Honors & Awards

  • Scholar-in-Training Award, American Association for Cancer Research (2012)
  • GlaxoSmithKline Award for 1st-ranked graduating student, University of Cambridge (2012)
  • Gates Cambridge Scholarship, Gates Cambridge Trust, University of Cambridge (2011)
  • Young Investigator Award Finalist, American College of Cardiology (2013)
  • Student Scholarship in Cardiovascular Disease and Stroke, American Heart Association (2012)
  • Medical Student Research Fellowship, American Heart Association (2010)
  • Phi Beta Kappa, Phi Beta Kappa Society (2008)

Education & Certifications

  • MPhil (Distinction), University of Cambridge, Epidemiology (2012)


Journal Articles

  • The combination of 9p21.3 genotype and biomarker profile improves a peripheral artery disease risk prediction model. Vascular medicine Downing, K. P., Nead, K. T., Kojima, Y., Assimes, T., Maegdefessel, L., Quertermous, T., Cooke, J. P., Leeper, N. J. 2014; 19 (1): 3-8


    Peripheral artery disease (PAD) is a highly morbid condition affecting more than 8 million Americans. Frequently, PAD patients are unrecognized and therefore do not receive appropriate therapies. Therefore, new methods to identify PAD have been pursued, but have thus far had only modest success. Here we describe a new approach combining genomic and metabolic information to enhance the diagnosis of PAD. We measured the genotype of the chromosome 9p21 cardiovascular-risk polymorphism rs10757269 as well as the biomarkers C-reactive protein, cystatin C, β2-microglobulin, and plasma glucose in a study population of 393 patients undergoing coronary angiography. The rs10757269 allele was associated with PAD status (ankle-brachial index < 0.9) independent of biomarkers and traditional cardiovascular risk factors (odds ratio=1.92; 95% confidence interval, 1.29-2.85). Importantly, compared to a previously validated risk factor-based PAD prediction model, the addition of biomarkers and rs10757269 significantly and incrementally improved PAD risk prediction as assessed by the net reclassification index (NRI=33.5%; p=0.001) and integrated discrimination improvement (IDI=0.016; p=0.017). In conclusion, a model including a panel of biomarkers, which includes both genomic information (which is reflective of heritable risk) and metabolic information (which integrates environmental exposures), predicts the presence or absence of PAD better than established risk models, suggesting clinical utility for the diagnosis of PAD.

    View details for DOI 10.1177/1358863X13514791

    View details for PubMedID 24323119

  • Self-reported history of childhood smoking is associated with an increased risk for peripheral arterial disease independent of lifetime smoking burden. PloS one Priest, J. R., Nead, K. T., Wehner, M. R., Cooke, J. P., Leeper, N. J. 2014; 9 (2)


    Atherosclerotic disorders are well known to be associated with obesity, lipid profile, smoking, hypertension and other medical comorbidities, and large cohort studies have explored the childhood correlates to these adult risk factors. However, there has been little investigation into the childhood risk factors for peripheral arterial disease (PAD). We endeavored to better understand the role of smoking in childhood in the risk for PAD in a well described cohort of 1,537 adults at high risk for cardiovascular disease. In a multivariate regression model, we observed an increased risk of PAD among those who reported a history of smoking during childhood (OR = 2.86; 95% CI, 1.99-4.11; P<0.001), which remained statistically significant after controlling for lifetime smoking burden (OR = 1.55; 95% CI, 1.00-2.41; P = 0.049). Our novel observation of disproportionate risk of PAD conferred by a history of childhood smoking may reflect an unrecognized biological mechanism such as a unique susceptibility to vascular injury or an unaccounted for covariate such as secondhand smoke exposure in childhood. This observation suggests further investigation is required into the pathophysiology of smoking in the developing vasculature and the need for detailed clinical data about patterns of childhood smoking and smoke exposure.

