Ankle-brachial index predicts change over time in functional status in the San Diego Population Study.

BACKGROUND: Peripheral artery disease (PAD) affects millions of people, both in the U.S. and worldwide. Even when asymptomatic, PAD and the ankle-brachial index (ABI), the major clinical diagnostic criterion for PAD, are associated with decreased functional status and quality of life, as well as mobility impairment. Whether the ABI or change in the ABI predicts decline in functional status over time has not been previously assessed in a population-based setting. METHODS: Participants were 812 non-Hispanic white, African American, Hispanic, and Asian men and women from the San Diego Population Study (SDPS) who attended a baseline examination (1994-1998), and follow-up clinic examination approximately 11 years later. The Medical Outcomes Study 36-Item Short Form (SF-36) was obtained at both the baseline and follow-up examinations, and the summary performance score (SPS) at the follow-up examination. Associations of the baseline ABI and clinically relevant change in the ABI (<-0.15 vs ≥-0.15) with change in SF-36 scores over time were assessed using growth curve models, a type of mixed model that accounts for within participant correlation of measurements over time, and using linear regression for SPS. Models were adjusted for baseline age, sex, race/ethnicity, body mass index, ever smoking, physical activity, hypertension, diabetes, and dyslipidemia. RESULTS: Mean ± standard deviation (SD) for the baseline ABI was 1.11 ± 0.10, and 50.8 ± 9.0 for the baseline Physical Component Score (PCS), 50.1 ± 9.5 for the baseline Mental Component Score (MCS), and 11.2 ± 1.9 for the SPS at the follow-up examination. In fully adjusted models, each SD lower of the baseline ABI was significantly associated with an average decrease over time of 0.6 (95% confidence interval [CI], -1.1 to -0.1; P = .02) units on SF-36 PCS. Each SD lower of the baseline ABI was also significantly associated with an average decrease over time of 1.2 units (95% CI, -2.3 to -0.2; P = .02) on the SF-36 physical functioning subscale, and a decrease of 1.3 units (95% CI, -2.3 to -0.3; P = .01) on the SF-36 energy/vitality subscale in fully adjusted models. Baseline ABI was not significantly associated with change in the SF-36 MCS over time, or the SPS at the follow-up examination. Change in the ABI was not associated with SF-36 PCS, MCS, or the SPS. CONCLUSIONS: In this multiethnic population of healthy middle-aged community-living men and women, we showed that participants with a lower baseline ABI had declines in functional status over 11 years. Findings suggest that small differences in the ABI, even within the normal range, may identify subclinical lower extremity PAD, which in turn may help to identify individuals at risk for declining functional status with age.

Global and regional burden of death and disability from peripheral artery disease: 21 world regions, 1990 to 2010.

