In 2007–2008, antiplatelet medications were prescribed at only 46.9% of visits for patients with ischemic vascular disease. The evidence of the benefit of aspirin with respect to cardiovascular outcomes underscores the substantial opportunity before clinicians and patients.

In this article, we examine the socioecological determinants—the biological, geographic, and built environment factors—that influence risk for prediabetes and type 2 diabetes. A socioecological perspective looks beyond the individual to evaluate a multitude of influences, from the surrounding home, work, school, and community environments to social determinants and the influence of public policy on individual behavior (1). Figure 1, adapted from the Institute of Medicine socioecological model of childhood obesity, provides a good framework for understanding potential socioecological determinants of risk for type 2 diabetes. Figure 1 Levels and sectors of influence on obesity and diabetes risk (progress in preventing childhood obesity) (© 2007 the National Academies Press). SES, socioeconomic status. In November 2012, the American Diabetes Association Prevention Committee convened a writing group to review the evidence on socioecological factors contributing to recent increases in prediabetes and type 2 diabetes. Drawing from the work of the committee, in this article we review the overarching evidence-based contributions of socioecological factors to risk for type 2 diabetes. Rather than incorporate the entire universe of relational observations, this scientific statement is intended to evaluate the extent to which data indicate a contributing role of social and environmental factors to the current epidemic of type 2 diabetes. The world is in the midst of parallel and rapidly advancing epidemics—obesity and type 2 diabetes—that began in the latter half of the 20th century and continue to grow, unchecked. Current prevalence rates are staggering and are expected to continue to climb over the ensuing decades. In the U.S., one-third of adults and 16–18% of youth are obese (2), up from 5 to 6% three decades ago (Fig. 2). Increases in rates of type 2 diabetes have closely followed the increases in obesity. In the U.S., diabetes affects 8.3% of the population, including 18.8 million with diagnosed …

OBJECTIVES:Evaluate the quality of care provided patients with acute myocardial infarction and compare with similar national and regional data.DESIGN:Case series.SETTING:The Strong Heart Study has extensive population-based data related to cardiovascular events among American Indians living in three rural regions of the United States.PARTICIPANTS:Acute myocardial infarction cases (72) occurring between 1/1/2001 and 12/31/2006 were identified from a cohort of 4549 participants.OUTCOME MEASURES:The proportion of cases that were provided standard quality of care therapy, as defined by the Healthcare Financing Administration and other national organizations.RESULTS:The provision of quality services, such as administration of aspirin on admission and at discharge, reperfusion therapy within 24 hours, prescription of beta blocker medication at discharge, and smoking cessation counseling were found to be 94%, 91%, 92%, 86% and 71%, respectively. The unadjusted, 30 day mortality rate was 17%.CONCLUSION:Despite considerable challenges posed by geographic isolation and small facilities, process measures of the quality of acute myocardial infarction care for participants in this American Indian cohort were comparable to that reported for Medicare beneficiaries nationally and within the resident states of this cohort.

Differences in utilization of health care services and the quality of those services between geographic regions of the United States exist. Public policy, guidelines, and health care organizations have attempted to address these differences. In 1992 the Healthcare Financing Administration, now the Center for Medicare/Medicaid Services (CMS), initiated the Cooperative Cardiovascular Project with the goal of improving the quality of care for acute myocardial infarction (AMI) nationally. Standards were developed for the evaluation of quality care based on the guidelines of the American College of Cardiology and the American Heart Association. The initial results from this national survey of AMI quality care was presented in 1998 and a follow-up survey reported in 2003. National performance since 1999 has been evaluated primarily on the basis of data from voluntary reporting systems, such as the National Registry of Myocardial Infarction, The National Cardiovascular Data Registry, the CMS and Hospital Quality Alliance Program (begun in 2004), and the American Heart Association’s Get With The Guidelines coronary artery disease program. There have been efforts to use these programs and quality measures to determine the role they play in the known cardiovascular disease disparities among minority populations. Cardiovascular disease accounts for a large proportion of morbidity and mortality among American Indians. Yet, studies of cardiovascular disease quality of care among American Indians are limited. The Strong Heart Study is a longitudinal cohort study of cardiovascular disease and its risk factors in American Indians. It is the longest-running population-based cohort study among American Indians with centers in three primarily rural geographic regions in the United States. It has rich demographic and clinical data including physician adjudicated cardiovascular events. In this study, we describe AMI quality care measures from the Strong Heart Study and then compare them to previously published studies from CMS.

