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Objectives: The aim of this study was to compare the impact of the European Society of Hypertension Guidelines 2016 (ESHG2016) and the American Academy of Pediatrics Guidelines 2017 (AAPG2017) on the screening of hypertension and classification of abnormal left ventricular geometry (ALVG) in overweight/obese youth., Methods: This study included 6137 overweight/obese youth; 437 had echocardiographic assessment. Hypertension was defined using either ESHG2016 or AAPG2017. ALVG was defined using 95th percentile for age and sex of left ventricular mass index (LVMi) and/or relative wall thickness (RWT) more than 0.38 (juvenile cut-offs) according to ESHG2016 or LVMi more than 51 g/h and/or RWT more than 0.42 (adult cut-offs) according to AAPG2017., Results: Prevalence of youth at a high risk of hypertension was 13% higher using AAPG2017 than ESHG2016. The increase was larger in overweight youth at least 13 years of age (+43%). Using the juvenile cut-offs for ALVG, youth at a high risk of hypertension by ESHG2016 had an odds ratio [95% confidence interval (95% CI)] of 3.03 (1.31-7.05) for left ventricular concentric remodelling (LVcr) and 2.53 (1.43-4.47) for concentric left ventricular hypertrophy (cLVH) as compared with youth with normal LVG. Similarly, in youth at a high risk of hypertension by AAPG2017, the odds ratio for LVcr was 3.28 (1.45-7.41, P < 0.001) and 3.02 (95% CI: 1.73-5.27, P < 0.001) for cLVH. Using the adult cut-offs, no significant difference in ALVG was found with both guidelines., Conclusion: The prevalence of overweight/obese youth at a high risk of hypertension increased by 13% comparing AAPG2017 vs. ESHG2016. The juvenile cut-offs for ALVG were more effective than the adult criteria in intercepting individuals with a potentially higher cardiovascular risk.

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.

Objective: Metabolic abnormalities have been shown to predict 8-year incident arterial hypertension in individuals with optimal blood pressure. As echocardiographic left ventricular mass has also been reported to predict incident hypertension in individuals with baseline blood pressure of less than 140/90 mmHg, we determined whether left ventricular mass predicts 4-year incident hypertension also in individuals with initial optimal blood pressure (<120/80 mmHg), independent of metabolic factors influencing blood pressure., Methods: We studied 777 of 3257 members of the American Indian population-based Strong Heart Study cohort with optimal blood pressure (34% men, 45% obese, and 35% diabetic), aged 57 +/- 7 years, and without prevalent cardiovascular disease., Results: Over 4 years, 159 individuals (20%, group H) developed hypertension (blood pressure >/=140/90 mmHg). They had a greater baseline BMI, waist girth, and blood pressure (112/69 vs. 109/68 mmHg, all P < 0.03) than those remaining normotensive (group N), with similar lipid profile and renal function. At baseline, left ventricular mass was significantly greater in group H than in group N (P < 0.004). The difference in left ventricular mass was confirmed after controlling for initial BMI, systolic blood pressure, homeostatic model assessment index, and diabetes. The probability of incident hypertension increased by 36% for each standard deviation of left ventricular mass index (P = 0.006), independent of covariates. Participants with left ventricular mass of more than 159 g (75th percentile of distribution) had 2.5-fold (95% confidence interval, 1.4-3.6; P < 0.001) higher adjusted risk of incident hypertension than those below this value., Conclusion: Left ventricular mass predicts incident arterial hypertension in individuals with initially optimal blood pressure. This association is independent of body build, prevalent diabetes, and initial blood pressure.

Background: Left ventricular wall motion (WM) abnormalities have recognized prognostic significance in patients with coronary or other heart diseases; however, whether abnormal WM predicts adverse events in adults without overt cardiovascular disease has not been assessed. Our objective was to determine whether echocardiographic WM abnormalities predict subsequent cardiovascular events in a population-based sample., Methods and Results: Participants (n=2864, mean age 60+/-8 years, 64% women) without clinically evident cardiovascular disease in the second Strong Heart Study examination who had complete echocardiographic WM assessment were studied. Echocardiographic assessment revealed that 5% of participants (n=140) had focal hypokinesia, and 1.5% (n=42) had WM abnormalities. Relationships between WM abnormalities and fatal and nonfatal cardiovascular events (including myocardial infarction, stroke, coronary artery disease, and heart failure; n=554) and cardiovascular death (n=182) during 8+/-2 years follow-up were examined. In Cox regression, after adjustment for age, gender, waist/hip ratio, systolic blood pressure, and diabetes mellitus, segmental WM abnormalities were associated with a 2.5-fold higher risk of cardiovascular events and a 2.6-fold higher risk of cardiovascular death (both P<0.0001). In similar multivariable models, global WM abnormalities were associated with a 2.4-fold higher risk of cardiovascular events (P=0.001) and a 3.4-fold higher risk of cardiovascular death (P=0.003)., Conclusions: Echocardiographic left ventricular WM abnormalities in adults without overt cardiovascular disease are associated with 2.4- to 3.4-fold higher risks of cardiovascular morbidity and mortality, independent of established risk factors.