    View details for DOI 10.1371/journal.pone.0088972

    View details for PubMedID 24558458

  • Alternative Ankle-Brachial Index Method Identifies Additional At-Risk Individuals JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY Nead, K. T., Cooke, J. P., Olin, J. W., Leeper, N. J. 2013; 62 (6): 553-559


    OBJECTIVES: To determine whether utilization of an alternative ankle-brachial index (ABI) calculation method improves mortality risk prediction compared to traditional methods. BACKGROUND: The ABI is used to diagnose peripheral arterial disease (PAD), and to identify those at risk for cardiovascular events. Traditionally, the ABI is calculated using the higher of the dorsalis pedis and posterior tibial ankle arteries. Studies directly comparing calculation methods are limited. METHODS: The ABI was calculated at baseline in 1,413 study participants undergoing non-emergent coronary angiography subsequently followed for all-cause and cardiovascular mortality. There were 224 individuals assigned to the traditional-PAD group (ABI < 0.90) using the traditional ABI method. Of those remaining, an alternative ABI method utilizing the lower of the two ankle pressures assigned 282 patients to the alternative-PAD group. The 862 individuals not assigned to PAD by either method were the no-PAD group. RESULTS: There were 163 mortalities during a median follow-up of 5.0 years. Adjusted Cox regression models showed that the alternative-PAD group had an increased risk for all-cause (HR=1.49; 95% CI, 1.01-2.19) and cardiovascular mortality (HR=3.21; 95% CI, 1.53-6.37) versus the no-PAD group. Additionally, in the no-PAD group, there was an 11% (HR=1.11; 95% CI, 1.05-1.17) increased risk of all-cause mortality per 1mm Hg increased difference between the left and right brachial systolic pressures. CONCLUSION: The implementation of an alternative ABI method and use of the brachial difference identifies individuals at an increased risk for mortality who are currently missed using traditional ABI methods. Current ABI protocols may need to be evaluated.

    View details for DOI 10.1016/j.jacc.2013.04.061

    View details for Web of Science ID 000322524300011

    View details for PubMedID 23707317

  • Walking impairment questionnaire improves mortality risk prediction models in a high-risk cohort independent of peripheral arterial disease status. Circulation. Cardiovascular quality and outcomes Nead, K. T., Zhou, M., Caceres, R. D., Olin, J. W., Cooke, J. P., Leeper, N. J. 2013; 6 (3): 255-261


    Background- The Walking Impairment Questionnaire (WIQ) is a subjective measure of patient-reported walking performance developed for peripheral arterial disease. The purpose of this study is to examine whether this simple tool can improve the predictive capacity of established risk models and whether the WIQ can be used in patients without peripheral arterial disease. Methods and Results- At baseline we assessed the walking distance, stair-climbing, and walking speed WIQ category scores among individuals who were undergoing coronary angiography. During a median follow-up of 5.0 years, there were 172 mortalities among 1417 study participants. Adjusted Cox proportional hazards models showed that all 3 WIQ categories independently predicted future all-cause and cardiovascular mortality, including among individuals without peripheral arterial disease (P<0.001). Compared with the cardiovascular risk factors model, we observed significantly increased risk discrimination with a C-index of 0.741 (change in C-index, 0.040; 95% confidence interval, 0.011-0.068) and 0.832 (change in C-index, 0.080; 95% confidence interval, 0.034-0.126) for all-cause and cardiovascular mortality, respectively. Examination of risk reclassification using the net reclassification improvement index showed a 48.4% (P<0.001) improvement for all-cause mortality and a 77.4% (P<0.001) improvement for cardiovascular mortality compared with the cardiovascular risk factors model. Conclusions- All 3 WIQ categories independently predicted future all-cause and cardiovascular mortality. Importantly, we found that this subjective measure of walking ability could be extended to patients without peripheral arterial disease. The addition of the WIQ scores to established cardiovascular risk models significantly improved risk discrimination and reclassification, suggesting broad clinical use for this simple, inexpensive test.