Background: Indigenous people across the globe have generally had suboptimal access to quality medical care and effective prevention programs. The available programs that existed have generally been poorly funded and have primarily focussed on infectious diseases. More recent trends denoting significant rising morbidity and mortality of chronic diseases have brought some limited medical focus on cardiovascular diseases, their risk factors and their prevention. However, there is a growing body of evidence published and unpublished of developed and developing successful programs to provide culturally appropriate and sensitive treatment for cardiovascular diseases and prevention. Within this report, we aim to describe some of these programs in order to understand common approaches and links that make them successful. Once this survey is completed, a template for successful CVD programs can be created for the development of future programs.Methods: We used several methods to gather information about successful Indigenous CVD programs: Pub Med search (keywords: Indigenous, native, First Nation, Aboriginal, cardiovascular, cardiac, etc.), online searches of government-based health programs (World Health Organization, Centers for Disease Control, etc.) and non-government health programs (World Heart Federation, Bill & Melinda Gates Foundation, etc.), and, importantly, personal communication with multiple thought leaders and program directors in the field of international CVD treatment and prevention.Results: Programs can be divided into: (1) epidemiologic programs, which focus on data collection, (2) focussed prevention programs and population approach to CVD prevention, and (3) clinical prevention and intervention programs.Discussion: Common themes that define successful Indigenous CVD programs include: dedicated focus on the Indigenous population, widespread community involvement within the Indigenous population, often through the use of Indigenous community health workers, a focus on high-risk individuals within the population and regularly scheduled contact between the program and participants. We recommend that these themes are incorporated during development of future CVD programs for Indigenous people. (Heart, Lung and Circulation 2010;19:351-360) (C) 2010 Australasian Society of Cardiac and Thoracic Surgeons and the Cardiac Society of Australia and New Zealand. All rights reserved.

Objectives Type 2 diabetes is accepted as a cause of heart failure, but direct cause–effect evidence independent of incident myocardial infarction (MI), hypertension and other coexisting risk factors is less well studied. We tested the hypothesis that diabetes predisposes to heart failure independently of hypertension and intercurrent MI. Methods We evaluated 12-year incident heart failure in 2740 participants (1781 women) without prevalent cardiovascular or severe kidney disease, at the time of the first exam of the Strong Heart Study cohort. Intercurrent MI was censored as a competing risk event. Results Diabetes was present in 1206 individuals (44%), and impaired fasting glucose (IFG) in 391 (14%). Diabetic participants more frequently had hypertension and/or central obesity (both P < 0.0001). Incident heart failure was ascertained in 64 participants with normal fasting glucose (NFG; 6%), 26 (7%) with IFG and 201 with diabetes (17%, hazard ratio = 4.04 vs. NFG, P < 0.0001). In Cox analysis adjusting for age, sex, obesity, central fat distribution, hypertension, antihypertensive medications, prevalent atrial fibrillation, glomerular filtration rate, urinary albumin/creatinine ratio, plasma cholesterol, Hb1Ac, smoking habit, alcohol use, educational level and physical activity, diabetes was associated with a two-fold greater risk of incident heart failure than NFG (hazard ratio = 2.45, P < 0.0001). Diabetes maintained 1.5-fold greater risk of heart failure than NFG (P < 0.03) even when intercurrent MI (n = 221) was censored as a competing risk event, similar to the adjusted hazard ratio for heart failure in hypertension. Conclusion Type 2 diabetes is a potent, independent risk factor for heart failure. Risk of heart failure in diabetic patients cannot be fully explained by incident MI and coexisting cardiovascular risk factors. Mechanisms directly related to diabetes and impairing cardiac function should be studied and identified.

