ISSN:0194-911X    

出版商:OVID    

年代:2002

数据来源: OVID

ISSN:0194-911X    

出版商:OVID    

年代:2002

数据来源: OVID

ISSN:0194-911X    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

Abstract—Obesity has become an increasingly important medical problem in children and adolescents. In national surveys from the 1960s to the 1990s, the prevalence of overweight in children grew from 5% to 11%. Outcomes related to childhood obesity include hypertension, type 2 diabetes mellitus, dyslipidemia, left ventricular hypertrophy, nonalcoholic steatohepatitis, obstructive sleep apnea, orthopedic problems, and psychosocial problems. Once considered rare, primary hypertension in children has become increasingly common in association with obesity and other risk factors, including a family history of hypertension and an ethnic predisposition to hypertensive disease. Obese children are at approximately a 3-fold higher risk for hypertension than nonobese children. In addition, the risk of hypertension in children increases across the entire range of body mass index (BMI) values and is not defined by a simple threshold effect. As in adults, a combination of factors including overactivity of the sympathetic nervous system (SNS), insulin resistance, and abnormalities in vascular structure and function may contribute to obesity-related hypertension in children. The benefits of weight loss for blood pressure reduction in children have been demonstrated in both observational and interventional studies. Obesity in childhood should be considered a chronic medical condition that is likely to require long-term management. Ultimately, prevention of obesity and its complications, including hypertension, is the goal.

ISSN:0194-911X    

出版商:OVID    

年代:2002

数据来源: OVID

ISSN:0194-911X    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

Abstract—The present study explored the possibility that estrogen may enhance the inhibitory effect of an angiotensin (Ang) II type 1 (AT1) receptor blocker on neointima formation in vascular injury, and investigated the signaling mechanism involved in their actions. Polyethylene cuff placement around the femoral artery of mice induced neointima formation and increased bromodeoxyuridine (BrdU) incorporation into vascular smooth muscle cells. These changes were significantly smaller in female mice than in male mice. Ovariectomy enhanced neointima formation and BrdU incorporation in the injured artery, which were reversed by 17&bgr;-estradiol (80 &mgr;g/kg per day) replacement. Treatment with a selective AT1receptor blocker, olmesartan (3 mg/kg per day), significantly inhibited neointima formation and BrdU incorporation, whereas the inhibitory effects of olmesartan were more marked in intact female mice than in male or ovariectomized mice. Phosphorylation of extracellular signal–regulated kinase (ERK), signal transducer and activator of transcription (STAT) 1, and STAT3 was increased in the injured artery. These increases were significantly smaller in intact female mice than in male or ovariectomized mice. Olmesartan or estrogen attenuated the phosphorylation of ERK and STAT in the injured artery, whereas these inhibitory effects were greater in intact female mice. Lower doses of olmesartan (0.5 mg/kg per day) or 17&bgr;-estradiol (20 &mgr;g/kg per day) did not influence neointima formation, BrdU incorporation, and ERK and STAT phosphorylation in ovariectomized mice, whereas coadministration of olmesartan and 17&bgr;-estradiol at these doses attenuated these parameters. These results indicate that estrogen and an AT1receptor blocker synergistically attenuate vascular remodeling, which is at least partly via inhibition of ERK and STAT activity.

ISSN:0194-911X    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

Abstract—Impaired fasting glucose (fasting plasma glucose 6.1 to 6.9 mmol/L [110 to 125 mg/dL]) is a common glycemic disorder which usually progress to diabetes mellitus. The relationships between impaired fasting glucose, other risk factors including blood pressure, and mortality have never been clearly investigated. We studied 63 443 consecutive men (ages 21 to 60 years), each of whom had a routine health examination with a fasting plasma glucose measurement. Men with known ischemic cardiac disease and treatment for diabetes or hypertension were excluded. Impaired fasting glucose was found in 10 773 (17.0%) of these men. Mean body mass index, serum triglyceride and cholesterol levels, and systolic, diastolic, and pulse blood pressure were significantly higher for men with impaired fasting glucose compared with those men with normal fasting glucose (fasting plasma glucose 3.9 to 6.0 mmol/L). When adjusted for confounding variables, relative risk of 8-year cardiovascular mortality associated with impaired fasting glucose was dependent on systolic blood pressure level (1.02 [95% CI: 0.62 to 1.70] when <140 mm Hg and 2.10 [95% CI: 1.16 to 3.80] between 140 and 160 mm Hg). Inversely, relative risk of 8-year cardiovascular mortality associated with moderate systolic hypertension (140 to 159 mm Hg) compared with normal systolic blood pressure (<140 mm Hg) was highly dependent on the glycemic status (2.97 [95% CI: 1.58 to 5.55] for men with impaired fasting glucose compared with 1.35 [95% CI: 0.84 to 2.18] in those with normal fasting glucose). Similar results were found concerning overall mortality. In conclusion, the presence of moderate systolic hypertension can identify subjects with impaired fasting glucose who are at risk of cardiovascular and overall mortality, and vice versa, probably through the metabolic syndrome.

