Article

Aortic Stiffness, Blood Pressure Progression, and Incident Hypertension

National Heart, Lung, and Blood Institute's Framingham Heart Study, Framingham, Massachusetts, USA.
JAMA The Journal of the American Medical Association (Impact Factor: 35.29). 09/2012; 308(9):875-81. DOI: 10.1001/2012.jama.10503
Source: PubMed

ABSTRACT

Vascular stiffness increases with advancing age and is a major risk factor for age-related morbidity and mortality. Vascular stiffness and blood pressure pulsatility are related; however, temporal relationships between vascular stiffening and blood pressure elevation have not been fully delineated.
To examine temporal relationships among vascular stiffness, central hemodynamics, microvascular function, and blood pressure progression.
Longitudinal community-based cohort study conducted in Framingham, Massachusetts. The present investigation is based on the 2 latest examination cycles (cycle 7: 1998-2001; cycle 8: 2005-2008 [last visit: January 25, 2008]) of the Framingham Offspring study (recruited: 1971-1975). Temporal relationships among blood pressure and 3 measures of vascular stiffness and pressure pulsatility derived from arterial tonometry (carotid-femoral pulse wave velocity [CFPWV], forward wave amplitude [FWA], and augmentation index) were examined over a 7-year period in 1759 participants (mean [SD] age: 60 [9] years; 974 women).
The primary outcomes were blood pressure and incident hypertension during examination cycle 8. The secondary outcomes were CFPWV, FWA, and augmentation index during examination cycle 8.
In a multivariable-adjusted regression model, higher FWA (β, 1.3 [95% CI, 0.5-2.1] mm Hg per 1 SD; P = .002) and higher CFPWV (β, 1.5 [95% CI, 0.5-2.6] mm Hg per 1 SD; P = .006) during examination cycle 7 were jointly associated with systolic blood pressure during examination cycle 8. Similarly, in a model that included systolic and diastolic blood pressure and additional risk factors during examination cycle 7, higher FWA (odds ratio [OR], 1.6 [95% CI, 1.3-2.0] per 1 SD; P < .001), augmentation index (OR, 1.7 [95% CI, 1.4-2.0] per 1 SD; P < .001), and CFPWV (OR, 1.3 [95% CI, 1.0-1.6] per 1 SD; P = .04) were associated with incident hypertension during examination cycle 8 (338 cases [32%] in 1048 participants without hypertension during examination cycle 7). Conversely, blood pressure during examination cycle 7 was not associated with CFPWV during examination cycle 8. Higher resting brachial artery flow (OR, 1.23 [95% CI, 1.04-1.46]) and lower flow-mediated dilation (OR, 0.80 [95% CI, 0.67-0.96]) during examination cycle 7 were associated with incident hypertension (in models that included blood pressure and tonometry measures collected during examination cycle 7).
In this cohort, higher aortic stiffness, FWA, and augmentation index were associated with higher risk of incident hypertension; however, initial blood pressure was not independently associated with risk of progressive aortic stiffening.