BACKGROUND: The Stop Atherosclerosis in Native Diabetics Study (SANDS) reported cardiovascular benefit of aggressive versus standard treatment targets for both low-density lipoprotein Cholesterol (LDL-C) and blood pressure (BP) in diabetic individualsOBJECTIVE: In this analysis. we examined within trial cost-effectiveness of aggressive targets of LDL-C <= 70 mg/dL and systolic BP <= 115 mmHg versus standard targets of LDL-C <= 100 mg/dL and systolic BP <= 130 mmHgDESIGN: Randomized, open label blinded-to-endpoint 3-year trialDATA SOURCES: SANDS clinical trial database, Quality of Wellbeing survey, Centers for Medicare and Medicaid Services, Wholesale Drug PricesTARGET POPULATION: American Indians >= age 40 years with type 2 diabetes and no previous cardiovascular eventsTIME HORIZON: April 2003 to July 2007PERSPECTIVE: Health payerINTERVENTIONS: Participants were randomized to aggressive versus standard groups with treatment algorithms defined for both.OUTCOME MEASURES: Incremental cost-effectivenessRESULTS OF BASE-CASE ANALYSIS: Compared with the standard group, the aggressive atom) had slightly lower costs of medical services (-$116) but a 54% greater cost for BP medication ($1,242) and a 116% greater cost for lipid-lowering medication ($2,863). resulting in an increased cost of $3.988 over 3 years Those in the aggressively treated group gained 0 0480 quality-adjusted life-years (QALY) over the standard group When a 3% discount rate or costs and outcomes was used, the resulting cost per QALY was $82,589RESULTS OF SENSITIVITY ANALYSIS: The use of a 25%, 50%, and 75% reduction in drug costs resulted in a cost per QALY of $61.329, $40,070. and $18,810, respectivelyLIMITATIONS: This study was limited by use of a single ethnic group and by its 3-year durationCONCLUSIONS: Within this 3-year study. treatment to lower BP and LDL-C below standard targets was not cost-effective because of the cost of the additional medications required to meet the lower targets With the anticipated availability of generic versions of the BP and lipid-lowering drugs used in SANDS, the cost-effectiveness of this intervention should improve Published by Elsevier Inc on behalf of the National Lipid Association

BACKGROUND: Lowering low-density lipoprotein cholesterol (LDL-C) with statins reduces atherosclerosis. LDL and high-density lipoprotein (HDL) are commonly measured by their cholesterol content, but non-HDL cholesterol, LDL particle number (LDL-P), or total apolipoprotein B (apoB) may better predict cardiovascular risk. Few studies have examined relations among lipoprotein levels and composition before and after interventions to lower LDL-C and non-HDL-C. OBJECTIVE: To measure changes in carotid artery intimal media thickness (CIMT) and lipid concentration and composition during 36 months of statin therapy. METHODS: Analyses were conducted on 418 diabetic individuals, with complete data and no prior cardiovascular events, who were randomized to aggressive (AG) versus standard (STD) treatment for LDL-C, non-HDL-C, and systolic blood pressure (SBP) as part of the Stop Atherosclerosis in Native Diabetics Study (SANDS). RESULTS: The AG group achieved average LDL-C and non-HDL-C of 71mg/dL and 100mg/dL and a decrease in CIMT. No significant interactions were observed between treatment effect and initial levels of LDL-C, non-HDL-C, HDL-C, triglycerides, apoB, or LDL-P. Decreases in LDL-C (p<.005) and non-HDL-C (p<.001) were independently correlated with CIMT regression in the AG group. Changes in apoB and LDL-P showed borderline correlations with CIMT regression (p=.07 and p=.09). CONCLUSIONS: In diabetic adults with no prior cardiovascular events, treatment to current targets for lipids and SBP reduces atherosclerosis progression and when more aggressive targets are met, atherosclerosis regresses. The aggressive targets for LDL-C and non-HDL-C appeared to be the main determinants of CIMT regression and were more predictive of this outcome than changes in LDL-P or apoB.

