The accurate measurement of blood pressure (BP) is essential for the diagnosis and management of hypertension. This article provides an updated American Heart Association scientific statement on BP measurement in humans. In the office setting, many oscillometric devices have been validated that allow accurate BP measurement while reducing human errors associated with the auscultatory approach. Fully automated oscillometric devices capable of taking multiple readings even without an observer being present may provide a more accurate measurement of BP than auscultation. Studies have shown substantial differences in BP when measured outside versus in the office setting. Ambulatory BP monitoring is considered the reference standard for out-of-office BP assessment, with home BP monitoring being an alternative when ambulatory BP monitoring is not available or tolerated. Compared with their counterparts with sustained normotension (ie, nonhypertensive BP levels in and outside the office setting), it is unclear whether adults with white-coat hypertension (ie, hypertensive BP levels in the office but not outside the office) have increased cardiovascular disease risk, whereas those with masked hypertension (ie, hypertensive BP levels outside the office but not in the office) are at substantially increased risk. In addition, high nighttime BP on ambulatory BP monitoring is associated with increased cardiovascular disease risk. Both oscillometric and auscultatory methods are considered acceptable for measuring BP in children and adolescents. Regardless of the method used to measure BP, initial and ongoing training of technicians and healthcare providers and the use of validated and calibrated devices are critical for obtaining accurate BP measurements.

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Abstract-Recent data suggest that visit-to-visit variability of blood pressure is associated with stroke incidence. Correlates of increased visit-to-visit variability in blood pressure and the relationship between variability and all-cause mortality were examined using data on US adults Ն20 years of age from the Third National Health and Nutrition Examination Survey (nϭ956). Three consecutive blood pressure readings were taken during 3 separate study visits from 1988 to 1994. Based on the mean of the second and third measurements from each visit, visit-to-visit blood pressure variability for each participant was defined using the standard deviation and coefficient of variation across visits. Mortality was assessed through December 31, 2006 (median follow-upϭ14 years; nϭ240 deaths). The mean of the standard deviation for systolic blood pressure across visits was 7.7 mm Hg. After multivariable adjustment, older age, female gender, history of myocardial infarction, higher mean systolic blood pressure and pulse pressure, and use of angiotensin converting enzyme inhibitors were associated with higher standard deviation in systolic blood pressure. The multivariable adjusted hazard ratios for all-cause mortality associated with a standard deviation of systolic blood pressure of 4.80 to 8.34 mm Hg and Ն8.35 mm Hg, versus Ͻ4.80 mm Hg, were 1.57 (95% CI, 1.07 to 2.18) and 1.50 (95% CI, 1.03 to 2.18), respectively. Results were similar when coefficient of variation for systolic blood pressure was evaluated. Visit-to-visit variability for diastolic blood pressure was not associated with mortality. In this populationbased study of US adults, higher levels of short-term visit-to-visit variability in systolic blood pressure were associated with increased all-cause mortality. (Hypertension. 2011;57:160-166.) • Online Data Supplement

As the worldwide prevalence of hypertension continues to increase, the primary prevention of hypertension has become an important global public health initiative. Physical activity is commonly recommended as an important lifestyle modification that may aid in the prevention of hypertension. Recent epidemiologic evidence has demonstrated a consistent, temporal, and dose-dependent relationship between physical activity and the development of hypertension. Experimental evidence from interventional studies have further confirmed a relationship between physical activity and hypertension as the favorable effects of exercise on blood pressure reduction have been well characterized in recent years. Despite the available evidence strongly supporting a role for physical activity in the prevention of hypertension, many unanswered questions regarding the protective benefits of physical activity in high-risk individuals, the factors that may moderate the relationship between physical activity and hypertension, and the optimal prescription for hypertension prevention remain. We review the most recent evidence for the role of physical activity in the prevention of hypertension and discuss recent studies that have sought to address these unanswered questions.

