Oxidative stress and inflammation link Life's Essential 8 with adverse cardiovascular events in adults with diabetes mellitus: NHANES 2011-2018.

In patients with diabetes, a high priority must be given to modification of the major risk factors for cardiovascular disease (CVD). There is growing evidence that control of these risk factors will reduce the likelihood of developing CVD and its complications in patients with diabetes.1 In clinical management of patients with diabetes, attention must be given to the following risk factors: smoking, hypertension, prothrombotic state, low-density lipoprotein (LDL) cholesterol and diabetic dyslipidemia, hyperglycemia, overweight/obesity, physical inactivity, and adverse nutrition. Specific considerations of Writing Group IV will be reviewed. They will be discussed in light of current recommendations for management of risk factors in diabetes as presented by the American Diabetes Association (ADA), the American Heart Association (AHA), and the national education programs sponsored by the National Heart, Lung, and Blood Institute (NHLBI).2–11⇓⇓⇓⇓⇓⇓⇓⇓⇓ These recommendations are summarized in the Table. View this table: Table 1107395. Goals for Risk Factor Management in Patients With Diabetes In addition to being a cause of many forms of cancer and chronic lung disease, cigarette smoking is a major cardiovascular risk factor. When a smoking patient also has diabetes, this patient is doubly at risk for CVD. Thus, every effort must be made to convince patients with diabetes who smoke to give up the smoking habit. This need is strongly reinforced by a position statement from the ADA.10 Elevated blood pressure is a major independent risk factor for multiple cardiovascular end points: coronary heart disease (CHD), stroke, chronic renal failure, and heart failure.11 Patients with diabetes have an increased prevalence of hypertension.12 Multiple factors undoubtedly contribute to hypertension in patients with diabetes, eg, obesity, insulin resistance, hyperinsulinemia, and renal disease. Systolic hypertension appears to be the main blood pressure–related risk factor in patients with diabetes.13 …

Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .e3 1. About These Statistics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .e7 2. American Heart Association's 2020 Impact Goals. . . . . . . . . . . . . . . . .e10 3. Cardiovascular Diseases . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . .e21 4. Subclinical Atherosclerosis . . . . . . . . . . . . . . . . . . . . .e45 5. Coronary Heart Disease, Acute Coronary Syndrome, and Angina Pectoris . . . . . . . . .e54 6. Stroke (Cerebrovascular Disease) . . . . . . . . . . . . . . . . . . . . . . . . . . . .e68 7. High Blood Pressure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . .e88 8. Congenital Cardiovascular Defects . . . . . . . . . . . . . . . . . . . . . . . . . . . .e97 9. Cardiomyopathy and Heart Failure . . . . . . . . . . . . . . . . . . . . . . . . . . . .e102 10. Disorders …

A long-standing association exists between elevated triglyceride levels and cardiovascular disease* (CVD).1,2 However, the extent to which triglycerides directly promote CVD or represent a biomarker of risk has been debated for 3 decades.3 To this end, 2 National Institutes of Health consensus conferences evaluated the evidentiary role of triglycerides in cardiovascular risk assessment and provided therapeutic recommendations for hypertriglyceridemic states.4,5 Since 1993, additional insights have been made vis-a-vis the atherogenicity of triglyceride-rich lipoproteins (TRLs; ie, chylomicrons and very low-density lipoproteins), genetic and metabolic regulators of triglyceride metabolism, and classification and treatment of hypertriglyceridemia. It is especially disconcerting that in the United States, mean triglyceride levels have risen since 1976, in concert with the growing epidemic of obesity, insulin resistance (IR), and type 2 diabetes mellitus (T2DM).6,7 In contrast, mean low-density lipoprotein cholesterol (LDL-C) levels have receded.7 Therefore, the purpose of this scientific statement is to update clinicians on the increasingly crucial role of triglycerides in the evaluation and management of CVD risk and highlight approaches aimed at minimizing the adverse public health–related consequences associated with hypertriglyceridemic states. This statement will complement recent American Heart Association scientific statements on childhood and adolescent obesity8 and dietary sugar intake9 by emphasizing effective lifestyle strategies designed to lower triglyceride levels and improve overall cardiometabolic health. It is not intended to serve as a specific guideline but will be of value to the Adult Treatment Panel IV (ATP IV) of the National Cholesterol Education Program, from which evidence-based guidelines will ensue. Topics to be addressed include epidemiology and CVD risk, ethnic and racial differences, metabolic determinants, genetic and family determinants, risk factor correlates, and effects related to nutrition, physical activity, and lipid medications. In the United States, the National Health and …