The Stop Atherosclerosis in Native Diabetics Study (SANDS) was a randomized open‐label clinical trial in type 2 diabetics designed to examine the effects of intensive reduction of blood pressure, aggressive vs standard goals (≤115/75 mm Hg vs ≤130/80 mm Hg), and low‐density lipoprotein (LDL) cholesterol on the composite outcome of change in carotid intimal‐medial thickness and cardiovascular events. The study demonstrated that in conjunction with a lower LDL cholesterol target of 70 mg/dL, aggressive systolic blood pressure–lowering resulted in a reduction in carotid intimal‐medial thickness and left ventricular mass without measurable differences in cardiovascular events. The blood pressure treatment algorithm included renin‐angiotensin system blockade, with other agents added if necessary. The authors conclude that both standard and more aggressive systolic blood pressure reduction can be achieved with excellent safety and good tolerability in patients with type 2 diabetes mellitus.

BACKGROUND: Lowering low-density lipoprotein cholesterol (LDL-C) with statins reduces atherosclerosis. LDL and high-density lipoprotein (HDL) are commonly measured by their cholesterol content, but non-HDL cholesterol, LDL particle number (LDL-P), or total apolipoprotein B (apoB) may be better predictors of cardiovascular risk. Few studies have examined the relationship arnong lipoprotein levels and composition before and after interventions to lower LDL-C and non-HDL-C.OBJECTIVE: We sought to measure changes in carotid artery intimal media thickness (CIMT) and lipid concentration and composition during 36 months of statin therapy.METHODS: Analyses were conducted on 418 diabetic individuals, with complete data and no previous cardiovascular events, who were randomized to aggressive (AG) versus standard treatment for LDL-C, non-HDL-C, and systolic blood pressure as part of the Stop Atherosclerosis in Native Diabetics Study (SANDS).RESULTS: The AG group achieved average LDL-C and non-HDL-C of 71 mg/dL and 100 mg/dL and a decrease in CIMT. No significant interactions were observed between treatment effect and initial levels of LDL-C, non-HDL-C, HDL-C, triglycerides, apoB, or LDL-P. Decreases in LDL-C (P < .005) and non-HDL-C (P < .001) were independently correlated with CIMT regression in the AG group. Changes in apoB and LDL-P demonstrated borderline correlations with CIMT regression (P = .07 and P = .09).CONCLUSIONS: In diabetic adults with no previous cardiovascular events, treatment to current targets for lipids and systolic blood pressure reduces atherosclerosis progression and when more aggressive targets are met, atherosclerosis regresses. The aggressive targets for LDL-C and non-HDL-C appeared to be the main determinants of CIMT regression and were more predictive of this outcome than changes in LDL-P or apoB. (C) 2009 National Lipid Association. All rights reserved.

Background and Purpose— American Indians have high rates of stroke. Improved risk stratification could enhance prevention, but the ability of biochemical and echocardiographic markers of preclinical disease to improve stroke prediction is not well-defined. Methods— We evaluated such markers as predictors of ischemic stroke in a community-based cohort of American Indians without prevalent cardiovascular or renal disease. Laboratory markers included C-reactive protein, fibrinogen, urine albumin-to-creatinine ratio, and glycohemoglobin (HbA1c), whereas echocardiographic parameters comprised left atrial diameter, left ventricular mass, mitral annular calcification, and the ratio of early to late mitral diastolic velocities. Predictive performance was judged by indices of discrimination, reclassification, and calibration. Results— After adjustment for standard risk factors, only HbA1c, albuminuria, and left atrial diameter were significantly associated with first ischemic stroke. Addition of HbA1c, although not urine albumin-to-creatinine ratio, to a basic clinical model significantly improved the C-statistic (0.714 versus 0.695; P =0.044), whereas left atrial diameter modestly enhanced integrated discrimination improvement (0.90%; P =0.004), but not the C-statistic (0.701; P =0.528). When combined with HbA1c, left atrial diameter further increased integrated discrimination improvement (1.81%; P <0.001) but not the C-statistic (0.716). No marker achieved significant net reclassification improvement. Conclusions— In this cohort at high cardiometabolic risk, HbA1c emerged as the foremost predictor of ischemic stroke when added to traditional risk factors, affording substantially improved discrimination, with a more modest contribution for left atrial diameter. These findings bolster the role of HbA1c in cardiovascular risk assessment among persons with glycometabolic disorders and provide impetus for further study of the incremental value of echocardiography in high-risk populations.

