T he ankle-brachial index (ABI) is the ratio of the systolic blood pressure (SBP) measured at the ankle to that measured at the brachial artery. Originally described by Winsor 1 in 1950, this index was initially proposed for the noninvasive diagnosis of lower-extremity peripheral artery disease (PAD). 2,3 Later, it was shown that the ABI is an indicator of atherosclerosis at other vascular sites and can serve as a prognostic marker for cardiovascular events and functional impairment, even in the absence of symptoms of PAD. 4 -6 Rationale for Standardization of the ABIThe current lack of standards for measurement and calculation of the ABI leads to discrepant results with significant impact from clinical, public health, and economic standpoints. Indeed, the estimated prevalence of PAD may vary substantially according to the mode of ABI calculation. [7][8][9] In a review of 100 randomly selected reports using the ABI, multiple variations in technique were identified, including the position of the patient during measurement, the sizes of the arm and leg cuffs, the location of the cuff on the extremity, the method of pulse detection over the brachial artery and at the ankles, whether the arm and ankle pressures were measured bilaterally, which ankle pulses were used, and whether a single or replicate measures were obtained. 10 There is controversy about what ABI threshold should be used to diagnose PAD. The ABI threshold most commonly used is Յ0.90 based on studies reporting Ͼ90% sensitivity and specificity to detect PAD compared with angiography. 2,3 These studies were limited in that they included mostly older white men with PAD or who were at high risk for PAD and compared them with a younger healthy group. A recent metaanalysis of 8 studies of diverse populations, including diabetic patients, confirmed a high specificity but lower sensitivity (at best Ͻ80%) than that reported in earlier studies. 11 Similar to other vascular markers such as carotid intimamedia thickness 12 or coronary artery calcium score, 13 standardization of the techniques used to measure the ABI and the calculation and interpretation of its values is necessary. Aims and ScopeThe goals for this document are to provide a comprehensive review of the relevant literature on the measurement of the The American Heart Association makes every effort to avoid any actual or potential conflicts of interest that may arise as a result of an outside relationship or a personal, professional, or business interest of a member of the writing panel. Specifically, all members of the writing group are required to complete and submit a Disclosure Questionnaire showing all such relationships that might be perceived as real or potential conflicts of interest.This statement was approved by the American Heart Association Science Advisory and Coordinating Committee on September 10, 2012. A copy of the document is available at http://my.americanheart.org/statements by selecting either the "By Topic" link or the "By Publication Date" link. To purchase additional repri...
Atherosclerosis is a chronic inflammatory disease of the vessel wall. Recent evidence suggests that chronic vascular inflammation ensues as an imbalance between pro-and anti-inflammatory mediators. Recently identified lipid mediators (eg, lipoxins and resolvins) play active roles in promoting the resolution of inflammation. Alterations in vascular smooth muscle cell (VSMC) phenotype, which manifest as a loss of contractile protein expression and increased proliferation and migration, are prominent mechanistic features of both atherosclerosis and restenosis following various interventions (eg, angioplasty and bypass grafting). We sought to determine whether human atherosclerosis is associated with a "resolution deficit" and whether lipoxins and resolvins influence VSMC phenotype. Here we report that plasma levels of aspirin-triggered lipoxin are significantly lower in patients with symptomatic peripheral artery disease than in healthy volunteers. Both aspirintriggered lipoxin and resolvin E1 block platelet-derived growth factor-stimulated migration of human saphenous vein SMCs and decrease phosphorylation of the platelet-derived growth factor receptor-. Importantly, receptors for aspirin-triggered lipoxin and resolvin E1 (ALX and ChemR23, respectively) were identified in human VSMCs. Overall, these results demonstrate that stimulatory lipid mediators confer a protective phenotypic switch in VSMCs and elucidate new functions for these mediators in the regulation of SMC biology. These results also suggest that peripheral artery disease is associated with an inflammation-resolution deficit and highlight a potential therapeutic opportunity for the regulation of vascular injury responses. (Am J Pathol
Background-Bilirubin, with recently recognized antioxidant and antiinflammatory activity, has emerged as a candidate for atheroprotection. We hypothesized that higher levels of bilirubin would reduce susceptibility to peripheral arterial disease (PAD