    View details for DOI 10.1161/CIRCOUTCOMES.111.000070

    View details for PubMedID 23633217

  • Usefulness of the Addition of Beta-2-Microglobulin, Cystatin C and C-Reactive Protein to an Established Risk Factors Model to Improve Mortality Risk Prediction in Patients Undergoing Coronary Angiography AMERICAN JOURNAL OF CARDIOLOGY Nead, K. T., Zhou, M. J., Caceres, R. D., Sharp, S. J., Wehner, M. R., Olin, J. W., Cooke, J. P., Leeper, N. J. 2013; 111 (6): 851-856


    Evidence-based therapies are available to reduce the risk for death from cardiovascular disease, yet many patients go untreated. Novel methods are needed to identify those at highest risk for cardiovascular death. In this study, the biomarkers ?2-microglobulin, cystatin C, and C-reactive protein were measured at baseline in a cohort of participants who underwent coronary angiography. Adjusted Cox proportional-hazards models were used to determine whether the biomarkers predicted all-cause and cardiovascular mortality. Additionally, improvements in risk reclassification and discrimination were evaluated by calculating the net reclassification improvement, C-index, and integrated discrimination improvement with the addition of the biomarkers to a baseline model of risk factors for cardiovascular disease and death. During a median follow-up period of 5.6 years, there were 78 deaths among 470 participants. All biomarkers independently predicted future all-cause and cardiovascular mortality. A significant improvement in risk reclassification was observed for all-cause (net reclassification improvement 35.8%, p = 0.004) and cardiovascular (net reclassification improvement 61.9%, p = 0.008) mortality compared to the baseline risk factors model. Additionally, there was significantly increased risk discrimination with C-indexes of 0.777 (change in C-index 0.057, 95% confidence interval 0.016 to 0.097) and 0.826 (change in C-index 0.071, 95% confidence interval 0.010 to 0.133) for all-cause and cardiovascular mortality, respectively. Improvements in risk discrimination were further supported using the integrated discrimination improvement index. In conclusion, this study provides evidence that ?2-microglobulin, cystatin C, and C-reactive protein predict mortality and improve risk reclassification and discrimination for a high-risk cohort of patients who undergo coronary angiography.

    View details for DOI 10.1016/j.amjcard.2012.11.055

    View details for Web of Science ID 000316537700013

    View details for PubMedID 23290308

  • The genetic susceptibility to type 2 diabetes may be modulated by obesity status: implications for association studies BMC MEDICAL GENETICS Cauchi, S., Nead, K. T., Choquet, H., Horber, F., Potoczna, N., Balkau, B., Marre, M., Charpentier, G., Froguel, P., Meyre, D. 2008; 9


    Considering that a portion of the heterogeneity amongst previous replication studies may be due to a variable proportion of obese subjects in case-control designs, we assessed the association of genetic variants with type 2 diabetes (T2D) in large groups of obese and non-obese subjects.We genotyped RETN, KCNJ11, HNF4A, HNF1A, GCK, SLC30A8, ENPP1, ADIPOQ, PPARG, and TCF7L2 polymorphisms in 1,283 normoglycemic (NG) and 1,581 T2D obese individuals as well as in 3,189 NG and 1,244 T2D non-obese subjects of European descent, allowing us to examine T2D risk over a wide range of BMI.Amongst non-obese individuals, we observed significant T2D associations with HNF1A I27L [odds ratio (OR) = 1.14, P = 0.04], GCK -30G>A (OR = 1.23, P = 0.01), SLC30A8 R325W (OR = 0.87, P = 0.04), and TCF7L2 rs7903146 (OR = 1.89, P = 4.5 x 10-23), and non-significant associations with PPARG Pro12Ala (OR = 0.85, P = 0.14), ADIPOQ -11,377C>G (OR = 1.00, P = 0.97) and ENPP1 K121Q (OR = 0.99, P = 0.94). In obese subjects, associations with T2D were detected with PPARG Pro12Ala (OR = 0.73, P = 0.004), ADIPOQ -11,377C>G (OR = 1.26, P = 0.02), ENPP1 K121Q (OR = 1.30, P = 0.003) and TCF7L2 rs7903146 (OR = 1.30, P = 1.1 x 10-4), and non-significant associations with HNF1A I27L (OR = 0.96, P = 0.53), GCK -30G>A (OR = 1.15, P = 0.12) and SLC30A8 R325W (OR = 0.95, P = 0.44). However, a genotypic heterogeneity was only found for TCF7L2 rs7903146 (P = 3.2 x 10-5) and ENPP1 K121Q (P = 0.02). No association with T2D was found for KCNJ11, RETN, and HNF4A polymorphisms in non-obese or in obese individuals.Genetic variants modulating insulin action may have an increased effect on T2D susceptibility in the presence of obesity, whereas genetic variants acting on insulin secretion may have a greater impact on T2D susceptibility in non-obese individuals.

