ISSN:0194-911X    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

Left ventricular hypertrophy is an independent predictor of cardiovascular morbidity and mortality. However, predictors of cardiac structure and function in youth are not completely understood. On 2 occasions (2.3 years apart), we examined 146 youth aged initially 10 to 19 years (mean age, 14.2±1.8 years). On the initial visit, hemodynamic function was assessed at rest, during laboratory stress (ie, orthostasis, car-driving simulation, video game, and forehead cold), and in the field (ie, ambulatory blood pressure). Quantitative M-mode echocardiograms were obtained on both visits. On both visits, black compared with white youth had higher resting laboratory systolic blood pressure (P<0.02), greater relative wall thickness (P<0.003), greater left ventricular mass indexed by either body surface area or height2.7(P<0.01 for both), and lower midwall fractional shortening ratio (P<0.05). Hierarchical stepwise regression analysis indicated that significant independent predictors of follow-up left ventricular mass/height2.7were the initial evaluation of left ventricular mass/height2.7, body mass index, gender (males more than females), and supine resting total peripheral resistance (final modelR2=0.53). Left ventricular mass/body surface area was predicted by initial left ventricular mass/body surface area, weight, gender, mean supine resting total peripheral resistance, and systolic pressure response to car-driving simulation (final modelR2=0.48). Midwall fractional shortening was predicted by initial midwall fractional shortening, race (white more than black), and lower mean supine total peripheral resistance (final modelR2=0.13). The clinical significance of these findings and their implications for improved prevention of cardiovascular diseases are yet to be determined.

ISSN:0194-911X    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

Appropriateness of left ventricular (LV) mass to cardiac workload can be evaluated by the ratio of observed LV mass to the value predicted for an individual's gender, height2.7, and stroke work at rest (%PLVM). It is unclear which pathophysiological factors are associated with inappropriately high LV mass in hypertensive subjects. Adequate LV mass was defined by the 90% confidence interval (73% to 128%) of the distribution of %PLVM in 393 normal-weight normotensive subjects. In 185 hypertensive subjects (aged 56±11 years; 60% male, 29% black), according to %PLVM, 164 (88%) had adequate LV mass, 16 (9%) had inappropriately high LV mass (%PLVM >128%), and 5 (3%) had %PLVM <73% (low LV mass). Age, gender, smoking habit, proportion of never-treated subjects, total cholesterol, triglycerides, and creatinine levels did not differ significantly between subjects with adequate and inappropriately high LV mass. Body mass index, fasting glucose, and proportion of black subjects were higher (allP<0.05), while HDL cholesterol was lower (P<0.05) in subjects with inappropriately high LV mass. Blood pressure at the echocardiogram was comparable between subjects with adequate and inappropriately high LV mass, but the latter group had higher ambulatory blood pressure (P<0.01). Subjects with inappropriately high LV mass also had higher aortic root dimension and LV relative wall thickness and relatively lower LV systolic performance than those with adequate LV mass (allP<0.001). Larger aortic root diameter and lower systolic function were also found in hypertensive subjects with inappropriate LV hypertrophy compared with those with adequate LV hypertrophy. In an exploratory case-control study that compared subjects with low %PLVM with age-matched counterparts with adequate LV mass, low %PLVM was associated with lower body mass index, more favorable metabolic profile, and higher LV myocardial contractility. Higher body mass index, larger aortic root, and black race were independent correlates of increased %PLVM. Thus, in arterial hypertension, levels of LV mass inappropriately high for gender, cardiac workload, and height2.7are associated with higher body mass index, higher ambulatory blood pressure, larger aortic root diameters, and relatively low myocardial contractility.

