Risk for myocardial infarction

Left Ventricular Hypertrophy, Subclinical Atherosclerosis, and Inflammation

Sameer K. Mehta; J. Eduardo Rame; Amit Khera; Sabina A. Murphy; Russell M. Canham; Ronald M. Peshock; James A. de Lemos; Mark H. Drazner
From the Donald W. Reynolds Cardiovascular Clinical Research Center and Divisions of Cardiology (S.K.M., J.E.R., A.K., R.M.C., R.M.P., J.A.d.L., M.H.D.), Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas; and the TIMI Study Group (S.A.M.), Boston, Mass.

To elucidate mechanisms by which left ventricular (LV) hypertrophy (LVH) increases the risk of atherosclerotic heart disease, we sought to determine whether LVH is independently associated with coronary artery calcium (CAC) and serum C-reactive protein (CRP) levels in the general population. The Dallas Heart Study is a population-based sample in which 2633 individuals underwent cardiac MRI to measure LV structure, electron beam CT to measure CAC, and measurement of plasma CRP. We used univariate and multivariable analyses to determine whether LV mass and markers of concentric LV hypertrophy or dilation were associated with CAC and CRP. Increasing quartiles of LV mass indexed to fat-free mass, LV wall thickness, and concentricity, but not LV volume, were associated with CAC in both men and women (P<0.001). After adjustment for traditional cardiovascular risk factors and statin use, LV wall thickness and concentricity remained associated with CAC in linear regression (P<0.001 for each). These associations were particularly robust in blacks. LV wall thickness and concentricity were also associated with elevated CRP levels (P=0.001 for both) in gender-stratified univariate analyses, although these associations did not persist in multivariable analysis. In conclusion, concentric LVH is an independent risk factor for subclinical atherosclerosis. LVH is also associated with an inflammatory state as reflected in elevated CRP levels, although this relationship appears to be mediated by comorbid conditions. These data likely explain in part why individuals with LVH are at increased risk for myocardial infarction.

Key Words: left ventricular hypertrophy • atherosclerosis • inflammation • myocardial infarction • coronary artery disease

Hypertension, June, 2007,Vol.49, №6; p.1385.
© 2007 American Heart Association, Inc.

Hypoadiponectinemia: Predictor of Hypertension

Hypoadiponectinemia as a Predictor for the Development of Hypertension: A 5-Year Prospective Study

Wing-Sun Chow; Bernard M.Y. Cheung; Annette W.K. Tso; Aimin Xu; Nelson M.S. Wat; Carol H.Y. Fong; Liza H.Y. Ong; Sidney Tam; Kathryn C.B. Tan; Edward D. Janus; Tai-Hing Lam; Karen S.L. Lam
From the Department of Medicine (W-S.C., B.M.Y.C., A.W.K.T., A.X., N.M.S.W., C.H.Y.F., L.H.Y.O., K.C.B.T., K.S.L.L.), the Research Centre of Heart, Brain, Hormone, and Healthy Aging (B.M.Y.C., A.X., K.C.B.T., K.S.L.L.), the Clinical Biochemistry Unit (S.T., E.D.J.), and the Department of Community Medicine (T-H.L.), University of Hong Kong, Queen Mary Hospital, Hong Kong, People’s Republic of China. Current address: Department of Medicine (E.D.J.), University of Melbourne, Western Hospital, Footscray, Australia.

Low circulating levels of adiponectin, an adipokine with insulin-sensitizing, antiatherogenic, and anti-inflammatory properties, are found in hypertensive patients. Adiponectin replenishment ameliorated hypertension in adiponectin-deficient mice or obese, hypertensive mice with hypoadiponectinemia, suggesting an etiologic role of adiponectin in hypertension.

We aimed to determine, in this 5-year prospective study, whether hypoadiponectinemia could predict the development of hypertension in a nondiabetic Chinese cohort. A total of 577 subjects (249 men and 328 women) were recruited from the population-based Hong Kong Cardiovascular Risk Factor Prevalence Study and prospectively followed up for 5 years.

