ISSN:0009-7322    

出版商:OVID    

年代:1999

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:1999

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:1999

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

BackgroundIn the presence of atherosclerosis, the coronary endothelial vasomotor response to acetylcholine is frequently abnormal but is variable between patients. We tested the hypothesis that the plasma concentration of alpha-tocopherol is associated with the preservation of nitric oxide-mediated endothelium-dependent vasomotion.Methods and Results-We studied 15 men and 6 women (mean age 61 +/- 10 years) at coronary angiography who were not taking vitamin supplements. Coronary endothelium-dependent and -independent vasomotion was assessed by intracoronary infusions of acetylcholine and nitroglycerin. The vasomotor responses were compared with the plasma concentration of alpha-tocopherol and the plasma alpha-tocopherol concentration relative to total lipid (total cholesterol plus triglycerides). The mean plasma alpha-tocopherol was 25.6 +/- 6.1 [micro sign]mol/L, total cholesterol 193 +/- 27 mg/dL, triglycerides 115 +/- 66 mg/dL, and alpha-tocopherol to total lipid 4.2 +/- 0.9 [micro sign]mol [middle dot] L-1[middle dot] (mmol/L)-10.05). The acetylcholine response remained significant after adjustment for other potential sources of oxidant stress (total cholesterol, diabetes mellitus, smoking, angina class) (P<0.01). The relative concentration of alpha-tocopherol to total lipid was not related to endothelial function (r=0.24, P=0.3, n=20).Conclusionsalpha-Tocopherol may preserve endothelial vasomotor function in patients with coronary atherosclerosis. This effect may be related primarily to the action of alpha-tocopherol in the vascular wall. Further studies that assess the impact of alpha-tocopherol supplementation as therapy of endothelial dysfunction are justified. (Circulation. 1999;100:219-221.)

ISSN:0009-7322    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

BackgroundSphygmomanometric blood pressure measurements induce an alerting reaction and thus an increase in the patient's blood pressure and heart rate. Whether and to what extent this "white-coat" effect is accompanied by detectable changes in sympathetic nerve traffic has never been investigated.Methods and Results-In 10 mild untreated essential hypertensives (age 37.9 +/- 3.8 years, mean +/- SEM), we measured arterial blood pressure (by Finapres), heart rate (by ECG), and postganglionic muscle and skin sympathetic nerve activity via microneurography. Measurements were performed with the subject supine during (1) a 15-minute control period, (2) a 10-minute visit by a doctor unfamiliar to the patient who was in charge of measuring his or her blood pressure by sphygmomanometry, and (3) a 15-minute recovery period after the doctor's departure. The entire procedure was performed twice at a 45-minute interval to obtain, in separate periods, muscle or skin sympathetic nerve traffic recordings, whose sequence was randomized. The doctor's visit induced a sudden, marked, and prolonged pressor and tachycardic response, accompanied by a significant increase in skin sympathetic nerve traffic (+38.6 +/- 6.7%, P<0.01). In contrast, muscle sympathetic nerve traffic was significantly inhibited (-25.5 +/- 4.1%, P<0.01). All changes persisted throughout the doctor's visit and, with the exception of skin sympathetic nerve traffic, showed a slow rate of disappearance after the doctor's departure.ConclusionsThus, the pressor and tachycardic responses to the alerting reaction that accompanies sphygmomanometric blood pressure measurement is characterized by a behavior of the adrenergic nervous system that causes muscle sympathoinhibition and skin sympathoexcitation. (Circulation. 1999;100:222-225.)

ISSN:0009-7322    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

BackgroundHypovolemic shock of marked severity and duration may progress to cardiovascular collapse unresponsive to volume replacement and drug intervention. On the basis of clinical observations, we investigated the action of vasopressin in an animal model of this condition.Methods and Results-In 7 dogs, prolonged hemorrhagic shock (mean arterial pressure [MAP] of [approximate]40 mm Hg) was induced by exsanguination into a reservoir. After [approximate]30 minutes, progressive reinfusion was needed to maintain MAP at [approximate]40 mm Hg, and by [approximate]1 hour, despite complete restoration of blood volume, the administration of norepinephrine [approximate]3 [micro sign]g [middle dot] kg (-1) [middle dot] min-1was required to maintain this pressure. At this moment, administration of vasopressin 1 to 4 mU [middle dot] kg-1[middle dot] min-1increased MAP from 39 +/- 6 to 128 +/- 9 mm Hg (P<0.001), primarily because of peripheral vasoconstriction. In 3 dogs subjected to similar prolonged hemorrhagic shock, angiotensin II 180 ng [middle dot] kg-1[middle dot] min-1had only a marginal effect on MAP (45 +/- 12 to 49 +/- 15 mm Hg). Plasma vasopressin was markedly elevated during acute hemorrhage but fell from 319 +/- 66 to 29 +/- 9 pg/mL before administration of vasopressin (P<0.01).ConclusionsVasopressin is a uniquely effective pressor in the irreversible phase of hemorrhagic shock unresponsive to volume replacement and catecholamine vasopressors. Vasopressin deficiency may contribute to the pathogenesis of this condition. (Circulation. 1999;100:226-229.)