CONTEXTIndividuals with diabetes are at increased risk for cardiovascular disease (CVD), but more aggressive targets for risk factor control have not been tested.OBJECTIVETo compare progression of subclinical atherosclerosis in adults with type 2 diabetes treated to reach aggressive targets of low-density lipoprotein cholesterol (LDL-C) of 70 mg/dL or lower and systolic blood pressure (SBP) of 115 mm Hg or lower vs standard targets of LDL-C of 100 mg/dL or lower and SBP of 130 mm Hg or lower.DESIGN, SETTING, AND PARTICIPANTSA randomized, open-label, blinded-to-end point, 3-year trial from April 2003-July 2007 at 4 clinical centers in Oklahoma, Arizona, and South Dakota. Participants were 499 American Indian men and women aged 40 years or older with type 2 diabetes and no prior CVD events.INTERVENTIONSParticipants were randomized to aggressive (n=252) vs standard (n=247) treatment groups with stepped treatment algorithms defined for both.MAIN OUTCOME MEASURESPrimary end point was progression of atherosclerosis measured by common carotid artery intimal medial thickness (IMT). Secondary end points were other carotid and cardiac ultrasonographic measures and clinical events.RESULTSMean target LDL-C and SBP levels for both groups were reached and maintained. Mean (95% confidence interval) levels for LDL-C in the last 12 months were 72 (69-75) and 104 (101-106) mg/dL and SBP levels were 117 (115-118) and 129 (128-130) mm Hg in the aggressive vs standard groups, respectively. Compared with baseline, IMT regressed in the aggressive group and progressed in the standard group (-0.012 mm vs 0.038 mm; P < .001); carotid arterial cross-sectional area also regressed (-0.02 mm(2) vs 1.05 mm(2); P < .001); and there was greater decrease in left ventricular mass index (-2.4 g/m(2.7) vs -1.2 g/m(2.7); P = .03) in the aggressive group. Rates of adverse events (38.5% and 26.7%; P = .005) and serious adverse events (n = 4 vs 1; P = .18) related to blood pressure medications were higher in the aggressive group. Clinical CVD events (1.6/100 and 1.5/100 person-years; P = .87) did not differ significantly between groups.CONCLUSIONSReducing LDL-C and SBP to lower targets resulted in regression of carotid IMT and greater decrease in left ventricular mass in individuals with type 2 diabetes. Clinical events were lower than expected and did not differ significantly between groups. Further follow-up is needed to determine whether these improvements will result in lower long-term CVD event rates and costs and favorable risk-benefit outcomes.TRIAL REGISTRATIONclinicaltrials.gov Identifier: NCT00047424.

Background-There are few published data on the incidence of fatal and nonfatal stroke in American Indians. The aims of this observational study were to determine the incidence of stroke and to elucidate stroke risk factors among American Indians.Methods and Results-This report is based on 4549 participants aged 45 to 74 years at enrollment in the Strong Heart Study, the largest longitudinal, population-based study of cardiovascular disease and its risk factors in a diverse group of American Indians. At baseline examination in 1989 to 1992, 42 participants (age-and sex-adjusted prevalence proportion 1132/100 000, adjusted to the age and sex distribution of the US adult population in 1990) had prevalent stroke. Through December 2004, 306 (6.8%) of 4507 participants without prior stroke suffered a first stroke at a mean age of 66.5 years. The age-and sex-adjusted incidence was 679/100 000 person-years. Nonhemorrhagic cerebral infarction occurred in 86% of participants with incident strokes; 14% had hemorrhagic stroke. The overall age-adjusted 30-day case-fatality rate from first stroke was 18%, with a 1-year case-fatality rate of 32%. Age, diastolic blood pressure, fasting glucose, hemoglobin A(1c), smoking, albuminuria, hypertension, prehypertension, and diabetes mellitus were risk factors for incident stroke.Conclusions-Compared with US white and black populations, American Indians have a higher incidence of stroke. The case-fatality rate for first stroke is also higher in American Indians than in the US white or black population in the same age range. Our findings suggest that blood pressure and glucose control and smoking avoidance may be important avenues for stroke prevention in this population.