The relationship of serum adiponectin with the development of hypertension (sitting blood pressure 140/90 mm Hg) was investigated in a nested case–control study consisting of 70 subjects who had developed hypertension on follow-up and 140 age- and sex-matched control subjects who were normotensive both at baseline and at year 5. At baseline, serum adiponectin level in the lowest sex-specific tertile was more likely to be associated with hypertension (P=0.003 versus the highest tertile, after adjusting for age, body mass index, fasting insulin, and high-sensitivity C-reactive protein).
At year 5, baseline serum adiponectin was a significant independent predictor of incident hypertension in the nested case–control study (P=0.015; age adjusted), together with mean arterial pressure (P<0.001), high-sensitivity C-reactive protein (P=0.018), and body mass index (P=0.004). Normotensive subjects with baseline serum adiponectin levels in the lowest sex-specific tertile had an increased risk of becoming hypertensive (adjusted odds ratio: 2.76; 95% CIs: 1.06 to 7.16; P=0.037 versus highest tertile).

Our data suggest that hypoadiponectinaemia may be involved in the pathogenesis of hypertension in humans.

Key Words: adiponectin • hypertension • Chinese • prediction • C-reactive protein

Hypertension, June, 2007,Vol.49, №6; p.1455.
© 2007 American Heart Association, Inc.

Obesity-Induced Hypertension: Activation Baroreflex

Prolonged Activation of the Baroreflex Abolishes Obesity-Induced Hypertension

Thomas E. Lohmeier; Terry M. Dwyer; Eric D. Irwin; Martin A. Rossing; Robert S. Kieval
From the Department of Physiology (T.E.L., T.M.D.), University of Mississippi Medical Center, Jackson; Trauma Services (E.D.I.), North Memorial Medical Center, Robbinsdale, Minn; and CVRx, Inc. (M.A.R., R.S.K.), Maple Grove, Minn.

Prolonged electrical activation of the carotid baroreflex produces sustained reductions in sympathetic activity and arterial pressure in normotensive dogs.
The main goal of this study was to assess the influence of prolonged baroreflex activation on arterial pressure and neurohormonal responses in 6 dogs with obesity-induced hypertension.
After control measurements, the diet was supplemented with cooked beef fat for 6 weeks, whereas sodium intake was held constant. After 4 weeks of the high-fat diet, there were increments in body weight from 25.8±0.7 to 38.6±1.0 kg, mean arterial pressure from 97±2 to 110±3 mm Hg, heart rate from 67±3 to 91±4 bpm, and plasma norepinephrine concentration from 141±35 to 280±52 pg/mL. Plasma glucose and insulin concentrations were elevated, but increases in plasma renin activity during the initial weeks of the high-fat diet were not sustained. During week 5, baroreflex activation resulted in sustained reductions in mean arterial pressure, heart rate, and plasma norepinephrine concentration; at the end of week 5, these values were 87±2 mm Hg, 77±4 bpm, and 166±45 pg/mL, respectively. These suppressed values returned to week 4 levels during a 7-day recovery period after baroreflex activation. There were no changes in plasma glucose or insulin concentrations, or plasma renin activity during prolonged baroreflex activation.
These findings indicate that baroreflex activation can chronically suppress the sympathoexcitation associated with obesity and abolish the attendant hypertension while having no effect on hyperinsulinemia or hyperglycemia.

Key Words: baroreflex • hypertension • heart rate • obesity • sympathetic nervous system • norepinephrine • renin–angiotensin system

Hypertension, June, 2007,Vol.49, №6; p.1307.
© 2007 American Heart Association, Inc.