Background: It has been suggested that the trophic effects of insulin may contribute to left ventricular (LV) hypertrophy in hypertension, but few population-based data exist to assess the potential impact of insulin level on LV structure or systolic function., Methods: Fasting plasma insulin levels (log-transformed) in 1,542 nondiabetic African American or white hypertensive participants in the Hypertension Genetic Epidemiology Network (HyperGEN) study were compared to indices of LV geometry and function, with adjustment for potential confounders (age, sex, ethnicity, blood pressure (BP), body mass index, height and antihypertensive drugs)., Results: In simple correlation analysis, a weak positive relation (r = 0.078, P =.002) was found between LV mass and insulin, principally due to positive correlations (r = 0.22 and 0.50) of both variables to body mass index. Multivariate analysis, adjusting for age, sex, ethnicity, body size, systolic BP, and antihypertensive drugs revealed a modest negative relation between insulin and LV mass (r = -0.08, P =.001) due to a negative relationship between insulin with LV chamber size (r = - 0.10, P <.001) and no significant relation to LV wall thicknesses. These results were confirmed in additional analysis controlling for a positive relation (r =.19, P <.0001) of insulin to heart rate, and the relation with insulin became slightly more negative when LV mass was indexed for height(2.7) (r = -0.13, P <.001). After adjustment for covariates, there were no significant relations of insulin to LV ejection fraction or stress-corrected midwall shortening; however, insulin was negatively related to stroke volume (r = -0.12, p < 0.001) and was weakly related positively to relative wall thickness (r =.053) (P =.04)., Conclusions: After adjustment for body mass index and other covariates, insulin in nondiabetic hypertensive individuals has weak negative relations to LV chamber size, mass, and stroke volume, and also has weak positive relations to relative wall thickness but not to measures of LV systolic function. Thus, native plasma insulin level may not play a major independent role in the pathogenesis of hypertensive LV hypertrophy or dysfunction.

The impact of different methods of indexation of left ventricular (LV) mass and systemic hemodynamic variables on prevalences and correlates of cardiovascular abnormalities in relation to level of obesity in populations remains unclear. We evaluated 1,672 participants in the Hypertension Genetic Epidemiology Network Study to investigate the relations of overweight and level of obesity to LV mass and prevalences of LV hypertrophy, abnormal cardiac output, and peripheral resistance detected using different indexations for body size. In our study population, 1,577 subjects were clinically healthy nondiabetic hypertensive and 95 were normotensive normal-weight nondiabetic reference subjects. Fat-free mass (FFM) did not differ between the reference group and the normal-weight hypertensive subjects, and increased with overweight. In hypertensive subjects, LV mass and cardiac output increased and total peripheral resistance decreased with overweight. Indexation of LV mass for FFM or body surface area (BSA) resulted in no difference or even lower prevalence of LV hypertrophy in severely obese compared with normal-weight hypertensive subjects. In contrast, indexation of LV mass for height(2.7) identified an increased prevalence of LV hypertrophy with overweight and obesity. Absolute cardiac output increased and total peripheral resistance decreased with overweight. Prevalence of elevated cardiac output indexed for height(1.83) increased and for elevated total peripheral resistance-height(1.83) index decreased with greater overweight, whereas opposite trends were seen when cardiac output and total peripheral resistance were indexed for BSA or FFM. Thus, in hypertensive subjects, FFM increases with overweight and is directly related to LV mass, stroke volume, and cardiac output, and inversely related to total peripheral resistance. Indexations of LV mass and systemic hemodynamics for FFM or BSA obscured associations of LV hypertrophy and abnormal cardiac and total peripheral resistance indexes with overweight, whereas LV mass/height(2,7), cardiac output/height(1.83), and total peripheral resistance-height(1.83) detected significant preclinical cardiovascular abnormalities with obesity.

Background: Although cardiac output (CO) plays the vital role of delivering nutrients to body tissues, few data are available concerning the relations of stroke volume (SV) and CO to body composition in large population samples., Methods and Results: Doppler and 2D echocardiography and bioelectric impedance in 2744 Strong Heart Study participants were used to calculate SV and CO and to relate them to fat-free body mass (FFM), adipose mass, and demographic variables. Both SV and CO were higher in men than women and in overweight than normal-weight individuals, but these differences were diminished or even reversed by normalization for FFM or body surface area. In both sexes, SV and CO were more strongly related to FFM than adipose mass, other body habitus measures, arterial pressure, diabetes, or age. In multivariate analyses using the average of Doppler and left ventricular SV to minimize measurement variability, FFM was the strongest correlate of SV and CO; other independent correlates were adipose mass, systolic pressure, diabetes, age, and use of digoxin and calcium channel and beta-blockers., Conclusions: In a population-based sample, SV and CO are more strongly related to FFM than other variables; increased FFM may be the primary determinant of increased SV and CO in obesity.