ISSN:0194-911X    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

To reduce cardiovascular complications, antihypertensive therapy should not only normalize blood pressure but also induce a regression of structural abnormalities, which are the expression of end-organ damage. We investigated the effects of transdermal 17β-estradiol, combined with standard antihypertensive therapy, on the modification of left ventricular anatomy and systolic performance in hypertensive postmenopausal women. In a randomized, double-blind, placebo-controlled study, we enrolled 169 postmenopausal women with mild or moderate hypertension. Eighty-six patients (group 1) received transdermal 17β-estradiol (50 μg/d) and norethisterone acetate (2.5 mg/d, orally), and 83 patients (group 2) received placebo. At baseline, all women underwent M-mode and 2-D echocardiogram, which was repeated after 6, 12, and 18 months of follow-up. After 18 months of treatment, we observed a significant decrease in left ventricular diastolic septal and posterior wall thickness and mass in both groups. Furthermore, after 18 months, left ventricular mass was significantly less than in the estrogen-treated group. No significant modifications were observed in left ventricular systolic and diastolic dimensions or in systolic performance, as expressed by left ventricular fractional shortening. In conclusion, transdermal 17β-estradiol, which is associated with antihypertensive therapy, may contribute in the reduction of left ventricular mass in hypertensive postmenopausal women.

ISSN:0194-911X    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

Leptin, the product of theobgene, has been shown to increase heart rate and blood pressure through a stimulation of cardiac sympathetic nervous system activity, a phenomenon also involved in the pathogenesis of left ventricular hypertrophy in hypertensives. Thus, we hypothesize that plasma leptin concentration is associated with left ventricular hypertrophy. Forty hypertensive males and 15 healthy male subjects underwent anthropometric and echocardiographic evaluations, assessment of insulin sensitivity through euglycemic glucose clamp combined with indirect calorimetry, and determination of fasting plasma leptin concentration. Fasting plasma leptin levels were higher in hypertensives than in controls (6.48±2.9 versus 4.62±1.5 ng/mL,P<0.05); these results were unchanged after adjustment for body mass index (P<0.05). In the whole group of patients (n=55), fasting plasma leptin concentration was correlated with body mass index (r=0.46,P<0.001) and waist/hip ratio (r=0.50,P<0.001); independent of body mass index and waist/hip ratio, fasting plasma leptin concentration was correlated (n=55) with whole-body glucose disposal (r=−0.27,P<0.04), interventricular septum thickness (r=0.34,P<0.001), posterior wall thickness (r=0.38,P<0.003), and the sum of wall thicknesses (r=0.68,P<0.001). In a multivariate analysis (n=55), age, body mass index, fasting plasma leptin concentration, plasma Na+concentration, whole-body glucose disposal, and diastolic blood pressure explained 68% of the variability of the sum of wall thicknesses with fasting plasma leptin concentration (P<0.03), whole body glucose disposal (P<0.002), and diastolic blood pressure (P<0.001), which were significantly and independently associated with the sum of wall thicknesses. In conclusion, our study demonstrates that fasting plasma leptin levels are associated with increased myocardial wall thickness independent of body composition and blood pressure levels in hypertensives.

ISSN:0194-911X    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

Angiotensin II (Ang II) is known to act as a growth factor and may be involved in cardiac remodeling. We have shown that insulin-like growth factor-I (IGF-I) is an autocrine mediator of growth responses to Ang II in vascular smooth muscle cells in vitro, and we hypothesized that IGF-I also serves as an important modulator of cardiovascular growth in vivo. To study the effect of Ang II on cardiac IGF-I, we infused rats for 3, 7, or 14 days with Ang II through osmotic minipumps. After 7 days, left ventricular mass normalized for body weight was increased by 20% (P<0.01) in Ang II rats compared with pair-fed control rats that were given a restricted amount of food identical to that eaten by the anorexic, Ang II-infused rats. Ang II increased left ventricular IGF-I mRNA levels by 1.5- to 1.8-fold compared with ad libitum-fed or pair-fed control rats (P<0.05). Cardiac IGF-I protein was increased correspondingly and was localized on the cardiomyocytes. Treatment with hydralazine abolished the induction of IGF-I mRNA, which indicates that Ang II induces cardiac IGF-I mRNA expression through a pressor-mediated mechanism. IGF-I receptor (IGF-IR) mRNA was induced 2.1-fold in Ang II rats compared with ad libitum-fed rats (P<0.01). However, this increase was also observed in pair-fed controls and is thus due to the anorexigenic effect of Ang II. We have recently shown that circulating IGF-I levels are reduced in response to Ang II infusion. Elevation of IGF-I levels by coinfusion of IGF-I and Ang II significantly increased left ventricular index by 16% compared with rats infused with Ang II alone (P<0.05). In conclusion, autocrine upregulation of cardiac IGF-I and IGF-IR mRNA by Ang II occurs through hemodynamic and nonhemodynamic mechanisms, respectively, and may modulate cardiac structural changes that occur in hypertension.