Modest Gains Confer Large Impact: Achievement of Optimal Cardiovascular Health in the US Population

Executive Summary: Heart Disease and Stroke Statistics—2011 Update

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An Institute of Medicine report titled U.S. Health in International Perspective: Shorter Lives, Poorer Health documents the decline in the health status of Americans relative to people in other high-income countries, concluding that “Americans are dying and suffering from illness and injury at rates that are demonstrably unnecessary.”1 The report blames many factors, “adverse economic and social conditions” among them. In an editorial in Science discussing the findings of the Institute of Medicine report, Bayer et al2 call for a national commission on health “to address the social causes that have put the USA last among comparable nations.” Although mortality from cardiovascular disease (CVD) in the United States has been on a linear decline since the 1970s, the burden remains high. It accounted for 31.9% of deaths in 2010.3 There is general agreement that the decline is the result, in equal measure, of advances in prevention and advances in treatment. These advances in turn rest on dramatic successes in efforts to understand the biology of CVD that began in the late 1940s.4,5 It has been assumed that the steady downward trend in mortality will continue into the future as further breakthroughs in biological science lead to further advances in prevention and treatment. This view of the future may not be warranted. The prevalence of CVD in the United States is expected to rise 10% between 2010 and 2030.6 This change in the trajectory of cardiovascular burden is the result not only of an aging population but also of a dramatic rise over the past 25 years in obesity and the hypertension, diabetes mellitus, and physical inactivity that accompany weight gain. Although there is no consensus on the precise causes of the obesity epidemic, a dramatic change in the underlying biology of Americans is …

BackgroundThe C-reactive protein-triglyceride-glucose index (CTI) has emerged as an innovative composite marker for evaluating metabolic-inflammatory dysregulation, integrating markers of insulin resistance and systemic inflammation. However, the association between CTI and cardiovascular disease (CVD) or its mortality has rarely been studied. This study sought to examine CTI's associations with CVD mortality, CVD incidence, and all-cause mortality.MethodsThis study included 8,679 adults from the National Health and Nutrition Examination Survey (NHANES) 2001–2010, 2015–2018. The CTI was derived as: 0.412* Ln (CRP [mg/L]) + Ln (TG [mg/dl] × FPG [mg/dl])/2, with participants categorized into quartiles. We employed Kaplan–Meier curves, cox proportional hazards model, logistic regression analyses, and restricted cubic spline (RCS) to evaluate CTI's associations with CVD mortality, total CVD incidence, and all-cause mortality across sex-stratified, age-specific, and glycemic subgroups.ResultsIn this study, CTI was significantly and positively associated with CVD mortality, total CVD incidence, and all-cause mortality. CTI significantly predicted both CVD mortality (HR 2.28 [1.69–3.24]) and all-cause mortality (HR 2.14 [1.76–2.55]). Additionally, the CTI index correlated with the risk of total CVD (OR 2.85, 95% CI 2.32–3.52), congestive heart failure (OR 3.66, 95% CI 2.46–5.35), coronary heart disease (OR 2.82, 95% CI 1.95–3.97), angina pectoris (OR 2.85, 95% CI 1.89–4.22), heart attack (OR 2.59, 95% CI 1.89–3.52), and stroke (OR 2.86, 95% CI 2.00–3.85). Specifically, the association was similar between male and female, and similar in young participants and elderly participants. In different glycemic status, high levels of CTI were found to be linked to an increased risk of CVD in individuals without diabetes mellitus (DM). However, this association was not observed in individuals with DM.ConclusionsOur analysis revealed that elevated CTI levels were significantly associated with CVD incidence and mortality. CTI may emerge as a unique predictive marker for CVD risk.Graphical abstractSupplementary InformationThe online version contains supplementary material available at 10.1186/s12933-025-02835-0.