ISSN:0009-7322    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

BackgroundElevated plasma concentrations of C-reactive protein (CRP) are associated with increased cardiovascular risk. We evaluated whether long-term therapy with pravastatin, an agent that reduces cardiovascular risk, might alter levels of this inflammatory parameter.Methods and Results-CRP levels were measured at baseline and at 5 years in 472 randomly selected participants in the Cholesterol and Recurrent Events (CARE) trial who remained free of recurrent coronary events during follow-up. Overall, CRP levels at baseline and at 5 years were highly correlated (r=0.60, P<0.001). However, among those allocated to placebo, median CRP levels and the mean change in CRP tended to increase over time (median change, +4.2%; P=0.2 and mean change, +0.07 mg/dL; P=0.04). By contrast, median CRP levels and the mean change in CRP decreased over time among those allocated to pravastatin (median change, -17.4%; P=0.004 and mean change, -0.07 mg/dL; P=0.002). Thus, statistically significant differences were observed at 5 years between the pravastatin and placebo groups in terms of median CRP levels (difference, -21.6%; P=0.007), mean CRP levels (difference, -37.8%; P=0.002), and absolute mean change in CRP (difference, -0.137 mg/dL; P=0.003). These effects persisted in analyses stratified by age, body mass index, smoking status, blood pressure, and baseline lipid levels. Attempts to relate the magnitude of change in CRP to the magnitude of change in lipids in both the pravastatin and placebo groups did not reveal any obvious relationships.ConclusionsAmong survivors of myocardial infarction on standard therapy plus placebo, CRP levels tended to increase over 5 years of follow-up. In contrast, randomization to pravastatin resulted in significant reductions in this inflammatory marker that were not related to the magnitude of lipid alterations observed. Thus, these data further support the potential for nonlipid effects of this agent. (Circulation. 1999;100:230-235.)

ISSN:0009-7322    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

BackgroundBalloon angioplasty (PTCA) of occluded coronary arteries is limited by high rates of restenosis and reocclusion. Although stenting improves results in anatomically simple occlusions, its effect on patency and clinical outcome in a broadly selected population with occluded coronary arteries is unknown.6 weeks' duration, baseline flow was TIMI grade 0 in 64%, and median treated segment length was 30.5 mm. With 95.6% angiographic follow-up, primary stenting resulted in a 44% reduction in failed patency (10.9% versus 19.5%, P=0.024) and a 45% reduction in clinically driven target-vessel revascularization at 6 months (15.4% versus 8.4%, P=0.03). The incidence of adverse cardiovascular events was similar for both strategies (PTCA, 23.6%; stent, 23.3%; P=NS). Stenting resulted in a larger mean 6-month minimum lumen dimension (1.48 versus 1.23 mm, P<0.01) and a reduced binary restenosis rate (55% versus 70%, P<0.01).ConclusionsPrimary stenting of broadly selected nonacute coronary occlusions is superior to PTCA alone, improving late patency and reducing restenosis and target-vessel revascularization. (Circulation. 1999;100:236-242.)

ISSN:0009-7322    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

BackgroundThe mechanisms leading to dobutamine-induced ischemia are not fully understood. In the present study, we investigated the effects of high-dose intravenous dobutamine on morphological and physiological indexes of coronary stenoses.Methods and Results-Twenty-two patients with normal left ventricular function and isolated coronary stenoses were studied. At catheterization, mean aortic pressure (Pa), mean distal coronary pressure (Pd), and Pd/Paas an index of myocardial resistance were recorded at rest, after intracoronary adenosine, and during intravenous infusion of dobutamine (10 to 40 [micro sign]g [middle dot] kg (-1) [middle dot] min-1). Reference vessel diameter and minimal luminal diameter, as assessed by coronary angiography, did not change during dobutamine infusion compared with baseline (2.84 +/- 0.49 versus 2.77 +/- 0.41 mm and 1.35 +/- 0.38 versus 1.27 +/- 0.31 mm, respectively; both P=NS). During peak dobutamine infusion, Pdand Pd/Pareached similar levels as during adenosine infusion (60 +/- 18 versus 59 +/- 18 mm Hg and 0.68 +/- 0.18 versus 0.68 +/- 0.17, respectively; all P=NS). In 9 patients, an additional bolus of intracoronary adenosine given at the peak dose of dobutamine failed to further decrease Pd/Pa. Furthermore, in patients with dobutamine-induced wall motion abnormalities, the maximal decrease in Pd/Pawas similar during dobutamine and adenosine infusions.ConclusionsHigh-dose intravenous infusion of dobutamine does not modify the dimensions of the epicardial coronary stenosis. However, much like the direct coronary vasodilator adenosine, dobutamine fully exhausts myocardial resistance regardless of the presence of mechanical dysfunction. (Circulation. 1999;100:243-249.)

ISSN:0009-7322    

出版商:OVID    

年代:1999

数据来源: OVID