ISSN:0194-911X    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

Previous studies have found that respiratory variations of ventricular response in atrial fibrillation are infrequent and inconsistent. This asynchrony between heart rate and respiration may characterize the physiological mechanisms coupling heart rate and systolic blood pressure oscillations in the respiratory band. The aim of this study was to evaluate whether synchronous variations in systolic blood pressure and respiration depend on a simultaneous change in heart rate. Univariate and bivariate spectral analyses were made of the R-R interval, systolic blood pressure, and respiratory signals during controlled respiration (16 breaths/min) in 24 patients with atrial fibrillation before and after efficacious electrical cardioversion and in 24 age- and sex-matched control subjects. During atrial fibrillation, the spectral coherence between respiration and heart rate was low (0.18±0.03), but there was a high level of coherence between respiration and systolic blood pressure (0.67±0.05). After cardioversion, the coherence between respiration and heart rate increased to 0.86±0.04, whereas the geometric mean values of the concomitant respiratory systolic blood pressure oscillations decreased by 72% (from 21.1 to 5.9 mm Hg2,P<0.001), which was similar to that observed in the control group (5.7 mm Hg2). These results confirm the inconsistent effect of respiration on heart rate response during atrial fibrillation and demonstrate that respiratory sinus arrhythmia is not a prerequisite for systolic blood pressure oscillations but may play an antioscillatory role in respiratory systolic blood pressure variability, which is probably mediated by arterial baroreflex mechanisms.

ISSN:0194-911X    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

The aim of this study was to investigate the activity of the parasympathetic limb of the baroreflex arch in a canine model of obesity-related hypertension. Twelve male beagle dogs were randomized into 2 groups. Six dogs were fed with normal canine food and 6 were submitted to a 10-week high-fat diet (HFD). We have evaluated the consequences of HFD on heart rate (HR) and blood pressure (BP) circadian cycles and methylscopolamine dose-response curves. Binding of [3H]-AF-DX 384 and adenylyl cyclase activity were investigated to determine the density and functionality of M2-cholinoceptors on right atrial membranes from control and HFD dogs. HFD induced a significant increase in body weight (15±1 vs 12±1 kg), systolic BP (161±5 vs 145±4 mm Hg), diastolic BP (92±3 vs 79±2 mm Hg), and HR (96±4 vs 81±3 bpm). Circadian rhythms of HR and BP observed in the baseline period were abolished after 9 weeks of HFD. After propranolol (1 mg/kg) pretreatment, the dose of methylscopolamine able to induce 50% maximum tachycardia was significantly increased after 9 weeks of HFD (7.4±0.3 vs 4.7±0.1 μg/kg). In the control group, the experimental period failed to modify these parameters. The numbers of M2-cholinoceptors measured in right atrial membranes were significantly lower in HFD than in control groups (54±6 vs 27±6 fmol/mg protein). The ability of carbachol to inhibit isoproterenol-stimulated adenylyl cyclase activity was significantly lower in HFD than in control groups (IC50=47±12 vs 6.4±1.4 μmol/L). However, the basal activity of adenylyl cyclase was unchanged by HFD. HFD decreases M2-cholinoceptor number and function in cardiomyocytes. This could explain the abolition of circadian rhythm of HR and the changes in chronotropic effect brought about by methylscopolamine.