    View details for DOI 10.1186/1471-2350-9-45

    View details for Web of Science ID 000256606000001

    View details for PubMedID 18498634

  • Platelet-rich plasma as a treatment for patellar tendinopathy: a double-blind, randomized controlled trial. American journal of sports medicine Dragoo, J. L., Wasterlain, A. S., Braun, H. J., Nead, K. T. 2014; 42 (3): 610-618


    BACKGROUND:Previous studies have shown improvement in patellar tendinopathy symptoms after platelet-rich plasma (PRP) injections, but no randomized controlled trial has compared PRP with dry needling (DN) for this condition. PURPOSE:To compare clinical outcomes in patellar tendinopathy after a single ultrasound-guided, leukocyte-rich PRP injection versus DN. STUDY DESIGN:Randomized controlled trial; Level of evidence, 1. METHODS:A total of 23 patients with patellar tendinopathy on examination and MRI who had failed nonoperative treatment were enrolled and randomized to receive ultrasound-guided DN alone (DN group; n = 13) or with injection of leukocyte-rich PRP (PRP group; n = 10), along with standardized eccentric exercises. Patients and the physician providing follow-up care were blinded. Participants completed patient-reported outcome surveys before and at 3, 6, 9, 12, and ≥26 weeks after treatment during follow-up visits. The primary outcome measure was the Victorian Institute of Sports Assessment (VISA) score for patellar tendinopathy at 12 weeks, and secondary measures included the visual analog scale (VAS) for pain, Tegner activity scale, Lysholm knee scale, and Short Form (SF-12) questionnaire at 12 and ≥26 weeks. Results were analyzed using 2-tailed paired and unpaired t tests. Patients who were dissatisfied at 12 weeks were allowed to cross over into a separate unblinded arm. RESULTS:At 12 weeks after treatment, VISA scores improved by a mean ± standard deviation of 5.2 ± 12.5 points (P = .20) in the DN group (n = 12) and by 25.4 ± 23.2 points (P = .01) in the PRP group (n = 9); at ≥26 weeks, the scores improved by 33.2 ± 14.0 points (P = .001) in the DN group (n = 9) and by 28.9 ± 25.2 points (P = .01) in the PRP group (n = 7). The PRP group had improved significantly more than the DN group at 12 weeks (P = .02), but the difference between groups was not significant at ≥26 weeks (P = .66). Lysholm scores were not significantly different between groups at 12 weeks (P = .81), but the DN group had improved significantly more than the PRP group at ≥26 weeks (P = .006). At 12 weeks, 3 patients in the DN group failed treatment and subsequently crossed over into the PRP group. These patients were excluded from the primary ≥26-week analysis. There were no treatment failures in the PRP group. No adverse events were reported. Recruitment was stopped because interim analysis demonstrated statistically significant and clinically important results. CONCLUSION:A therapeutic regimen of standardized eccentric exercise and ultrasound-guided leukocyte-rich PRP injection with DN accelerates the recovery from patellar tendinopathy relative to exercise and ultrasound-guided DN alone, but the apparent benefit of PRP dissipates over time.