Cardiovascular disease (CVD) is a leading cause of morbidity and mortality in American Indian people. In 2022, the American Heart Association developed the Life's Essential 8 goals to promote cardiovascular health (CVH) for Americans, composed of diet, physical activity, nicotine exposure, sleep, body mass index, blood lipids, blood pressure, and blood glucose. We examined whether achievement of Life's Essential 8 goals was associated with incident CVD among SHFS (Strong Heart Family Study) participants. A total of 2139 SHFS participants without CVD at baseline were included in analyses. We created a composite CVH score based on achievement of Life's Essential 8 goals, excluding sleep. Scores of 0 to 49 represented low CVH, 50 to 69 represented moderate CVH, and 70 to 100 represented high CVH. Incident CVD was defined as incident myocardial infarction, coronary heart disease, congestive heart failure, or stroke. Cox proportional hazard models were used to examine the relationship of CVH and incident CVD. The incidence rate of CVD at the 20-year follow-up was 7.43 per 1000 person-years. Compared with participants with low CVH, participants with moderate and high CVH had a lower risk of incident CVD; the hazard ratios and 95% CIs for incident CVD for moderate and high CVH were 0.52 (95% CI, 0.40-0.68) and 0.25 (95% CI, 0.14-0.44), respectively, after adjustment for age, sex, education, and study site. Better CVH was associated with lower CVD risk which highlights the need for comprehensive public health interventions targeting CVH promotion to reduce CVD risk in American Indian communities.

Health hazards of obesity have been recognized for centuries, appearing, for example, in writings attributed to Hippocrates. From the later decades of the 20th century through the present, there have been numerous epidemiological studies of the relationship between excess weight and the total, or all-cause, mortality rate,1 a critical cumulative measure of the public health impact of any health condition. Using body mass index (BMI), an indicator of relative weight for height (weight [kg]/height [m]2) and a frequently used surrogate for assessment of excess body fat, these studies have found linear, U-shaped, or J-shaped relationships between total mortality and BMI. That is, in some studies, both the thin and the obese were more likely to die than those in between. There is, however, always a point at which increasing BMI is associated with increasing mortality risk, but the BMI at which this occurs varies across studies and populations.2 Currently,3 overweight in adults is defined as a BMI of 25.0 to <30.0 kg/m2 and obesity as a BMI of ≥30.0 kg/m2 (Table 1). A number of studies have found no significant relationship between BMI in the overweight range and mortality rate4 and have shown the nadir of mortality risk to be in the overweight range. In particular, commentaries in both the lay press5–7 and scientific literature2,8,9 subsequent to recent reports from National Health and Nutrition Examination Surveys (NHANES)10,11 have highlighted the confusion and controversy regarding this issue. Some have interpreted the recent data to mean that overweight is not detrimental to health and is not in itself a public health concern and that drawing attention to the need for weight loss in this range will have negative effects on the health and well-being of the general population.8 Others have argued …

Author(s): Go, Alan S; Mozaffarian, Dariush; Roger, Veronique L; Benjamin, Emelia J; Berry, Jarett D; Blaha, Michael J; Dai, Shifan; Ford, Earl S; Fox, Caroline S; Franco, Sheila; Fullerton, Heather J; Gillespie, Cathleen; Hailpern, Susan M; Heit, John A; Howard, Virginia J; Huffman, Mark D; Judd, Suzanne E; Kissela, Brett M; Kittner, Steven J; Lackland, Daniel T; Lichtman, Judith H; Lisabeth, Lynda D; Mackey, Rachel H; Magid, David J; Marcus, Gregory M; Marelli, Ariane; Matchar, David B; McGuire, Darren K; Mohler, Emile R; Moy, Claudia S; Mussolino, Michael E; Neumar, Robert W; Nichol, Graham; Pandey, Dilip K; Paynter, Nina P; Reeves, Matthew J; Sorlie, Paul D; Stein, Joel; Towfighi, Amytis; Turan, Tanya N; Virani, Salim S; Wong, Nathan D; Woo, Daniel; Turner, Melanie B; American Heart Association Statistics Committee and Stroke Statistics Subcommittee