Rationale: Basic science research suggests a causal role for endothelial dysfunction in chronic obstructive pulmonary disease (COPD). Clinical studies examining endothelial function are lacking, particularly early in the disease. Flow-mediated dilation (FMD) is a physiologic measure of endothelial reactivity to endogenous nitric oxide. Objectives: We hypothesized that lower FMD among former smokers would be associated with lower post-bronchodilator FEV 1 , higher percentage of emphysema using computed tomography (CT) and lower diffusing capacity. Methods: We measured FMD, pulmonary function, and CT percentage of emphysema in a random sample of 107 cotinine-confirmed former smokers in the ongoing EMCAP study. FMD was defined as percentage change in the brachial artery diameter with reactive hyperemia. Generalized additive models were used to adjust for potential confounders and assess linearity. Measurements and Main Results: Mean age of participants was 71 6 5 years, 46% were female, and pack-years averaged 48 6 26. Mean FMD was 3.8 6 3.1%; mean post-bronchodilator FEV 1 , 2.3 6 0.8 L; and mean CT percentage of emphysema, 26 6 10%. A 1 SD decrease in FMD was associated with a 132-ml (95% confidence interval, 16-248 ml; P 5 0.03) decrement in post-bronchodilator FEV 1 and a 2.6% (95% confidence interval, 0.5-4.7%; P 5 0.02) increase in CT percentage of emphysema in fully adjusted models. These associations were linear across the spectrum from normality to disease, independent of smoking history, and also significant among participants without COPD. Associations with diffusing capacity were consistent but nonsignificant (P 5 0.09). The FMD-FEV 1 association was entirely attributable to percentage of emphysema. Conclusions: Impaired endothelial function, as measured by FMD, was associated with lower FEV 1 and higher CT percentage of emphysema in former smokers early in COPD.Keywords: pulmonary disease, chronic obstructive; bronchitis, chronic; pulmonary emphysema; endothelial dysfunction Recent research on the pathogenesis of chronic obstructive pulmonary disease (COPD) suggests that perturbations in the vasculature and, specifically, endothelial health may occur early in COPD (1). Decreased expression of vascular endothelial growth factor (VEGF) causes endothelial apoptosis, epithelial apoptosis, and emphysema (2-4). The second messenger lipid ceramide mediates VEGF blockade-induced apoptosis in COPD and ceramide instillation acutely triggers apoptosis in pulmonary endothelial cells, causing emphysema in mice (5).Apoptotic endothelial cells are present in the lungs of smokers with COPD (6, 7), and there are significant morphologic differences in the endothelium of smokers with mild, moderate, and severe COPD compared with smokers without COPD (8). Furthermore, nitric oxide (NO)-mediated, endotheliumdependent relaxation provoked by adenosine diphosphate and acetylcholine is attenuated in the excised pulmonary arteries of patients with COPD compared with those of smoking and nonsmoking control subjects (9, 10). Publ...

Background Depressive symptoms are an established predictor of mortality and major adverse cardiac events (defined as nonfatal myocardial infarction or hospitalization for unstable angina or urgent/emergency revascularizations) in patients with acute coronary syndrome (ACS). This study was conducted to determine the acceptability and efficacy of enhanced depression treatment in patients with ACS. Methods A 3-month observation period to identify patients with ACS and persistent depressive symptoms was followed by a 6-month randomized controlled trial. From January 1, 2005, through February 29, 2008, 237 patients with ACS from 5 hospitals were enrolled, including 157 persistently depressed patients randomized to intervention (initial patient preference for problem-solving therapy and/or pharmacotherapy, then a stepped-care approach; 80 patients) or usual care (77 patients) and 80 nondepressed patients who underwent observational evaluation. The primary outcome was patient satisfaction with depression care. Secondary outcomes were depressive symptom changes (assessed with the Beck Depression Inventory), major adverse cardiac events, and death. Results At the end of the trial, the proportion of patients who were satisfied with their depression care was higher in the intervention group (54% of 80) than in the usual care group (19% of 77) (odds ratio, 5.4; 95% confidence interval [CI], 2.2–12.9 [P<.001]). The Beck Depression Inventory score decreased significantly more (t155=2.85 [P=.005]) for intervention patients (change, −5.7; 95% CI, −7.6 to −3.8; df=155) than for usual care patients (change, −1.9; 95% CI, −3.8 to −0.1; df=155); the depression effect size was 0.59 of the standard deviation. At the end of the trial, 3 intervention patients and 10 usual care patients had experienced major adverse cardiac events (4% and 13%, respectively; log-rank test, χ12=3.93 [P=.047]), as well as 5 nondepressed patients (6%) (for the intervention vs nondepressed cohort, χ12=0.48 [P=.49]). Conclusion Enhanced depression care for patients with ACS was associated with greater satisfaction, a greater reduction in depressive symptoms, and a promising improvement in prognosis.