A comprehensive and systematic assessment of disability and mortality due to lower extremity peripheral artery disease (PAD) is lacking. Therefore, we estimated PAD deaths, disability-adjusted life years (DALYs), and years of life lost in 21 regions worldwide for 1990 and 2010. We used the GBD (Global Burden of Diseases 2010) study causes of death database, and the cause of death ensemble modeling approach to assess levels and trends of PAD deaths and years of life lost over time, by age, sex, and region. Assessment of DALYs employed estimates of PAD prevalence from systematic reviews of epidemiologic data using a Bayesian meta-regression method. In 1990, the age-specific PAD death rate per 100,000 population ranged from 0.05 (95% confidence interval [CI]: 0.03 to 0.09) among those 40 to 44 years old to 16.63 (95% CI: 10.47 to 25.31) among the 80+ years group. In 2010, the corresponding estimates were 0.07 (95% CI: 0.04 to 0.13) and 28.71 (95% CI: 18.3 to 43.06). Death rates increased consistently with age in 1990 and 2010, and the rates in 2010 were higher than they were in 1990 in all age categories. The largest relative change in median death rate of +6.03 per 100,000 (95% CI: 1.50 to 11.85) was noted in the Asia Pacific-High Income region and was largely driven by higher rates in women: +17.36 (95% CI: 1.79 to 32.01) versus +1.25 (95% CI: 0.13 to 2.39) in men. The overall relative change in median DALYs was larger in developing nations than in developed nations: 1.15 (95% CI: 0.80 to 1.66) versus 0.77 (95% CI: 0.55 to 1.08). Of note, the overall relative change in median DALYs was higher among both men and women in developing versus developed countries: men: 1.18 (95% CI: 0.82 to 1.65) versus 0.51 (95% CI: 0.30 to 0.81), and women: 1.11 (95% CI: 0.58 to 2.02) versus 1 (95% CI: 0.67 to 1.47). Within developed nations, the overall relative change in median DALY rates was larger in women than in men: +1.00 (95% CI: 0.67 to 1.47) versus +0.51 (95% CI: 0.3 to 0.81). Similarly, the overall relative change in median years of life lost rate in developed countries was larger in women than in men: +1.64 (95% CI: 1.17 to 2.34) versus +0.53 (95% CI: 0.24 to 0.94). The relative increases in median years lived with nonfatal disease disability (YLD) rates in men and women were larger in developing versus developed nations: men: 0.87 (95% CI: 0.59 to 1.2) versus 0.49 (95% CI: 0.29 to 0.73), and women: 0.75 (95% CI: 0.46 to 1.09) versus 0.49 (95% CI: 0.29 to 0.73). Disability and mortality associated with PAD has increased over the last 20 years, and this increase in burden has been greater among women than among men. In addition, the burden of PAD is no longer confined to the elderly population, but now involves young adults. Furthermore, the relative increase in PAD burden in developing regions of the world is striking and exceeds the increases in developed nations.

Global and regional burden of aortic dissection and aneurysms: mortality trends in 21 world regions, 1990 to 2010.

A comprehensive and systematic assessment of the global burden of aortic aneurysms (AA) has been lacking. Therefore, we estimated AA regional deaths and years of life lost (YLL) in 21 regions worldwide for 1990 and 2010. We used the GBD (Global Burden of Disease) 2010 study causes of death database and the cause of death ensemble modeling approach to assess levels and trends of AA deaths by age, sex, and GBD region. The global AA death rate per 100,000 population was 2.49 (95% CI: 1.78 to 3.27) in 1990 and 2.78 (95% CI: 2.04 to 3.62) in 2010. In 1990 and 2010, the highest mean death rates were in Australasia and Western Europe: 8.82 (95% CI: 6.96 to 10.79) and 7.69 (95% CI: 6.11 to 9.57) in 1990 and 8.38 (95% CI: 6.48 to 10.86) and 7.68 (95% CI: 6.13 to 9.54) in 2010. YLL rates by GBD region mirrored the mortality rate pattern. Overall, men had higher AA death rates than women: 2.86 (95% CI: 1.90 to 4.22) versus 2.12 (95% CI: 1.33 to 3.00) in 1990 and 3.40 (95% CI: 2.26 to 5.01) versus 2.15 (95% CI: 1.44 to 2.89) in 2010. The relative change in median death rate was +0.22 (95% CI: 0.10 to 0.33) in developed nations versus +0.71 (95% CI: 0.28 to 1.40) in developing nations. The smallest relative changes in median death rate were noted in North America high income, Central Europe, Western Europe, and Australasia, with estimates of +0.07 (95% CI: -0.26 to 0.37), +0.08 (95% CI: -0.02 to 0.23), +0.09 (95% CI: -0.02 to 0.21), and +0.22 (95% CI: -0.08 to 0.46), respectively. The largest increases were in Asia Pacific high income, Southeast Asia, Latin America tropical, Oceania, South Asia, and Central Sub-Saharan Africa. Women rather than men drove the increase in the Asia Pacific high-income region: the relative change in median rates was +2.92 (95% CI: 0.6 to 4.35) versus +1.05 (95% CI: 0.61 to 2.42). In contrast to high-income regions, the observed pattern in developing regions suggests increasing AA burden, which portends future health system challenges in these regions.

Estimation of global and regional incidence and prevalence of abdominal aortic aneurysms 1990 to 2010.