Microalbuminuria (MA) has been increasingly identified as a marker of cardiovascular risk. Although poor cognitive function has been implicated as a sequelae of increased cardiovascular burden, little is known about the association between MA and cognitive function. Population-based cross-sectional study. National Health and Nutrition Examination Survey 1999-2002 in the USA. 2049 noninstitutionalized adults (>/=60 years) with nonmissing values in cognitive test, urinary albumin-to-creatinine ratio (UACR) and ankle-brachial blood pressure index (ABPI) was analysed. Participants with UACR >300 microg mg(-1) were excluded. The UACR, in the unit of microg mg(-1), was calculated by dividing the urinary albumin value by the urinary creatinine concentration. MA was defined as UACR between 30 and 300 microg mg(-1). Cognitive function was measured by a 2-min Digit Symbol Substitution Test (DSST). Peripheral artery disease (PAD) was defined as an ABPI <0.9 in either leg. Overall speaking, MA was inversely associated with DSST score after controlling for age, sex, race, body mass index and educational level (regression coefficient = -2.8, P = 0.002). There was an effect modification of PAD on the association between MA and the DSST score. Amongst participants with PAD, the DSST score for those with MA was lower than those without MA (beta = -6.3, P = 0.003) after multivariate adjustment. Moreover, participants with PAD in the highest quartile of UACR had significantly lower DSST score compared to those in the lowest quartile (beta = -8.7, P = 0.001). There was no association between MA and cognitive function amongst participants without PAD. We observed an additive effect of MA and PAD on DSST score. Participants with both MA and PAD had a lower mean DSST score compared to those without both conditions (beta = -6.2, P = 0.003). The presence of MA or a higher level of urinary albumin excretion was inversely associated with cognitive function in participants with PAD.

Nonalcoholic fatty liver disease (NAFLD) is a common comorbidity in hypertension. However, the impact of NAFLD and related fibrosis on hypertension and its control of cardiovascular disease (CVD) and mortality outcomes remains unclear. Participants with hypertension were sourced from two cohorts, with 12 907 individuals from the National Health and Nutrition Examination Survey (NHANES) and 120 639 from the UK Biobank (UKBB). Mendelian randomization analyses explored the causal relationship among hypertension, NAFLD, and CVD. Cox regression models estimated the hazard ratios for CVD and mortality associated with NAFLD (defined by fatty liver index) and liver fibrosis (defined by fibrosis-4 index or NAFLD fibrosis score). The NHANES documented 3376 deaths over a median follow-up of 8.5 years, and the UKBB documented 15 864 deaths, 4062 incident ischemic strokes, and 5314 incident myocardial infarctions over a median follow-up of 13.5 years. The hazard ratios for CVD and mortality increased in accordance with NAFLD grading (ischemic stroke, 1.16 [95% CI, 1.01-1.33]; myocardial infarction, 1.64 [95% CI, 1.44-1.86] in UKBB; and all-cause mortality, 1.29 [95% CI, 1.09-1.54] in NHANES). High-risk fibrosis increased the hazard ratios for all-cause mortality by 91% and ischemic stroke by 42% in patients with NAFLD in UKBB and for all-cause mortality by 95% in NHANES. NAFLD partially mediates the risk of hypertension for incident CVD and mortality (NHANES, 6.45% of all-cause mortality; UKBB, 5.17% of all-cause mortality; and 8.20% of myocardial infarction). NAFLD and related liver fibrosis are associated with a higher risk of incident CVD and mortality in hypertensives. NAFLD and related liver fibrosis seem to partially mediate hypertension-induced CVD and mortality.

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World Kidney Day 2011: Protect Your Kidneys, Save Your Heart