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RATIONALE: Blacks compared with whites have a greater risk of adverse cardiovascular outcomes. Impaired regenerative capacity, measured as lower levels of circulating progenitor cells (CPCs), is a novel determinant of adverse outcomes; however, little is known about racial differences in CPCs. OBJECTIVE: To investigate the number of CPCs, PC-mobilizing factors, PC mobilization during acute myocardial infarction and the predictive value of CPC counts in blacks compared with whites. METHODS AND RESULTS: CPCs were enumerated by flow cytometry as CD45med+ blood mononuclear cells expressing CD34+, CD133+, VEGF2R+, and CXCR4+ epitopes in 1747 subjects, mean age 58.4±13, 55% male, and 26% self-reported black. Patients presenting with acute myocardial infarction (n=91) were analyzed separately. Models were adjusted for relevant clinical variables. SDF-1α (stromal cell-derived factor-1α), VEGF (vascular endothelial growth factor), and MMP-9 (matrix metallopeptidase-9) levels were measured (n=561), and 623 patients were followed for median of 2.2 years for survival analysis. Blacks were younger, more often female, with a higher burden of cardiovascular risk, and lower CPC counts. Blacks had fewer CD34+ cells (-17.6%; [95% confidence interval (CI), -23.5% to -11.3%]; P<0.001), CD34+/CD133+ cells (-15.5%; [95% CI, -22.4% to -8.1%]; P<0.001), CD34+/CXCR4+ cells (-17.3%; [95% CI, -23.9% to -10.2%]; P<0.001), and CD34+/VEGF2R+ cells (-27.9%; [95% CI, -46.9% to -2.0%]; P=0.04) compared with whites. The association between lower CPC counts and black race was not affected by risk factors or cardiovascular disease. Results were validated in a separate cohort of 411 patients. Blacks with acute myocardial infarction had significantly fewer CPCs compared with whites ( P=0.02). Blacks had significantly lower plasma MMP-9 levels ( P<0.001) which attenuated the association between low CD34+ and black race by 19% (95% CI, 13%-33%). However, VEGF and SDF-1α levels were not significantly different between the races. Lower CD34+ counts were similarly predictive of mortality in blacks (hazard ratio, 2.83; [95% CI, 1.12-7.20]; P=0.03) and whites (hazard ratio, 1.79; [95% CI, 1.09-2.94]; P=0.02) without significant interaction. CONCLUSIONS: Black subjects have lower levels of CPCs compared with whites which is partially dependent on lower circulating MMP-9 levels. Impaired regenerative capacity is predictive of adverse outcomes in blacks and may partly account for their increased risk of cardiovascular events.

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BACKGROUND: Truncal obesity is associated with metabolic syndrome and cardiovascular risk. Although vascular health is influenced by weight, it is not known whether changes in fat distribution modulate arterial function. OBJECTIVE: We assessed how changes in truncal (android) fat at 1 year affect arterial stiffness and endothelial function. METHODS: We recruited 711 healthy volunteers (235 males, age 48 ± 11 years) into the Emory Predictive Health Study; 498 returned at 1 year. Measurements included anthropometric and chemistry panels, fat mass using dual-energy X-ray absorptiometry, arterial stiffness indices (pulse wave velocity [PWV], augmentation index [AIx], and subendocardial viability ratio [SEVR]; Sphygmocor), flow-mediated dilation (FMD), and reactive hyperemia index (Endo-PAT). RESULTS: At baseline, measures of body mass correlated with PWV, AIx, SEVR, and FMD. In a multivariable analysis including body mass index (BMI) and traditional risk factors, BMI remained an independent predictor of PWV, AIx, SEVR, and FMD. In a model including BMI and measures of fat distribution, android fat remained an independent predictor of PWV (ß = 0.31, P = .004), AIx (ß = 0.24, P = .008), and SEVR (ß = -0.41, P < .001). The 1-year change in android fat correlated negatively with change in SEVR (ß = -0.13, P = .005) and FMD (ß = -0.13, P = .006) after adjustment for change in gynoid fat. CONCLUSION: In addition to BMI, android fat is a determinant of arterial stiffness, independent of traditional risk factors. Changes in android fat over time are associated with simultaneous changes in vascular function, indicating fat distribution's effect on vascular health.

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AIMS: Mental stress-induced myocardial ischemia (MSIMI) in patients with coronary artery disease (CAD) is associated with adverse cardiovascular outcomes. We aim to assess hemodynamic, neuro-hormonal, endothelial, vasomotor and vascular predictors of MSIMI. METHODS AND RESULTS: We subjected 660 patients with stable CAD to 99mTc sestamibi myocardial perfusion imaging at rest, with mental (speech task) and with conventional (exercise/pharmacological) stress. Endothelium-dependent flow-mediated dilation (FMD), microvascular reactivity [reactive hyperemia index (RHI)] and arterial stiffness [pulse wave velocity (PWV)] were measured at rest and 30-min after mental stress. The digital microvascular vasomotor response during mental stress was assessed using peripheral arterial tonometry (PAT). A total of 106(16.1%) patients had MSIMI. Mental stress was accompanied by significant increases in rate-pressure-product (heart rate x systolic blood pressure; RPP), epinephrine levels and PWV, and significant decreases in FMD and PAT ratio denoting microvascular constriction. In comparison to those with no MSIMI, patients with MSIMI had higher hemodynamic and digital vasoconstrictive responses (p<0.05 for both), but did not differ in epinephrine, endothelial or macrovascular responses. Only presence of ischemia during conventional stress (OR of 7.1, 95%CI of 4.2, 11.9), high hemodynamic response (OR for RPP response≥vs