Hypertension and Polycystic ovary syndrome

Relationship Between Androgen Levels and Blood Pressure in Young Women With Polycystic Ovary Syndrome

Mei-Jou Chen; Wei-Shiung Yang; Jehn-Hsiahn Yang; Chi-Ling Chen; Hong-Nerng Ho; Yu-Shih Yang
Departments of Obstetrics and Gynecology (M.-J.C., J.-H.Y., H.-N.H., Y.-S.Y.) and Internal Medicine (W.-S.Y.), National Taiwan University Hospital, Taipei, Taiwan, Republic of China; Graduate Institute of Clinical Medicine (M.-J.C., W.-S.Y., C.-L.C.), College of Medicine, National Taiwan University, Taipei, Taiwan, Republic of China; and the Institute of Biomedical Science (W.-S.Y.), Academia Sinica, Taipei, Taiwan, Republic of China

The role of testosterone on the development of hypertension is controversial, especially in women with polycystic ovary syndrome (PCOS) who have higher prevalence of obesity and insulin resistance than women without PCOS.
Little is known about the association between serum testosterone level and blood pressure in young women with PCOS. In the 151 young Taiwanese women with PCOS enrolled in this cross-sectional study, we measured the body mass index, waist circumference, blood pressure, fasting glucose, fasting insulin, lipid profile, and hormone profiles. The free androgen index, total testosterone, and sex hormone-binding globulin, but not the level of dehydroepiandrosterone sulfate, significantly correlated with both systolic blood pressure (SBP) and diastolic blood pressure (DBP).
In multiple linear regression models adjusted for age, body mass index, and other anthropometric, metabolic, and hormonal variables, the level of serum free androgen index or total testosterone, but not the sex hormone-binding globulin, were independently related to SBP and DBP. The age- and body mass index–adjusted least-square mean of serum-free androgen index levels were significantly different between the highest quartile and other quartiles of the SBP and DBP levels. The high bioavailable testosterone levels (free androgen index: 19%) in women with PCOS increased the risk of elevated blood pressure (SBP 130 mm Hg and/or DBP 85 mm Hg) with an odds ratio of 3.817 (P=0.029; 95% CI: 1.14 to 12.74) after adjustment for age, anthropometric measures, and metabolic profiles.
Our results suggest that the characteristic hyperandrogenemia in young women with PCOS was associated with an elevated SBP and DBP independent of age, insulin resistance, obesity, or dyslipidemia.

Key Words: polycystic ovary syndrome • testosterone • systolic blood pressure • diastolic blood pressure • hypertension

Hypertension, June, 2007,Vol.49, №6; p.1442.
© 2007 American Heart Association, Inc.

Maternal smoking in pregnancy

Similar Associations of Parental Prenatal Smoking Suggest Child Blood Pressure Is Not Influenced by Intrauterine Effects

Marie-Jo A. Brion; Sam D. Leary; George Davey Smith; Andy R. Ness
Departments of Social Medicine (M.-J.A.B., S.D.L., G.D.S.) and Oral and Dental Science (A.R.N.), University of Bristol, Bristol, United Kingdom

Maternal smoking in pregnancy may be associated with higher offspring blood pressure; however, results of previous studies have been inconsistent and included varying confounder adjustments.
We studied the association between maternal smoking in pregnancy and offspring blood pressure at 7 years in the Avon Longitudinal Study of Parents and Children, accounting for important social and environmental confounders and using partner smoking to investigate intrauterine effects.
Analysis was carried out in 6509 children with maternal smoking data and 7149 children with partner smoking data. In models adjusting for child age and sex, modest differences in systolic blood pressure were observed between children of mothers who did and did not smoke during pregnancy (ß=0.64 mm Hg; 95% CI: 0.09 to 1.20; P=0.02). Adjusting for all of the confounders attenuated this difference toward the null (ß=0.05 mm Hg; 95% CI: –0.59 to 0.68; P=0.9), mostly because of adjustment for breastfeeding, maternal education, and family social class.
Associations were similar between maternal and partner smoking with offspring systolic blood pressure (for partner smoking: ß=0.62 mm Hg; 95% CI: 0.17 to 1.07; P=0.07 minimally adjusted and ß=0.26 mm Hg; 95% CI: –0.36 to 0.87; P=0.4 fully adjusted), providing further evidence that differences in child blood pressure observed in minimally adjusted models are not because of a biological influence of maternal smoking on the intrauterine environment.

Keywords: ALSPAC • blood pressure • child • confounding factors (epidemiology), cohort • maternal smoking • prenatal exposure delayed effects

Hypertension, June, 2007,Vol.49, №6; p.1422.
© 2007 American Heart Association, Inc.