    View details for DOI 10.1177/0363546513518416

    View details for PubMedID 24481828

  • International Prevalence of Indoor Tanning: A Systematic Review and Meta-analysis. JAMA dermatology Wehner, M. R., Chren, M. M., Nameth, D., Choudhry, A., Gaskins, M., Nead, K. T., Boscardin, W. J., Linos, E. 2014


    IMPORTANCE Indoor tanning is a known carcinogen, but the scope of exposure to this hazard is not known. OBJECTIVE To summarize the international prevalence of exposure to indoor tanning. DATA SOURCES Studies were identified through systematic searches of PubMed (1966 to present), Scopus (1823 to present), and Web of Science (1898 to present) databases, last performed on March 16, 2013. We also hand searched reference lists to identify records missed by database searches and publicly available data not yet published in the scientific literature. STUDY SELECTION Records reporting a prevalence of indoor tanning were eligible for inclusion. We excluded case-control studies, reports with insufficient study information, and reports of groups recruited using factors related to indoor tanning. Two independent investigators performed searches and study selection. Our search yielded 1976 unique records. After exclusions, 161 records were assessed for eligibility in full text, and 88 were included. DATA EXTRACTION AND SYNTHESIS Two independent investigators extracted data on characteristics of study participants, inclusion/exclusion criteria, data collection format, outcomes, and statistical methods. Random-effects meta-analyses were used to summarize the prevalence of indoor tanning in different age categories. We calculated the population proportional attributable risk of indoor tanning in the United States, Europe, and Australia for nonmelanoma skin cancer (NMSC) and melanoma. MAIN OUTCOMES AND MEASURES Ever and past-year exposure to indoor tanning. RESULTS The summary prevalence of ever exposure was 35.7% (95% CI, 27.5%-44.0%) for adults, 55.0% (33.0%-77.1%) for university students, and 19.3% (14.7%-24.0%) for adolescents. The summary prevalence of past-year exposure was 14.0% (95% CI, 11.5%-16.5%) for adults, 43.1% (21.7%-64.5%) for university students, and 18.3% (12.6%-24.0%) for adolescents. These results included data from 406 696 participants. The population proportional attributable risk were 3.0% to 21.8% for NMSC and 2.6% to 9.4% for melanoma, corresponding to more than 450 000 NMSC cases and more than 10 000 melanoma cases each year attributable to indoor tanning in the United States, Europe, and Australia. CONCLUSIONS AND RELEVANCE Exposure to indoor tanning is common in Western countries, especially among young persons. Given the large number of skin cancer cases attributable to indoor tanning, these findings highlight a major public health issue.

    View details for DOI 10.1001/jamadermatol.2013.6896

    View details for PubMedID 24477278

  • Exercise capacity is the strongest predictor of mortality in patients with peripheral arterial disease JOURNAL OF VASCULAR SURGERY Leeper, N. J., Myers, J., Zhou, M., Nead, K. T., Syed, A., Kojima, Y., Caceres, R. D., Cooke, J. P. 2013; 57 (3): 728-733


    The objective of this study was to assess the predictive value of clinical and exercise test variables in patients with peripheral arterial disease (PAD).A customized symptom-limited ramp treadmill protocol was used to assess 725 PAD patients referred for exercise testing at the Palo Alto Veterans Hospital between 1997 and 2011. Detailed clinical and exercise test data were collected at baseline, and patients were followed up for a mean of 11.3 ± 6.3 years.During follow-up, there were 364 deaths. Baseline exercise capacity was 7.0 ± 2.6 metabolic equivalents (METs) among survivors and 5.5 ± 2.4 METs in those who died (P < .001). Although several physiologic parameters differed between survivors and nonsurvivors, age-adjusted Cox regression revealed that exercise capacity was the strongest independent predictor of death. Each additional MET achieved was associated with age-adjusted 18% and 20% reductions in all-cause and cardiovascular mortality, respectively (P < .001 for both). This variable surpassed all classical risk factors (including smoking and history of congestive heart failure) and all measured exercise test responses (including symptoms and electrocardiograph abnormalities).Among PAD patients, reduced exercise capacity is the most powerful harbinger of long-term mortality. This factor has predictive power beyond traditional risk factors and confirms the critical importance of fitness in this cohort.

