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:

Damage of large arteries is a major factor in the high cardiovascular morbidity and mortality of patients with end-stage renal disease (ESRD). Increased aortic pulse wave velocity (PWV) and brachial pulse pressure (PP) are the principal arterial markers of cardiovascular mortality described in these patients. Whether central (carotid) PP and brachial-carotid PP amplification may predict all-cause (including cardiovascular) mortality has never been investigated. A cohort of 180 patients with ESRD who were undergoing hemodialysis was studied between January 1990 and March 2000. The mean duration of follow-up was 52±36 months (mean±SD). Mean age at entry was 51.5±16.3 years. Seventy deaths occurred, including both cardiovascular and noncardiovascular fatal events. At entry, patients underwent carotid PP measurements (pulse wave analysis), echocardiography, and aortic PWV (Doppler ultrasonography), together with standard clinical and biochemical analyses. On the basis of Cox analyses, after adjustment of age, time on dialysis before inclusion, and previous cardiovascular events, 3 factors emerged as predictors of all-cause mortality: carotid PP, brachial/carotid PP, and aortic PWV. Adjusted hazard ratios for 1-SD increments were 1.4 (1.1 to 1.8) for carotid PP, 0.5 (0.3 to 0.8) for brachial/carotid PP, and 1.3 (1.0 to 1.7) for PWV. Brachial blood pressure, including PP, had no predictive value for mortality after adjustment. These results provide the first direct evidence that in patients with ESRD, the carotid PP level and, mostly, the disappearance of PP amplification are strong independent predictors of all-cause (including cardiovascular) mortality.

ISSN:0194-911X    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

Left ventricular hypertrophy has been suggested to mediate the relation between hypertension and left atrial enlargement, with associated risks of atrial fibrillation and stroke. However, less is known about correlates of left atrial size in hypertensive patients with left ventricular hypertrophy. We assessed left atrial size by echocardiography in 941 hypertensive patients, age 55 to 80 (mean, 66) years, with electrocardiographic left ventricular hypertrophy at baseline in the Losartan Intervention For Endpoint reduction in hypertension study. Enlarged left atrial diameter (women, >3.8 cm; men, >4.2 cm) was present in 56% of women and 38% of men (P<0.01). Compared with the 512 patients with normal left atrial size, the 429 patients with enlarged left atrium more often had mitral regurgitation, atrial fibrillation, and echocardiographic left ventricular hypertrophy. They also had higher age, systolic blood pressure, pulse pressure, weight, body mass index, left ventricular internal chamber dimension, stroke volume, and mass and lower relative wall thickness and ejection fraction (all,P<0.05). In logistic regression analysis, left atrial enlargement was related to left ventricular hypertrophy and eccentric geometry; greater body mass index, systolic blood pressure, and age; female gender; mitral regurgitation; and atrial fibrillation (all,P<0.05). Thus, left atrial size in hypertensive patients with electrocardiographic left ventricular hypertrophy is influenced by gender, age, obesity, systolic blood pressure, and left ventricular geometry independently of left ventricular mass and presence of mitral regurgitation or atrial fibrillation.

ISSN:0194-911X    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

Previous studies have shown that in the population, only a minority of treated hypertensive patients achieve blood pressure (BP) control. Whether and to what extent this inadequate control has reflection on hypertension-related organ damage has never been systematically examined. In 2051 subjects belonging to the PAMELA (Pressioni Arteriose Monitorate E Loro Associazioni) Study population, we measured office, home, and 24-hour ambulatory BP values, together with echocardiographic left ventricular mass and wall thickness. Based on the fraction on antihypertensive treatment and on measurements of increased or normal office, home, or 24-hour ambulatory BP values, subjects were classified as normotensives, untreated hypertensives, treated hypertensives with inadequate BP control, and treated hypertensives with effective BP control. Compared with values in the normotensive group, left ventricular mass index, left ventricular wall thickness, and prevalence of left ventricular hypertrophy were markedly increased not only in untreated hypertensive patients but also in treated hypertensives with inadequate BP control. Echocardiographic abnormalities were less in treated hypertensives with BP control than in patients with inadequate BP control, but values were still clearly greater than in normotensive subjects. This was the case regardless whether BP control was assessed by office, home, and/or ambulatory values. Our data provide evidence that in the hypertensive fraction of the population, cardiac structural alterations can be frequently found in both the presence and absence of antihypertensive treatment. They also imply that even effective treatment of hypertension does not allow complete reversal of the cardiac organ damage characterizing high BP states.

ISSN:0194-911X    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

Left ventricular hypertrophy is associated with significant excess mortality and morbidity. The study and treatment of this condition, in particular the prognostic implications of changes in left ventricular mass, require an accurate, safe, and reproducible method of measurement. Cardiovascular magnetic resonance is a suitable tool for this purpose, and this review assesses the technique in comparison with others and examines the clinical and research implications of the improved reproducibility.