ISSN:0194-911X    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

We hypothesized that during hypertension, the impairment of mediation of shear stress-induced dilation by nitric oxide (NO) is due to the prevailing hemodynamic forces, and that mediation of this response by NO should still be present in young spontaneously hypertensive rats (SHR). Thus, responses to increases in perfusate flow eliciting increases in wall shear stress were investigated in pressurized (80 mm Hg), isolated arterioles (≈70 to 100 μm) of the left or right gracilis muscle obtained from the same WKY and SHR at 4 and 12 weeks of age. Flow-induced dilations were similar in WKY and SHR at 4 weeks (maximum, 26.5±1.8 and 24.2±2.0 μm, respectively). Also, the middle of the upward portion of the shear stress-diameter curves was similar in arterioles of the 2 strains. Inhibition of NO synthase withNω-nitro-L-arginine (L-NNA) or inhibition of synthesis of prostaglandins (PGs) with indomethacin elicited an ≈50% reduction in flow-dependent dilation, whereas their combined administration eliminated the responses in both groups. In arterioles of 12-week-old WKY, flow-induced dilation became significantly greater (maximum, 46.1±2.3 μm) than responses of arterioles of 4-week-old WKY and 12-week-old SHR (maximum, 18.3±5.9 μm), which shifted only the shear stress-diameter curve of the 12-week-old WKY significantly to the left. Also, at 12 weeks of age, flow-dependent dilation of arterioles from SHR is mediated solely by PGs. Thus, shear stress-induced arteriolar dilation is mediated by NO and PGs in 4-week-old WKY and SHR. With aging, the release of NO and PGs increases in normotensive rats, whereas the contribution of NO to the regulation of shear stress disappears in 12-week-old SHR, which suggests that this change is probably caused by the increase in intraluminal pressure as hypertension develops.

ISSN:0194-911X    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

Capillary hyperperfusion precedes and contributes to the occurrence of diabetic microangiopathy. Vascular tone is regulated by the balance of vasodilating and vasoconstricting factors, of which nitric oxide (NO; an endothelium dependent vasodilator) and norepinephrine (NE; a potent vasoconstrictor), respectively, are of primary importance. To investigate the role of these factors in hyperperfusion, we measured forearm blood flow (FBF) in 50 patients with noncomplicated type 1 diabetes (DP) and 50 healthy control subjects (CS) under baseline conditions and during intrabrachial infusion ofNG-monomethyl-L-arginine (L-NMMA), an endothelium-dependent vasoconstrictor, and acetylcholine (ACh), an endothelium-dependent vasodilator. Furthermore, we determined arterial plasma NE concentration at baseline and then determined α-adrenergic receptor sensitivity by measuring FBF response to intra-arterially infused NE. We found that basal FBF was increased in DP (2.9±0.1 versus 2.0±0.1 mL · min−1· dL−1in CS;P<0.01). L-NMMA caused a similar vasoconstriction in both groups (28.5±1.7% in DP versus 31.2±2.2% in CS;P=NS). Maximum blood flow during infusion of ACh was not different (23.3±1.9 mL · min−1· dL−1in DP versus 20.1±1.6 in CS). Arterial plasma NE concentrations were significantly decreased in DP (0.57±0.03 versus 0.81±0.05 nmol/L in CS;P<0.01). The vasoconstrictive effect of NE was increased in DP (slope log dose-response curve, 31.3±1.5 versus 24.3±1.8 in CS;P<0.01). We conclude that basal FBF is increased in noncomplicated type 1 diabetes. We found no evidence of a disturbance of basal or stimulated NO production. Arterial plasma NE concentrations are decreased in noncomplicated type 1 diabetes. This may explain the vasodilatation at baseline and the increased vascular response to intra-arterially NE.

ISSN:0194-911X    

出版商:OVID    

年代:1999

数据来源: OVID