    View details for DOI 10.1016/j.jvs.2012.07.051

    View details for Web of Science ID 000315944400019

    View details for PubMedID 23044259

  • SirT1 Regulates Adipose Tissue Inflammation DIABETES Gillum, M. P., Kotas, M. E., Erion, D. M., Kursawe, R., Chatterjee, P., Nead, K. T., Muise, E. S., Hsiao, J. J., Frederick, D. W., Yonemitsu, S., Banks, A. S., Qiang, L., Bhanot, S., Olefsky, J. M., Sears, D. D., Caprio, S., Shulman, G. I. 2011; 60 (12): 3235-3245


    Macrophage recruitment to adipose tissue is a reproducible feature of obesity. However, the events that result in chemokine production and macrophage recruitment to adipose tissue during states of energetic excess are not clear. Sirtuin 1 (SirT1) is an essential nutrient-sensing histone deacetylase, which is increased by caloric restriction and reduced by overfeeding. We discovered that SirT1 depletion causes anorexia by stimulating production of inflammatory factors in white adipose tissue and thus posit that decreases in SirT1 link overnutrition and adipose tissue inflammation.We used antisense oligonucleotides to reduce SirT1 to levels similar to those seen during overnutrition and studied SirT1-overexpressing transgenic mice and fat-specific SirT1 knockout animals. Finally, we analyzed subcutaneous adipose tissue biopsies from two independent cohorts of human subjects.We found that inducible or genetic reduction of SirT1 in vivo causes macrophage recruitment to adipose tissue, whereas overexpression of SirT1 prevents adipose tissue macrophage accumulation caused by chronic high-fat feeding. We also found that SirT1 expression in human subcutaneous fat is inversely related to adipose tissue macrophage infiltration.Reduction of adipose tissue SirT1 expression, which leads to histone hyperacetylation and ectopic inflammatory gene expression, is identified as a key regulatory component of macrophage influx into adipose tissue during overnutrition in rodents and humans. Our results suggest that SirT1 regulates adipose tissue inflammation by controlling the gain of proinflammatory transcription in response to inducers such as fatty acids, hypoxia, and endoplasmic reticulum stress.

    View details for DOI 10.2337/db11-0616

    View details for Web of Science ID 000297715100018

    View details for PubMedID 22110092

  • The threshold hypothesis: solving the equation of nurture vs nature in type 1 diabetes DIABETOLOGIA Wasserfall, C., Nead, K., Mathews, C., Atkinson, M. A. 2011; 54 (9): 2232-2236


    For more than 40 years, the contributions of nurture (i.e. the environment) and nature (i.e. genetics) have been touted for their aetiological importance in type 1 diabetes. Disappointingly, knowledge gains in these areas, while individually successful, have to a large extent occurred in isolation from each other. One reason underlying this divide is the lack of a testable model that simultaneously considers the contributions of genetic and environmental determinants in the formation of this and potentially other disorders that are subject to these variables. To address this void, we have designed a model based on the hypothesis that the aetiological influences of genetics and environment, when evaluated as intersecting and reciprocal trend lines based on odds ratios, result in a method of concurrently evaluating both facets and defining the attributable risk of clinical onset of type 1 diabetes. The model, which we have elected to term the 'threshold hypothesis', also provides a novel means of conceptualising the complex interactions of nurture with nature in type 1 diabetes across various geographical populations.

