ISSN:0009-7322    

出版商:OVID    

年代:1995

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:1995

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:1995

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Background Vascular endothelial growth factor (VEGF) is a hypoxia-inducible direct angiogenic factor. Upregulation of VEGF is thought to mediate many of the angiogenic effects of growth factors that are not direct endothelial cell mitogens. Like VEGF, basic fibroblast growth factor (bFGF) is considered to induce angiogenesis by a direct effect on endothelial cells. This study investigated the possibility that bFGF may also act indirectly by regulating VEGF expression in vascular smooth muscle cells (VSMCs).Methods and Results Incubation of confluent and quiescent cultures of rabbit VSMCs with bFGF caused a time- and concentration-dependent increase in steady-state levels of VEGF mRNA, as analyzed by Northern blot hybridization. Exposure of VSMCs to a threshold hypoxic stimulus (2.5% O2) caused a modest increase in VEGF mRNA levels. However, the combination of 2.5% O2with bFGF had a marked synergistic effect. This effect was specific for VEGF as hypoxia did not enhance bFGF-induced expression of the proto-oncogene c-myc. Synergistic upregulation of VEGF mRNA expression also was observed between hypoxia and TGF- beta1.Conclusions These results suggest that bFGF may promote angiogenesis both by a direct effect on endothelial cells and also indirectly by the upregulation of VEGF in VSMCs. The synergy demonstrated between hypoxia and either bFGF or TGF- beta1suggests that multiple diverse stimuli may interact via the upregulation of VEGF expression in VSMCs to amplify the angiogenic response. (Circulation. 1995;92:11-14.)

ISSN:0009-7322    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Background Phosphorus-31 metabolite measurements in the human heart by magnetic resonance spectroscopy (MRS) have been reported previously. By use of a method in which metabolite content was quantified with reference to a standard located outside the chest, it has become possible to measure the content of phosphocreatine (PCr) and ATP in vivo in the human heart. In this study, PCr and ATP contents were measured by Phosphorus-31 MRS and compared in human myocardium with reversible ischemia or scar diagnosed by exercise thallium scintigraphy.RD(-), 4.35+-1.52 micromole/g wet heart tissue, P<.05).Conclusions Compared with healthy control subjects, PCr content decreased significantly in patients with both reversible and fixed Thallium-201 defects, and ATP content decreased significantly in subjects with fixed thallium defects. These results suggest that the measurement of ATP content in the human heart by Phosphorus-31 MRS is a clinically important method for the evaluation of myocardial viability. (Circulation. 1995;92:15-23.)

ISSN:0009-7322    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Background Women are protected from coronary artery disease until the menopause. Ovarian hormones are vasoactive substances that influence both hemodynamic parameters and atheroma formation. Intravenous ethinyl estradiol has been shown to reverse acetylcholine-induced vasoconstriction in cynomolgus monkeys and humans, and 17 beta -estradiol improves exercise-induced myocardial ischemia in female patients. We investigated the effect of the naturally occurring estrogen 17 beta -estradiol on the coronary circulation in postmenopausal women and men with coronary artery disease..05). Isosorbide dinitrate (1 mg) caused dilatation of the coronary arteries by 11+-2% (P<.005). In men, acetylcholine 1.6 and 16 micrograms/min caused constriction both before and after the administration of 17 beta -estradiol and caused similar increases in coronary blood flow both before and after the intracoronary administration of 17 beta -estradiol. Infusion of intracoronary placebo in six female control patients 55+-3 years old and six male control patients 56+-3 years old did not change coronary diameter responses or coronary blood flow responses to acetylcholine.Conclusions 17 beta -Estradiol modulates acetylcholine-induced coronary artery responses of female but not male atherosclerotic coronary arteries in vivo. These human data confirm reports from studies in cynomolgus monkeys that estrogen modulates the responses of atherosclerotic coronary arteries. An enhancement of endothelium-dependent relaxation by natural estrogen (as used in most hormone replacement therapy) may be important in postmenopausal women with established coronary heart disease and may contribute to the acute effect of 17 beta -estradiol on blood flow and its long-term protective effect on the development of coronary artery disease. (Circulation. 1995;92:24-30.)

