unrelated to vessel wall thickness.
In this issue of the journal, Giannattasio et al12 studied 54 normoglycemic, normotensive, healthy offspring of 2 parents with type 2 diabetes mellitus and 55 age- and sex-matched healthy control subjects. They found that blood pressure, blood glucose, glycohemoglobin, and insulin sensitivity were normal and similar in the offspring of diabetic parents compared with the control subjects. However, in the subjects with diabetic parents, arterial stiffness was increased. They correctly point out that alterations in large artery wall thickness and a reduction in arterial distensibility are not late consequences of the diabetic state but that there are almost no data on arterial stiffness in normoglycemic subjects predisposed to diabetes. The limitations posed by this study prevent definitive statements from being made, eg, as an explorative study, few data were available from the literature regarding variability and, as such, the authors were unable to reliably estimate sample size and power. Also, the pulse pressure difference is large (
10 mm Hg), and this is an important observation given the age of the participants (mean: 37 years). This could shift the artery to a stiffer point on the pressure-stiffness curve and may simply be a transient, not permanent, reflection of greater stiffness. In addition, no multivariable adjustment was done in the analysis to test whether the difference in pulse pressure explained the differences between groups. Finally, although obesity in general is emphasized, abdominal obesity and triglyceride levels are different between the offspring of diabetic subjects compared with the normal subjects. Although homeostasis model assessment was equal, the offspring were showing early signs of the metabolic syndrome in terms of waist circumference and dyslipidemia. Thus, this study does not exclude the possibility that the observations were a result of early metabolic derangements caused by the observed increased pulse pressure, which, in turn, resulted in greater carotid stiffness. Nonetheless, this study should provide future researchers with an improved ability to further study this very interesting area.
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Acknowledgments |
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Disclosures
None.
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Footnotes |
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The opinions expressed in this editorial are not necessarily those of the editors or of the American Heart Association.
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References |
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 Top References |
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12. Giannattasio C, Failla M, Capra A, Scanziani E, Amigoni M, Boffi L, Whistock C, Gamba P, Paleari F, Mancia G. Increased arterial stiffness in normoglycemic normotensive offspring of type 2 diabetic parents. Hypertension. 2008; 51: 182–187.
Related Article:
Hypertension 2008 51: 182-187.
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