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Mobile health (mHealth) is the utilisation of mobile technologies in healthcare and has particular relevance in improving lifestyle behaviours which may ultimately reduce cardiovascular disease risk. Various intervention studies for example integrate self-monitoring of diet and physical activity with text messaging systems to improve intermediate outcomes. Currently the future progress of mHealth technologies in formal diagnostic and therapeutic roles is pending and includes the need to validate and standardise accelerometer and heart rate data from various devices. Data also needs to be integrated from such devices into the medical record system to facilitate communication between providers and patients. Although short-term behaviour changes have been found with technologies such as Fitbit® (Fitbit, Inc., San Francisco, California, USA), whether such technologies/interventions lead to sustained behaviour change and reduced risk of myocardial infarction and death remains to be seen.

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BACKGROUND: Lifestyle modifications are first-line measures for cardiovascular disease prevention. Whether lifestyle intervention also preserves cardiovascular health is less clear. Our study examined the role of a Health Partner-administered lifestyle intervention on metrics of ideal cardiovascular health. METHODS AND RESULTS: A total of 711 university employees (48±11 years; 66% women, 72% Caucasian/22.5% African Americans) enrolled in a program that promoted healthier lifestyles at Emory University (Atlanta, GA). Anthropometric, laboratory, and physical activity measurements were performed at baseline and at 6 months, 1 year, and 2 years of follow-up. Results were utilized by the Health Partner to generate a personalized plan aimed at meeting ideal health metrics. Compared to baseline, at each of the 6-month, 1-year, and 2-year follow-up visits, systolic blood pressure was lower by 3.6, 4.6, and 3.3 mm Hg (P<0.001), total cholesterol decreased by 5.3, 6.5, and 6.4 mg/dL (P<0.001), body mass index declined by 0.33, 0.45, and 0.38 kg/m2 (P<0.001), and the percentage of smokers decreased by 1.3%, 3.5%, and 3.5% (P<0.01), respectively. Changes were greater in those with greater abnormalities at baseline. Finally, the American Heart Association "Life's Simple 7" ideal cardiovascular health score increased by 0.28, 0.40, and 0.33 at 6 month, 1 year, and 2 years, respectively, compared to baseline visit. CONCLUSIONS: A personalized, goal-directed Health Partner intervention significantly improved the cardiometabolic risk profile and metrics of cardiovascular health. These effects were evident at 6 months following enrollment and were sustained for 2 years. Whether the Health Partner intervention improves long-term morbidity and mortality and is cost-effective needs further investigation.

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BACKGROUND: Clinical outcomes of cardiac resynchronization therapy (CRT) in patients over the age of 80 have not been well described. METHODS: We retrospectively identified 96 consecutive patients ≥ 80 years old who underwent an initial implant or an upgrade to CRT, with or without defibrillator (CRT-D vs. CRT-P), at our institution between January 2003 and July 2008. The control cohort consisted of 177 randomly selected patients < 80 years old undergoing CRT implant during the same time period. The primary efficacy endpoint was all-cause mortality at 36 months, assessed by Kaplan-Meier time to first event curves. RESULTS: In the octogenarian cohort, mean age at CRT implant was 83.1 ± 2.9 years vs. 60.1 ± 8.8 years among controls (P < 0.001). Across both groups, 70% were male, mean left ventricular ejection fraction (LVEF) was 24.8% ± 14.1% and QRS duration was 154 ± 24.8 ms, without significant differences between groups. Octogenarians were more likely to have ischemic cardiomyopathy (74% vs. 37%, P < 0.001) and more likely to undergo upgrade to CRT instead of an initial implant (42% vs. 19%, P < 0.001). The rate of appropriate defibrillator shocks was lower among octogenarians (14% vs. 27%, P = 0.02) whereas the rate of inappropriate shocks was similar (3% vs. 6%, P = 0.55). At 36 months, there was no significant difference in the rate of all-cause mortality between octogenarians (11%) and controls (8%, P = 0.381). CONCLUSION: Appropriately selected octogenarians who are candidates for CRT have similar intermediate-term mortality compared to younger patients receiving CRT.

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AIMS: Even though the Middle East and North Africa (MENA) region had the highest comparative prevalence of diabetes in 2012, little is known about the nuances of diabetes risk and capacity to address the burdens. To provide a comprehensive overview, we reviewed the literature on diabetes in the MENA region. METHODS: We conducted a systematic search in PubMed between January 1990 and January 2012 for studies on diabetes in the MENA region without language restriction. RESULTS: There was a paucity of country-specific epidemiology data in the region. Diabetes prevalence varied widely across studies, from 2.5% in 1982 to 31.6% in 2011. Older age and higher body mass index were the most strongly associated risk factors for diabetes. Among people with diabetes, over half did not meet recommended care targets. In addition, macrovascular and microvascular complications were observed in 9-12% and 15-54% of diabetes population, respectively. CONCLUSIONS: This review suggests a need for more representative surveillance data in this noteworthy focal point of the global diabetes epidemic. Such actions will not only help to understand the actual burden of diabetes but also motivate actions on design and implementation of diabetes prevention and control programs.

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