ISSN:0009-7322    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Background Fibrinogen is a risk factor for cardiovascular disease and is related to the severity of coronary atherosclerosis. Its role in restenosis after coronary angioplasty remains unknown. Although platelets and thrombosis contribute to the pathogenesis of restenosis, few clinical data are available concerning the relations between restenosis and proteins of the coagulation and fibrinolytic systems.3.5 g/L at follow-up had higher restenosis rates than patients with a concentration <3.5 g/L: 55% versus 22% (P=.001), 68% versus 31% (P=.002), 63% versus 37% (P=.01), and 74% versus 26% (P=.002) for definitions 1 through 4, respectively. The loss index was lower (P=.003) and the net gain higher (P=.03) in patients with a fibrinogen level <3.5 g/L. There was a significant correlation between fibrinogen level and angiographic loss index (r=.41; P<.0001). Multivariate analysis confirmed that the fibrinogen level predicted restenosis with all definitions.Conclusions An independent relation exists between von Willebrand factor measured immediately after angioplasty and restenosis defined by the degree of intraluminal renarrowing. An elevated fibrinogen level during follow-up is a strong biochemical predictor of restenosis. Therefore, fibrinogen should be considered at least as an independent marker of restenosis and perhaps as a common risk factor for both spontaneous coronary atherosclerosis and postangioplasty restenosis, which is an accelerated form of atherosclerosis. (Circulation. 1995;92:31-38.)

ISSN:0009-7322    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Background Myocardial fractional flow reserve (FFR sub myo) is a functional index of stenosis severity that can be derived from intracoronary pressure measurements performed during maximal vasodilatation. It is defined as the maximal myocardial perfusion during hyperemia in the presence of a stenosis in the epicardial artery expressed as a fraction of its normal maximal expected value. To determine threshold values of FFRmyo, of hyperemic translesional pressure gradient (Delta Pmax), and of resting translesional pressure gradient (Delta Prest) that are uniformly associated with exercise-induced ischemia, we studied the relation between these pressure-derived indexes and the results of exercise ECG.=0.1 mV) were compared with FFRmyo, Delta Pmax, and Delta Prest. Thirty-seven patients had an abnormal and 23 patients a normal exercise ECG. A significant linear correlation was found between the magnitude of ST-segment depressions and both FFRmyoand Delta Pmax(r=-.75, SEE=0.53; r=.71, SEE=0.56). A weaker correlation was noted between ST-segment depressions and Delta Prest(r=.53, SEE=0.67). Sensitivity and specificity curves were constructed for the prediction of an abnormal exercise ECG for the three pressure-derived indexes. The values that most accurately predicted an abnormal exercise ECG were 66% for FFRmyo, 31 mm Hg for Delta Pmax, and 12 mm Hg for Delta Prest. No patient with a FFRmyo72% showed an abnormal exercise ECG. In addition, receiver operating characteristic curves demonstrated a greater accuracy of FFRmyoand of Delta Pmaxthan of Delta Prestfor predicting the results of the exercise ECG.Conclusions In the present study, cutoff values of FFR sub myo and translesional pressure gradients are established from the relation between intracoronary pressure-derived indexes and ECG signs of myocardial ischemia during maximal exercise. These values can be helpful for clinical decision making in cases with dubious angiographic results. Furthermore, our data support the concept that stenosis physiology is better reflected by hyperemic than by basal measurements. (Circulation. 1995;92:39-46.)

ISSN:0009-7322    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Background Patients with heart failure frequently report exertional dyspnea and fatigue. These symptoms are usually attributed to circulatory dysfunction and therefore are typically treated with cardiovascular medications. Serial assessment of exertional symptoms has also become the principal method used to assess drug efficacy in heart failure. Nevertheless, the relation between exertional symptoms in heart failure and circulatory dysfunction remains uncertain.20 mm Hg during exercise. Despite these markedly different hemodynamic responses, all three groups exhibited similar levels of fatigue and dyspnea at comparable workloads and had comparable total scores for the Minnesota Living With Heart Failure Questionnaire and the Yale Dyspnea-Fatigue Index. There was no relation between the Living With Heart Failure Questionnaire and peak exercise Vo2and only a weak correlation between the Dyspnea-Fatigue Index and peak Vo2(r=.48).Conclusions The level of exercise intolerance perceived by patients with heart failure has little or no relation to objective measures of circulatory, ventilatory, or metabolic dysfunction during exercise. In patients who report severe exertional symptoms, it may be desirable to directly measure hemodynamic response to exercise to ensure that these symptoms are due to circulatory dysfunction. (Circulation. 1995;92:47-53.)

ISSN:0009-7322    

出版商:OVID    

年代:1995

数据来源: OVID