    View details for DOI 10.1007/s00125-011-2244-z

    View details for Web of Science ID 000293544900007

    View details for PubMedID 21773685

  • Low lifetime recreational activity is a risk factor for peripheral arterial disease JOURNAL OF VASCULAR SURGERY Wilson, A. M., Sadrzadeh-Rafie, A. H., Myers, J., Assimes, T., Nead, K. T., Higgins, M., Gabriel, A., Olin, J., Cooke, J. P. 2011; 54 (2): 427-432


    The relationship between lifetime physical activity and the risk of developing peripheral arterial disease (PAD) is not known.We studied 1381 patients referred for elective coronary angiography in a point prevalence analysis. PAD was defined as ankle-brachial index (ABI) <0.9 at the time or a history of revascularization of the lower extremities regardless of ABI measure. We used a validated physical activity questionnaire to retrospectively measure each patient's lifetime recreational activity (LRA). Multivariate and logistic regression analyses were used to assess the independent association of LRA to ABI and the presence of PAD.PAD was present in 19% (n = 258) of all subjects. Subjects reporting no regular LRA had greater diastolic blood pressure and were more likely to be female. They had lower average ABI, and a higher proportion had PAD (25.6%). In a regression model, including traditional risk factors and LRA, multivariate analysis showed that age (P < .001), female gender (P < .001), systolic blood pressure (P = .014), fasting glucose (P < .001), serum triglycerides (P = .02), and cumulative pack years (P < .001) were independent negative predictors of ABI, and LRA was a positive predictor of ABI (P < .001). History of sedentary lifestyle independently increased the odds ratio for PAD (odds ratio, 0.46; 95% confidence interval, 1.01-2.10) when assessed by logistic regression. Intriguingly, there is a correlation between physical activity and gender, such that women with low LRA are at greatest risk.Recalled LRA is positively correlated to ABI and associated with PAD. Whereas the mechanism for this effect is not clear, LRA may be a useful clinical screening tool for PAD risk, and strategies to increase adult recreational activity may reduce the burden of PAD later in life.

    View details for DOI 10.1016/j.jvs.2011.02.052

    View details for Web of Science ID 000293814400025

    View details for PubMedID 21664093

  • Sex differences in the prevalence of peripheral artery disease in patients undergoing coronary catheterization VASCULAR MEDICINE Rafie, A. H., Stefanick, M. L., Sims, S. T., Phan, T., Higgins, M., Gabriel, A., Assimes, T., Narasimhan, B., Nead, K. T., Myers, J., Olin, J., Cooke, J. P. 2010; 15 (6): 443-450


    To determine whether there are sex differences in the prevalence of peripheral artery disease, we performed an observational study of 1014 men and 547 women, aged ? 40 years, referred for elective coronary angiography. Women were slightly older, more obese, had higher low-density lipoprotein cholesterol (LDL-C) levels and systolic blood pressure (BP), and were more likely to be African American. Women had higher high-density lipoprotein cholesterol (HDL-C) levels, lower diastolic BP, and were less likely to smoke or to have a history of cardiovascular disease. Women had less prevalent (62% vs 81%) and less severe coronary artery disease (CAD) (p < 0.001 for both) by coronary angiography, but more prevalent peripheral artery disease (PAD) as determined by the ankle-brachial index (ABI) than men (23.6% versus 17.2%). Independent predictors of lower ABI were female sex, black race, older age, tobacco use, CAD, diabetes, and triglyceride level. In a full multivariable logistic regression model, women had a risk-adjusted odds ratio for PAD of 1.78 (95% CI 1.25-2.54) relative to men. Among patients referred for coronary angiography, women have less prevalent and less severe CAD, but more prevalent PAD, a sex difference that is not explained by traditional cardiovascular disease risk factors or CAD severity. Clinical Trial Registration-URL: Unique identifier: NCT00380185.

    View details for DOI 10.1177/1358863X10388345

    View details for Web of Science ID 000285574400002

    View details for PubMedID 21183651

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