Objectives This secondary analysis from the SANDS (Stop Atherosclerosis in Native Diabetics Study) trial examines the effects of lowering low-density lipoprotein cholesterol (LDL-C) with statins alone versus statins plus ezetimibe on common carotid artery intima-media thickness (CIMT) in patients with type 2 diabetes and no prior cardiovascular event.Background It is unknown whether the addition of ezetimibe to statin therapy affects subclinical atherosclerosis.Methods Within an aggressive group (target LDL-C <= 70 mg/dl; non-high-density lipoprotein cholesterol <= 100 mg/dl; systolic blood pressure <= 115 mm Hg), change in CIMT over 36 months was compared in diabetic individuals >40 years of age receiving statins plus ezetimibe versus statins alone. The CIMT changes in both aggressive subgroups were compared with changes in the standard subgroups (target LDL-C <= 100 mg/dl; non-high-density lipoprotein cholesterol <= 130 mg/dl; systolic blood pressure <= 130 mm Hg).Results Mean (95% confidence intervals) LDL-C was reduced by 31 (23 to 37) mg/dl and 32 (27 to 38) mg/dl in the aggressive group receiving statins plus ezetimibe and statins alone, respectively, compared with changes of 1 (-3 to 6) mg/dl in the standard group (p < 0.0001) versus both aggressive subgroups. Within the aggressive group, mean CIMT at 36 months regressed from baseline similarly in the ezetimibe (-0.025 [-0.05 to 0.003] mm) and nonezetimibe subgroups (-0.012 [-0.03 to 0.008] mm) but progressed in the standard treatment arm (0.039 [0.02 to 0.06] mm), intergroup p < 0.0001.Conclusions Reducing LDL-C to aggressive targets resulted in similar regression of CIMT in patients who attained equivalent LDL-C reductions from a statin alone or statin plus ezetimibe. Common carotid artery IMT increased in those achieving standard targets. (Stop Atherosclerosis in Native Diabetics Study [SANDS]; NCT00047424) (J Am Coll Cardiol 2008; 52: 2198-205) (C) 2008 by the American College of Cardiology Foundation

OBJECTIVE— This study analyzed which definition of the metabolic syndrome is more predictive of cardiovascular events in both diabetic and nondiabetic members of a population-based sample. RESEARCH DESIGN AND METHODS— A 10-year, longitudinal follow-up of the Strong Heart Study cohort has been evaluated. The analysis included 3,945 participants (2,384 female) with complete data (1,700 with diabetes and 1,468 with arterial hypertension) for evaluation of metabolic syndrome. Those with prevalent cardiovascular disease were excluded (n = 287, of whom 127 were female). Prevalence of metabolic syndrome was assessed based on the World Health Organization (WHO), the National Cholesterol Education Program Adult Treatment Panel (NCEP ATP) III, and International Diabetes Federation (IDF) definitions. The main outcome was 10-year incidence of combined fatal and nonfatal cardiovascular events, including stroke, coronary heart disease, and congestive heart failure. RESULTS— Fatal and nonfatal cardiovascular events occurred in 1,120 participants. After adjusting for age, sex, and diabetes, metabolic syndrome by all definitions was significantly associated with higher incidence of cardiovascular events (all P < 0.0001). In nondiabetic individuals, incident cardiovascular event rates were about 30–40% higher in those with metabolic syndrome, without a significant difference among definitions (0.03 < P < 0.001), and remained significant in WHO and NCEP ATP III definitions even after further adjustment for obesity, hypertension, and low HDL cholesterol. In the diabetic group, metabolic syndrome risk for cardiovascular events was greatest using the WHO definition (P < 0.002 vs. other models). CONCLUSIONS— In individuals without diabetes, metabolic syndrome is associated with incident cardiovascular disease, especially with WHO and NCEP ATP III definitions. Metabolic syndrome also predicts higher cardiovascular event rates in diabetic participants, a prediction that is greatest using the WHO definition.