The diagnosis and management of hypertension, a common cardiovascular risk factor among the general population, have been based primarily on the measurement of blood pressure (BP) in the office. BP may differ considerably when measured in the office and when measured outside of the office setting, and higher out-of-office BP is associated with increased cardiovascular risk independent of office BP. Self-measured BP monitoring, the measurement of BP by an individual outside of the office at home, is a validated approach for out-of-office BP measurement. Several national and international hypertension guidelines endorse self-measured BP monitoring. Indications include the diagnosis of white-coat hypertension and masked hypertension and the identification of white-coat effect and masked uncontrolled hypertension. Other indications include confirming the diagnosis of resistant hypertension and detecting morning hypertension. Validated self-measured BP monitoring devices that use the oscillometric method are preferred, and a standardized BP measurement and monitoring protocol should be followed. Evidence from meta-analyses of randomized trials indicates that self-measured BP monitoring is associated with a reduction in BP and improved BP control, and the benefits of self-measured BP monitoring are greatest when done along with cointerventions. The addition of self-measured BP monitoring to office BP monitoring is cost-effective compared with office BP monitoring alone or usual care among individuals with high office BP. The use of self-measured BP monitoring is commonly reported by both individuals and providers. Therefore, self-measured BP monitoring has high potential for improving the diagnosis and management of hypertension in the United States. Randomized controlled trials examining the impact of self-measured BP monitoring on cardiovascular outcomes are needed. To adequately address barriers to the implementation of self-measured BP monitoring, financial investment is needed in the following areas: improving education and training of individuals and providers, building health information technology capacity, incorporating self-measured BP readings into clinical performance measures, supporting cointerventions, and enhancing reimbursement.

Genome-wide association studies (GWASs) have identified many SNPs underlying variations in plasma-lipid levels. We explore whether additional loci associated with plasma-lipid phenotypes, such as high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), total cholesterol (TC), and triglycerides (TGs), can be identified by a dense gene-centric approach. Our meta-analysis of 32 studies in 66,240 individuals of European ancestry was based on the custom ∼50,000 SNP genotyping array (the ITMAT-Broad-CARe array) covering ∼2,000 candidate genes. SNP-lipid associations were replicated either in a cohort comprising an additional 24,736 samples or within the Global Lipid Genetic Consortium. We identified four, six, ten, and four unreported SNPs in established lipid genes for HDL-C, LDL-C, TC, and TGs, respectively. We also identified several lipid-related SNPs in previously unreported genes: DGAT2, HCAR2, GPIHBP1, PPARG, and FTO for HDL-C; SOCS3, APOH, SPTY2D1, BRCA2, and VLDLR for LDL-C; SOCS3, UGT1A1, BRCA2, UBE3B, FCGR2A, CHUK, and INSIG2 for TC; and SERPINF2, C4B, GCK, GATA4, INSR, and LPAL2 for TGs. The proportion of explained phenotypic variance in the subset of studies providing individual-level data was 9.9% for HDL-C, 9.5% for LDL-C, 10.3% for TC, and 8.0% for TGs. This large meta-analysis of lipid phenotypes with the use of a dense gene-centric approach identified multiple SNPs not previously described in established lipid genes and several previously unknown loci. The explained phenotypic variance from this approach was comparable to that from a meta-analysis of GWAS data, suggesting that a focused genotyping approach can further increase the understanding of heritability of plasma lipids.