ISSN:0194-911X    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

Abstract—Several clinical trials using a blood pressure (BP) treatment algorithm focused on a predetermined goal have achieved better control rates than those of national survey data. These trials reached the Sixth Joint National Committee on the Prevention, Detection, Evaluation and Treatment of High Blood Pressure (JNC VI) diastolic blood pressure (DBP) goal of <90 mm Hg in >90% of volunteers and systolic blood pressure (SBP) goal of <140 mm Hg in >60% of volunteers. We evaluated BP control of 437 consecutive patients after at least one year of follow up in a specialist clinic which employed “goal-oriented management,” ie, treating to a specific BP goal without a formal drug treatment algorithm, to determine whether JNC VI goals could be achieved. Overall, 276 (63%) patients achieved SBP goal, with 376 (86%) at DBP goal and 358 (59%) at both goals. Only 23% of patients were on monotherapy, with 34% requiring 2 drugs and 37% requiring 3 or more medications. There was no substantial difference in BP control rates among age, gender, and ethnicity subgroups. However, in the 20% of patients who were diabetic, only 52% had a BP of <140 mm Hg and <90 mm Hg, whereas fewer (22% and 15%, respectively) achieved the more stringent goals of JNC VI and the American Diabetic Association (ADA)/National Kidney Foundation (NKF). Goal-oriented management achieved dramatically better control rates than what is reported. Although DBP control was easy to achieve, achieving SBP goal still remained difficult. Employing goal-oriented management can translate BP control results achieved in clinical trials into outpatient practice.

ISSN:0194-911X    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

Abstract—To evaluate the prognostic impact of left ventricular (LV) mass exceeding individual needs to compensate hemodynamic load, the percentage of excess of echocardiographic LV mass in relation to individual ideal value predicted by gender, stroke work, and height (in meter2.7) from a reference population was assessed in 1019 white hypertensives (627 women [24% obese] and 392 men [17% obese,P<0.02 versus women]) without prevalent cardiovascular disease or type 1 diabetes, from the Italian multicenter, prospective study MAVI. Low LV mass (<73% of predicted) was found in 36 patients (3.5%), 661 had appropriate LV mass, and 322 (37%) had inappropriate LV mass. During follow-up (35±11 months), 52 fatal or nonfatal primary cardiovascular events occurred. Age, systolic blood pressure, and LV mass as a percentage of the predicted value were significant predictors of cardiovascular events (allP<0.01), independently of gender, glycemia, antihypertensive treatments, and body mass index, even in subgroups with or without LV hypertrophy. Survival analysis showed that cardiovascular risk increased stepwise from the lowest to the highest quintile of LV mass as a percentage of predicted value (P<0.01). The excess LV mass showed incremental prognostic value compared with assessment of traditional LV mass (P<0.01). Thus, inappropriate LV mass predicts a risk of cardiovascular events, independently of risk factors, and remains a significant predictor of risk either in the presence or in the absence of traditionally defined LV hypertrophy.

ISSN:0194-911X    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

Abstract—Increased reactive oxygen species (ROS) production is implicated in the pathophysiology of left ventricular (LV) hypertrophy and heart failure. However, the enzymatic sources of myocardial ROS production are unclear. We examined the expression and activity of phagocyte-type NADPH oxidase in LV myocardium in an experimental guinea pig model of progressive pressure-overload LV hypertrophy. Concomitant with the development of LV hypertrophy, NADPH-dependent O2−production in LV homogenates, measured by lucigenin (5 &mgr;mol/L) chemiluminescence or cytochrome c reduction assays, significantly and progressively increased (by ≈40% at the stage of LV decompensation;P<0.05). O2−production was fully inhibited by diphenyleneiodonium (100 &mgr;mol/L). Immunoblotting revealed a progressive increase in expression of the NADPH oxidase subunits p22phox, gp91phox, p67phox, and p47phoxin the LV hypertrophy group, whereas immunolabeling studies indicated the presence of oxidase subunits in cardiomyocytes and endothelial cells. In parallel with the increase in O2−production, there was a significant increase in activation of extracellular signal–regulated kinase 1/2, extracellular signal–regulated kinase 5, c-Jun NH2-terminal kinase 1/2, and p38 mitogen-activated protein kinase. These data indicate that an NADPH oxidase expressed in cardiomyocytes is a major source of ROS generation in pressure overload LV hypertrophy and may contribute to pathophysiological changes such as the activation of redox-sensitive kinases and progression to heart failure.

ISSN:0194-911X    

出版商:OVID    

年代:2002

数据来源: OVID