ISSN:0009-7322    

出版商:OVID    

年代:1996

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:1996

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:1996

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:1996

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:1996

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

BackgroundFenestration of the Fontan circulation that results in a residual right-to-left shunt has improved operative survival rates among high-risk patients. Late closure of the fenestration by use of a transcatheter umbrella device has achieved separation of the systemic and pulmonary venous circulations, "completing" the Fontan pathway. Because use of umbrella devices is restricted, many institutions continue to perform only nonfenestrated Fontan procedures.Methods and ResultsFive children 3.5 to 8.3 years old (mean, 5.1 years) underwent cardiac catheterization 0.5 to 24 months (mean, 10 months) after operation for the purpose of occluding a persistently patent Fontan fenestration. Once candidacy was determined, an 8-mm x 10-cm Gianturco coil was delivered to straddle the fenestration with established techniques for coil occlusion of patent ductus arteriosus. Complete occlusion occurred in 4 of 5 patients, in 2 of the 4 before they left the catheterization laboratory. One patient had a residual angiographic shunt but had complete closure within 24 hours by echocardiography. In 1 patient who had a residual shunt at 24 hours, the fenestration was completely closed at 1 month after coil placement. One patient had residual shunting at 2 months but saturations have increased 15% to 17% since coil placement. No embolizations (early or late), clinical hemolysis, thromboembolic events, or hemodynamic deterioration occurred among patients during 1- to 14-month follow-up periods.ConclusionsA persistently patent fenestration after Fontan operation may be closed with a Gianturco coil. This universally available alternative to umbrella devices may make the fenestrated Fontan a more appealing option to centers that had not previously considered its use. (Circulation. 1996;94:249-252.)

ISSN:0009-7322    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

BackgroundTemperatures near 50 degrees C can cause reversible loss of excitability in myocardial cells.Methods and Results90%.ConclusionsLow-temperature radiofrequency applications that cause transient AP block predict permanent success when a higher-temperature application is delivered at the same site. The time to achieve conduction block is a function of the temperature set point, and low-temperature tests produce reversible conduction block, suggesting minimal permanent injury. (Circulation. 1996;94:253-257.)

ISSN:0009-7322    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

BackgroundAngiotensin-converting enzyme (ACE) inhibitors may exert some of their benefits in the therapy of hypertension, congestive heart failure, and acute myocardial infarction by their improvement of endothelial dysfunction. TREND (Trial on Reversing ENdothelial Dysfunction) investigated whether quinapril might improve endothelial dysfunction in normotensive patients with coronary artery disease and no heart failure, cardiomyopathy, or major lipid abnormalities so that confounding variables that affect endothelial dysfunction could be minimized.Methods and ResultsUsing a double-blind, randomized, placebo-controlled design, we measured the effects of quinapril (40 mg daily) on coronary artery diameter responses to acetylcholine using quantitative coronary angiography. The primary response variable was the net change in the acetylcholine-provoked constriction of target segments between the baseline (prerandomization) and 6-month follow-up angiograms. The constrictive responses to acetylcholine were comparable in the placebo (n = 54) and quinapril (n = 51) groups at baseline. After 6 months, only the quinapril group showed significant net improvement in response to incremental concentrations of acetylcholine (4.5 +/- 3.0% [mean +/- SEM] versus -0.1 +/- 2.8% at 10 sup -6 mol/L and 12.1 +/- 3.0% versus -0.8 +/- 2.9% at 10 sup -4 mol/L, quinapril versus placebo, respectively; overall P = .002).ConclusionsTREND shows that ACE inhibition with quinapril improved endothelial dysfunction in patients who were normotensive and who did not have severe hyperlipidemia or evidence of heart failure. These benefits of ACE inhibition are likely due to attenuation of the contractile effects and superoxide-generating effects of angiotensin II and to enhancement of endothelial cell release of nitric oxide secondary to diminished breakdown of bradykinin. (Circulation. 1996;94:258-265.)

ISSN:0009-7322    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

BackgroundCoronary spasm can be induced by acetylcholine, serotonin, ergonovine, or histamine, all of which cause vasodilation when the endothelium is intact by releasing nitric oxide (NO). Coronary spasm is promptly relieved by nitroglycerin, which vasodilates through its conversion to NO. It is thus possible that NO release may be deficient in the spasm arteries in patients with coronary spastic angina (CSA). The aim of this study was to determine whether NO release is deficient in coronary arteries of patients with CSA.Methods and ResultsNG-monomethyl-L-arginine (L-NMMA), an inhibitor of NO synthase, was infused into coronary arteries in 21 patients with coronary spastic angina (CSA) and in 28 control patients. Coronary spasm was induced by intracoronary injection of acetylcholine and was documented angiographically in all patients with CSA. L-NMMA dose-dependently decreased basal luminal diameter of coronary arteries in control patients, whereas it had no effect on basal diameter of the spasm arteries in patients with CSA. L-NMMA abolished the dilator response to acetylcholine and enhanced the constrictor response to acetylcholine in control arteries, whereas it had no effect on the constrictor response to acetylcholine in spasm arteries. Intracoronary infusion of L-arginine did not affect the diameter of spasm or control arteries. The dilator response to nitroglycerin was increased markedly in spasm arteries compared with control arteries, whereas response to diltiazem did not differ between them.ConclusionsThere is a deficiency in endothelial NO activity in spasm arteries, which leads to the supersensitivity of the artery to the vasodilator effect of nitroglycerin and to the vasoconstrictor effect of acetylcholine in patients with CSA. This deficient endothelial NO activity plays an important role in the pathogenesis of coronary spasm. (Circulation. 1996;94:266-272.)

ISSN:0009-7322    

出版商:OVID    

年代:1996

数据来源: OVID