ISSN:0194-911X    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

The renin-angiotensin-aldosterone-system appears to be involved in the development of cardiac fibrosis in rodents, characterized by nonepithelial cell proliferation and changes in the extracellular matrix. The aim of our study was to investigate the effect of high aldosterone concentrations on the proliferation of human cardiac interstitial cells in vitro. In addition, the effect of d-glucose as another risk factor for fibrosis, eg, in the diabetic heart, was investigated. Human cardiac myofibroblast cultures were established, and growth rates were measured by WST-1 assay in fetal calf serum-free Dulbecco’s modified Eagle’s medium (DMEM). Cells in culture showed a significant increase in number between 24 to 72 hours of cultivation under basal conditions (DMEM, 10% fetal calf serum). Aldosterone at high concentrations (10−8and 10−7mol/L) significantly (P<0.01) increased the proliferation of cultured cardiac myofibroblasts. Comparable effects were observed after incubation of the cells with high d-glucose concentrations (15 and 25 mmol/L,P<0.01). No additive growth stimulation was evident when the cells were incubated in medium containing both aldosterone and d -glucose. These results suggest a role for aldosterone and glucose in mediating the cardiac fibrosis through stimulation of myofibroblast growth in patients with dysregulated renin-angiotensin-aldosterone-system (especially hyperaldosteronism) and impaired glucose homeostasis.

ISSN:0194-911X    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

Previous works have shown that exaggerated blood pressure response to exercise is a valid risk marker for future hypertension, yet the use of an exercise test as a means of early prediction of hypertension still requires methodological development and confirmation. The purpose of this study was to determine abnormal ranges of blood pressure responses in relation to heart rate increase during exercise and to examine the clinical utility of exercise blood pressure measurement in evaluating individual risk for developing hypertension. We examined exercise test data from a population-based sample of 1033 nonmedicated normotensive men (mean age, 42.9±8.5 years; range, 20 to 59 years). Percentile curves of systolic and diastolic blood pressure responses to relative heart rate increments during submaximal exercise were constructed using a third-order polynomial model with multiple regression analysis. Of the original study sample, a cohort of 726 subjects was followed for hypertensive outcome for an average period of 4.7 years. Progression to hypertension, defined as a blood pressure of ≥140/90 mm Hg or the initiation of antihypertensive therapy, was found in 114 subjects (15.4%). Kaplan-Meier survival estimates showed that the cumulative incidence of hypertension increased progressively with higher percentiles of systolic and diastolic blood pressure response (both,P<0.01). A Cox proportional survival analysis revealed a significantly increased risk for developing hypertension associated with exaggerated blood pressure response to exercise after multivariable adjustments for traditional risk factors (relative risk, 3.8; 95% confidence interval, 2.3 to 6.1). These results suggest that an exaggerated blood pressure response to heart rate during exercise is predictive of future hypertension independent of other important risk factors and lend further support to the concept that blood pressure measurement during exercise test is a valuable means of identifying normotensive individuals at high risk for developing hypertension.

ISSN:0194-911X    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

Bradykinin stimulates tissue plasminogen activator release from human endothelium through a flow-independent, B2receptor–dependent mechanism. The present study tests the hypothesis that smoking impairs bradykinin-stimulated tissue plasminogen activator release. Graded doses of nitroprusside (1.6 to 6.4 &mgr;g/min), methacholine (3.2 to 12.8 &mgr;g/min), and bradykinin (100 to 400 ng/min) were infused in the brachial artery in random order in 20 smokers and 12 nonsmokers matched for age, gender, and body mass index. Forearm blood flow was measured by strain-gauge plethysmography. All 3 drugs caused a dose-dependent increase in forearm blood flow, with no significant difference between smokers and nonsmokers. Bradykinin (P=0.001) and methacholine (P=0.001) caused significant dose-dependent increases in net tissue plasminogen activator release. The tissue plasminogen activator response to bradykinin was significantly greater than the tissue plasminogen activator response to methacholine in the nonsmokers (maximal net tissue plasminogen activator release, 73.2±21.5 versus 27.6±7.2 ng/min per 100 mL;P=0.001) but not in the smokers (maximal net tissue plasminogen activator release, 44.5±10.7 versus 24.8±9.3 ng/min per 100 mL;P=0.154). The effect of bradykinin (P=0.037), but not methacholine (P=0.978), on net tissue plasminogen activator release was significantly reduced in smokers compared with nonsmokers. The vascular tissue plasminogen activator response to bradykinin, but not methacholine, is impaired in smokers. Stimulated tissue plasminogen activator release may be a more sensitive measure of endothelial function than vasodilation.

ISSN:0194-911X    

出版商:OVID    

年代:2002

数据来源: OVID