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    • "However, it has been controversial whether the risk factors directly cause the increase in arterial stiffness, or whether the increased vascular stiffness exacerbates the disease state, such as has been analyzed in the case of hypertension (Mitchell, 2014). Notably, a recent Framingham study found increased arterial stiffness precedes hypertension (Kaess et al., 2012), and this has supported the concept that arterial stiffness is not necessarily caused by hypertension but may be a good predictor of risk for hypertension development and its subsequent complications (Boutouyrie et al., 2002; Laurent et al., 2003; Tomiyama et al., 2013). It has also been conjectured that the presence of arterial stiffness may complicate the management of cardiovascular disease. "
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    ABSTRACT: In recent decades, the pervasiveness of increased arterial stiffness in patients with cardiovascular disease has become increasingly apparent. Though, this phenomenon has been well documented in humans and animal models of disease for well over a century, there has been surprisingly limited development in a deeper mechanistic understanding of arterial stiffness. Much of the historical literature has focused on changes in extracellular matrix proteins—collagen and elastin. However, extracellular matrix changes alone appear insufficient to consistently account for observed changes in vascular stiffness, which we observed in our studies of aortic stiffness in aging monkeys. This led us to examine novel mechanisms operating at the level of the vascular smooth muscle cell (VSMC)—that include increased cell stiffness and adhesion to extracellular matrix—which that may be interrelated with other mechanisms contributing to arterial stiffness. We introduce these observations as a new concept—the Smooth Muscle Cell Stiffness Syndrome (SMCSS)—within the field of arterial stiffness and posit that stiffening of vascular cells impairs vascular function and may contribute stiffening to the vasculature with aging and cardiovascular disease. Importantly, this review article revisits the structural basis of arterial stiffness in light of these novel findings. Such classification of SMCSS and its contextualization into our current understanding of vascular mechanics may be useful in the development of strategic therapeutics to directly target arterial stiffness.
    Full-text · Article · Nov 2015 · Frontiers in Physiology
    • "Arterial stiffness or arterial compliance, used as physiological markers of peripheral vascular function, are independent predictors of coronary heart disease and stroke [13]. Arterial stiffness increases (or compliance decreases) with age [14], and is associated with a higher risk for hypertension [15]. In addition , the plasma concentration of asymmetric dimethylarginine (ADMA) is considered as a novel risk marker of cardiovascular disease [16]. "
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    ABSTRACT: Hypertension is a major contributor to the global burden of cardiovascular diseases and its prevalence increases progressively with ageing. Therefore the identification of effective, age-friendly exercise and nutritional interventions which lower blood pressure (BP) is a research priority. To undertake a pilot RCT examining the efficacy of isometric handgrip exercise (IHGE) and beetroot juice (a rich source of inorganic nitrate) consumption in modifying clinic and 24-h ambulatory BP (24-h ABP), peripheral arterial function and plasma asymmetric dimethylarginine (ADMA) in older overweight and obese adults. Thirty middle age and older adults (62±5 years) were randomised to: (a) bilateral IHGE at 50% of maximal voluntary contraction (8min/day), (b) 140ml/day of concentrated beetroot juice, or (c) no-intervention (control group), for 7 days. All groups followed a standardised diet to control nitrate intake. Clinic and 24-h ABP, peripheral arterial function quantified by pulse wave velocity (PWV) and arterial volume distensibility were assessed before and after intervention. Clinical ageing research unit, Newcastle University. At baseline, there were no between-group differences in age, handgrip strength, clinic or 24-h ABP, BMI, waist circumference, fat mass, physical activity level, energy intake or urinary and plasma nitrate concentrations. After intervention, there were no significant effects on clinic systolic and diastolic BP or 24-h ABP, PWV (p=0.54), arterial volume distensibility (p=0.89), or ADMA (p=0.45). IHGE or beetroot juice consumption for 7 days did not affect BP or peripheral arterial function in overweight and obese middle age and older adults. Ageing may reduce the effects of these interventions on vascular function and studies are needed to test this hypothesis. Copyright © 2015. Published by Elsevier Ireland Ltd.
    No preview · Article · Aug 2015 · Maturitas
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    • "Current thought holds that the influence of proximal stiffening on the risk for cardiovascular disease is primarily exerted at a late stage in life (O'Rourke, 2007; Kaess et al. 2012). Yet pre-existing structural abnormalities established in utero may lead to a premature cycle of wall stiffening and associated endothelial dysfunction. "
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    ABSTRACT: The association between intrauterine growth restriction (IUGR) and hypertension is well- established, yet the interaction between IUGR and other pathogenic contributors remains ill-defined. This study examined the independent and interactive effects of fetal growth reduction resulting in low birth weight (LBW), and postnatal western diet (WD) on vascular function. Growth reduction was induced in pregnant guinea pigs by uterine artery ablation. LBW and normal birth weight (NBW) offspring were randomly assigned to a control diet (CD) or a WD. In young adulthood, length-tension curves were generated in aortic rings and responses to methacholine (MCh) were evaluated in the carotid and aorta using wire myography. Relative to NBW/CD, aortae of NBW/WD offspring were stiffer as determined by a left-ward shift in the length-tension curve, yet the shift in LBW/CD curve was considerably greater. Aortic stiffening was most severe in LBW/WD (slope: NBW/CD, 1.97 ± 0.04; NBW/WD, 2.16 ± 0.04; LBW/CD, 2.28 ± 0.05; LBW/WD, 2.34 ± 0.07). Maximal responses (Emax) to MCh were significantly blunted in the aorta of LBW/CD vs. NBW/CD (p < 0.05) and in LBW/WD vs. NBW/WD offspring (p < 0.05); but WD alone had no influence on MCh responses. Emax for carotid responses to MCh were reduced in LBW/CD vs. NBW/CD (p < 0.05). Thus, aortic stiffening was influenced more by LBW than by a postnatal WD and the most severe stiffening was observed in LBW/WD offspring. In contrast, blunted endothelial responses in LBW/CD offspring were not exacerbated by WD. IUGR may have a greater independent impact on vascular function than a postnatal WD.This article is protected by copyright. All rights reserved
    Full-text · Article · Oct 2014 · The Journal of Physiology
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