The global burden of abdominal aortic aneurysm (AAA) has not been studied previously. Such information is important given the emergence of cardiovascular diseases in developing countries. We conducted a systematic literature review and estimated the global and regional incidence and prevalence of AAA in 21 world regions by age and sex. The search for prevalence and incidence of AAA using standard clinical and epidemiological terms was conducted using MEDLINE (1950 to 2010), EMBASE (1980 to 2010), AMED (1985 to 2010), CINAHL (1982 to 2010), and LILACS (2008 to 2010). Data abstracted from the systematic review served as priors for Bayesian meta-regression analyses. The analysis drew from 26 high-quality studies to estimate AAA prevalence and incidence. In 1990, the global age-specific prevalence rate per 100,000 ranged from 8.43 (95% CI: 7.03 to 10.14) in the 40 to 44 years age group to 2,422.53 (95% CI: 2,298.63 to 2,562.25) in the 75 to 79 years age group; the corresponding range in 2010 was 7.88 (95% CI: 6.54 to 9.59) to 2,274.82 (95% CI: 2,149.77 to 2,410.17). Prevalence was higher in developed versus developing nations, and the rates within each development stratum decreased between 1990 and 2010. Globally, the age-specific annual incidence rate per 100,000 in 1990 ranged from 0.89 (95% CI: 0.66 to 1.17) in 40 to 44 years age group to 176.08 (95% CI: 162.72 to 190.28) in the 75 to 79 years age group. In 2010, this range was 0.83 (95% CI: 0.61 to 1.11) to 164.57 (95% CI: 152.20 to 178.78). The highest prevalence in 1990 was in Australasia and North America high income regions: 382.65 (95% CI: 356.27 to 410.88) and 300.59 (95% CI: 280.93 to 321.54), respectively. Australasia had the highest prevalence in 2010, although the prevalence decreased to 310.27 (95% CI: 289.01 to 332.94). Regional prevalence increased in Oceania, tropical Latin America, Asia Pacific high income, Southern Sub-Saharan Africa (SSA), Central SSA, South Asia, Western SSA, and Central Asia. AAA global prevalence and incidence rates have decreased over the last 20 years. However, rising rates in some regions highlight the need for policies to enhance global disease surveillance and prevention.

The association between lipoprotein-associated phospholipase A2 and cardiovascular disease and total mortality in vascular medicine patients.

INTRODUCTION: In some community-based studies, lipoprotein-associated phospholipase A(2) (Lp-PLA(2)) has been shown to be independently predictive of future fatal and nonfatal cardiovascular disease (CVD) events. We tested the hypothesis that Lp-PLA(2) is independently predictive of mortality in high-risk patients from a vascular laboratory. METHODS: Between 1990 and 1994, patients seen in the previous 10 years for noninvasive lower extremity arterial testing were invited to return for a vascular examination of the lower extremities. By medical record review, we identified 2265 eligible patients; of these, 508 returned for interviews, blood collection, and arterial examination and represent those who had survived, could be located, and were willing to participate. The 508 subjects were followed up for an average of 6.7 years until the end of the study period on December 31, 2001. Vital status was ascertained by multiple searches of the Social Security Death Index. The primary outcomes for this study were time to any, CVD, and coronary heart disease (CHD) mortality. RESULTS: The mean age was 68.2 years, 88% were men, 87% were non-Hispanic white, 39.1% were diagnosed with peripheral arterial disease only, 9.2% with other CVD only, and 28.5% with both peripheral arterial disease and other CVD. During the entire follow-up period, 299 (59.7%) patients died, 167 from CVD, of which 88 deaths were due to coronary heart disease. With adjustment for CVD risk factors and baseline peripheral arterial disease and other CVD, an increment of one standard deviation in Lp-PLA(2) activity was associated with a 40% higher risk for CHD mortality at 5 years of follow-up (P = .04). Additional adjustment for triglycerides, high-density lipoprotein, and low-density lipoprotein cholesterol reduced this association to nonsignificance (hazard risk, 1.12). CONCLUSION: In a vascular laboratory patient population, higher levels of LpPLA(2) mass and activity were not significantly associated with total, CVD, or CHD mortality at 5 years of follow-up and after adjustment for traditional CVD risk factors and the presence of PAD and other CVD at baseline. An apparent elevated risk of CHD death associated with elevated Lp-PLA2 was largely explained by associated elevations in lipids and lipoproteins.