Background Whether individuals with peripheral artery disease (PAD) identified by screening ankle-brachial index (ABI) benefit from preventative therapies to reduce cardiovascular risk is unknown. We aimed to determine the number of US adults with PAD not receiving preventative therapies and whether treatment is associated with reduced mortality in PAD subjects without known cardiovascular disease (CVD). Methods and Results We analyzed data from the National Health and Nutrition Examination Survey (NHANES) 1999-2004 with mortality follow-up through December 31, 2006. PAD was defined as ABI ≤ 0.90. Of 7458 eligible participants ≥ 40 years, weighted PAD prevalence was 5.9% ± SE 0.3%, corresponding to approximately 7.1 million US adults with PAD. Statin use was reported in only 30.5% ± 2.5%, angiotensin converting enzyme inhibitor/angiotensin receptor blocker (ACEI/ARB) use in 24.9% ± 1.9%, and aspirin use in 35.8% ± 2.9%, corresponding to 5.0 million adults with PAD not taking statins, 5.4 million not taking ACEI/ARBs, and 4.5 million not receiving aspirin. Adjusting for age, gender, and race/ethnicity, PAD was associated with all-cause mortality (HR 2.4 [1.9-2.9], p<0.0001). Even after excluding individuals with known CVD, subjects with PAD had higher mortality rates (16.1% ± 2.1%) than subjects without PAD or CVD (4.1% ± 0.3%) with adjusted HR 1.9 [1.3-2.8], p=0.001. Among PAD subjects without CVD, use of multiple preventative therapies was associated with 65% lower all-cause mortality (HR 0.35 [0.20-0.86], p=0.02). Conclusions Millions of US adults with PAD are not receiving secondary prevention therapies. Treatment with multiple therapies is associated with reduced all-cause mortality.
Background-Bilirubin inhibits experimental atherosclerosis, is inversely associated with carotid plaque burden, and confers neuroprotection in experimental stroke. Clinical data addressing the association of bilirubin with stroke are not available. We hypothesized that higher bilirubin levels would be associated with reduced stroke prevalence and improved stroke outcomes.
Anemia and vitamin D deficiency are conditions that both result in significant morbidity and increase with age. The potential relationship between them remains poorly understood, particularly in the elderly. We used the Third National Health and Nutrition Examination Survey to examine the association of vitamin D deficiency with anemia subtypes in persons aged > 60 years. Vitamin D deficiency was defined as serum levels < 20 ng/mL, and anemia was defined according to World Health Organization criteria. Vitamin D deficiency was associated with anemia prevalence independent of age, sex, or race/ ethnicity (odds ratio, 1.47; 95% confidence interval, 1.06-2.05; P ؍ .02) and varied significantly by anemia subtype (P overall ؍ .003). The prevalence of vitamin D deficiency was 33.3% in the nonanemic population, 56% in anemia of inflammation (AI; P ؍ .008), and 33.0% in unexplained anemia (P ؍ .55). NonHispanic blacks had a 7-fold increased risk of AI compared with whites, and this was partially attenuated after adjusting for vitamin D deficiency. These data show that vitamin D deficiency is associated with specific subtypes of anemia in the elderly, especially in those with AI. Vitamin D may suppress inflammatory pathways, and studies to determine whether vitamin D supplementation ameliorates AI are warranted. (Blood. 2011;117(10):2800-2806)
Background-Although the role of inflammation in the pathophysiology of peripheral arterial disease (PAD) is well established, the contribution of insulin resistance (IR) to PAD is less clear. We hypothesized that IR is associated with PAD and that the presence of IR would influence the association between C-reactive protein (CRP) and PAD, an association established predominantly in healthy individuals. Methods and Results-We analyzed data from 3242 adults in the National Health and Nutrition Examination Survey (NHANES) 1999 to 2004 who underwent measurement of ankle brachial index, CRP, and fasting glucose and insulin, enabling calculation of homeostasis model of IR (HOMA-IR). Odds ratios (ORs) and 95% CIs were estimated by logistic regression. The mean prevalence of PAD (defined as an ankle brachial index Յ0.9) was 5.5% (SE, 0.47%). HOMA-IR was independently associated with PAD (OR, 2.06; 95% CI, 1.1 to 4.0; Pϭ0.03 for quartile 4, P for trend across quartilesϭ0.047) after adjustment for age, gender, race/ethnicity, hypertension, hyperlipidemia, smoking, body mass index, chronic kidney disease, and CRP. Elevated CRP (Ͼ3 mg/L) also was strongly associated with PAD (OR, 2.2; 95% CI, 1.3 to 3.6; Pϭ0.003 versus CRP Ͻ1 mg/L). Stratifying subjects on the basis of median HOMA-IR, we found that CRP Ͼ3 mg/L was no longer significantly associated with PAD in subjects with IR (OR, 1.3; 95% CI, 0.8 to 2.1; Pϭ0.3, P for interactionϭ0.08). Conclusions-These
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