Risk Factors for Arterial Hypertension in Adults With Initial Optimal Blood Pressure

Whether metabolic factors and their change over time influence development of arterial hypertension in adults with initially optimal blood pressure (BP) is unknown. We analyzed associations of BP in the optimal range (<120/80 mm Hg), metabolic risk factors, and their changes over 4-year follow-up, with 8-year incident hypertension, in a cohort of American Indians with a high prevalence of obesity. At baseline, 967 participants with optimal BP and no prevalent cardiovascular disease (69.5% women; mean age, 54±7 years) were evaluated and reexamined after 4 (second examination) and 8 years to evaluate predictors of 8-year incident arterial hypertension. In participants with normal glucose tolerance, baseline BP and decrease in high-density lipoprotein cholesterol from baseline to the second examination were the most potent predictors of 8-year arterial hypertension (both P <0.0001), with additional effects of baseline waist circumference and its increase, increase in BP, and presence of diabetes at the second examination (all P <0.04). In participants with impaired glucose tolerance or diabetes, the most potent predictor of 8-year incident hypertension was diabetes at the second examination ( P <0.0001) followed by a increase in BP and LDL cholesterol over the first 4 years (both P <0.001). Thus, incident arterial hypertension can be predicted by initial metabolic profile and unfavorable metabolic variations over time, in addition to initial BP. At optimal levels of initial BP, increasing abdominal obesity, and abnormal lipid profile are major predictors of development of arterial hypertension. Possible implications of these findings for primary cardiovascular prevention should be tested in prospective studies

Markers of Inflammation, Metabolic Risk Factors, and Incident Heart Failure in American Indians: The Strong Heart Study

Inflammation may play a role in increased risk of heart failure (HF) that is associated with obesity, metabolic syndrome (MS), and diabetes. This study investigated associations between inflammatory markers, MS, and incident HF in a population with high prevalence of diabetes, obesity, and MS. The cohort consisted of 3098 American Indians, without prevalent cardiovascular disease who had C-reactive protein (CRP) and fibrinogen measured at the SHS Phase II exam. Independent associations between inflammatory markers, MS, and HF were analyzed by Cox hazard models. During mean follow-up of 11 years, 218 participants developed HF. After the adjustment for cardiovascular risk factors, fibrinogen, (HR 1.36, 95% C.I.:1.15–1.59) but not CRP, (HR 1.25, 95% C.I.:0.97–1.32) remained significant HF predictor. In individuals without diabetes, concomitant presence of MS and elevated CRP or fibrinogen increased HF risk (for MS and CRP: HR 2.02, 95% C.I.: 0.95–4.31; for CRP and fibrinogen: HR 1.75, 95% C.I.:0.83–3.72). In a population with high prevalence of obesity, MS, and diabetes, elevated CRP and fibrinogen predict increased HF risk. These associations are attenuated by the adjustments for conventional risk factors suggesting that inflammation acts in concert with metabolic and clinical risk factors in increasing HF risk

Genetic influence on variation in serum uric acid in American Indians: the strong heart family study

Hyperuricemia is associated with the metabolic syndrome, gout, renal and cardiovascular disease (CVD). American Indians have high rates of CVD and 25 % of individuals in the Strong Heart Family Study (SHFS) have high serum uric acid levels. The aim of this study was to investigate the genetic determinants of serum uric acid variation in American Indian participants of the SHFS. A variance component decomposition approach (implemented in SOLAR) was used to conduct univariate genetic analyses in each of three study centers and the combined sample. Serum uric acid was adjusted for age, sex, age*sex, BMI, estimated glomerular filtration rate, alcohol intake, diabetic status and medications. Overall mean ± SD serum uric acid for all individuals was 5.14 ± 1.5 mg/dl. Serum uric acid was found to be significantly heritable (0.46 ± 0.03 in all centers, and 0.39 ± 0.07, 0.51 ± 0.05, 0.44 ± 0.06 in Arizona, Dakotas and Oklahoma, respectively). Multipoint linkage analysis showed significant evidence of linkage for serum uric acid on chromosome 11 in the Dakotas center (logarithm of odds score (LOD) = 3.02) and in the combined sample (LOD = 3.56) and on chromosome 1 (LOD = 3.51) in the combined sample. A strong positional candidate gene in the chromosome 11 region is solute carrier family22, member 12 (SLC22A12) that encodes a major uric acid transporter URAT1. These results show a significant genetic influence and a possible role for one or more genes on chromosomes 1 and 11 on the variation in serum uric acid in American Indian populations