ISSN:0009-7322    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

Key WordsEditorials, angioplasty, stents, heparin, coronary disease.

ISSN:0009-7322    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

Key WordsEditorials, clinical outcome, quality control.

ISSN:0009-7322    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

BackgroundTorsade de pointes often occurs with underlying hypokalemia and bradycardia. A common effect of many drugs producing torsade de pointes is block of the rapidly activating component of the cardiac delayed rectifier (IKr). In this study, we evaluated the effect of changing extracellular potassium ([K sup +]o) on IKrblock by the nonspecific agent quinidine and by the specific IKrblocker dofetilide.Methods and ResultsIKrwas measured in AT-1 cells, where contaminating outward currents are absent. The drug concentration producing 50% inhibition of IKrtails (IC50) was strikingly [K sup +]o-dependent. Elevating [K sup +]ofrom 1 to 8 mmol/L increased the IC50for dofetilide block from 2.7 plus/minus 0.9 to 79 plus/minus 32 nmol/L and for quinidine block from 0.4 plus/minus 0.1 to 3.8 plus/minus 1.2 micro mol/L.Conclusions(1) The increase in drug block with low [K sup +]oprovides a mechanism to explain the link between hypokalemia and torsade de pointes. (2) Elevations in [K sup +]ooccur with myocardial ischemia and with rapid pacing. Possible consequences of blunted drug block with high [K sup +]oinclude loss of drug efficacy with ischemia and with rapid pacing; the latter may contribute to "reverse use-dependent" action potential prolongation. Extracellular potassium is a critical determinant of drug block of IKr, with substantial clinical implications. (Circulation. 1996;93:407-411.)Key Wordspotassium, torsade de pointes, ions.

ISSN:0009-7322    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

BackgroundThe purpose of the Benestent-II Pilot Study was to evaluate the safety of delaying and eliminating anticoagulant therapy in patients receiving a heparin-coated stent in conjunction with antiplatelet drugs.Methods and ResultsThe study consisted of three initial phases (I, II, III) during which resumption of heparin therapy after sheath removal was progressively deferred by 6, 12, and 36 hours. In phase IV, coumadin and heparin were replaced by 250 mg ticlopidine and 100 mg aspirin. Of the 207 patients with stable angina pectoris and a de novo lesion in whom heparin-coated stent implantation was attempted, implantation was successful in 202 patients (98%). Stent thrombosis did not occur during all four phases, and the overall clinical success rate at discharge was 99%. Bleeding complications requiring blood transfusion or surgery fell from 7.9% in phase I to 5.9%, 4%, and 0% in the three following phases. Hospital stay was 7.4, 6.1, 7.2, and 3.1 days for the consecutive phases. The restenosis rate for the combined four phases was 13% (15% in phase I, 20% in phase II, 11% in phase III, and 6% in phase IV). The overall rate of reintervention for the four phases was 8.9%. At 6 months, 84%, 75%, 94%, and 92% of the patients of phases I to IV, respectively, were event free. For the four phases, the event-free rate was 86%, which compares favorably with the rate observed in the Benestent-I study (80%; relative risk, 0.68 [0.45 to 1.04]).ConclusionsThe implantation of stents coated with polyamine and end-point-attached heparin in stable patients with one significant de novo coronary lesion is well tolerated, is associated with no (sub)acute stent thrombosis, and results in a favorable event-free survival after 6 months. (Circulation. 1996;93:412-422.)Key Wordsheparin, stents, anticoagulants, angina, coating.

ISSN:0009-7322    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

BackgroundThe use of stents improves the result after balloon coronary angioplasty. Thrombogenicity of stents is, however, a concern. In the present study, we compared stents with an antithrombotic coating with regular stents.Methods and ResultsRegular stents were placed in coronary arteries of pigs receiving no aspirin (group 1; n = 8) or aspirin over 4 weeks (group 2, n = 10) or 12 weeks (group 3, n = 9). Stents coated with heparin (antithrombin III uptake, 5 pmol/stent) were placed in 7 pigs that did not receive aspirin (group 4). The other animals received aspirin and coated stents with a heparin activity of 12 pmol antithrombin III/stent (group 5, n = 10) or 20 pmol/stent (group 6, n = 10; group 7, n = 10). Quantitative arteriography was performed at implantation and after 4 (groups 1, 2, and 4 through 6) or 12 weeks (groups 3 and 7). In an additional 5 animals, five regular and five coated stents (20 pmol/stent) were placed and explanted after 5 days for examination of the early responses to the implants. Thrombotic occlusion of the regular stent occurred in 9 of 27 in groups 1 through 3. However, in 0 of 30 of the animals receiving high-activity heparin-coated stents (groups 5 through 7), thrombotic stent occlusion was observed (P < .001). Histological analysis at 4 weeks showed that the neointima in group 6 was thicker compared with its control group 2 (259 plus/minus 104 and 117 plus/minus 36 micro meter, P < .01), but at 12 weeks the thickness was similar (152 plus/minus 61 and 198 plus/minus 49 micro meter, respectively). Comparison at 5 days suggested delayed endothelialization of the coating.ConclusionsHigh-activity heparin coating of stents eliminates subacute thrombosis in porcine coronary arteries. (Circulation. 1996;93:423-430.)Key Wordsstents, thrombosis, heparin.

ISSN:0009-7322    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

BackgroundMedical consumers are increasingly requesting methods to discriminate among the results of different providers. Standards for appropriate modeling, risk adjustment, and evaluation ("scorecarding") in this setting are not well developed, although such evaluation is being performed by the medical insurance industry and by several states in the United States. Our objectives were to develop and examine clinically meaningful methodology for assessing the operator-specific results for percutaneous coronary revascularization.Methods and ResultsFrom a multicenter database of patients treated since January 1, 1990, we used training and validation samples (n = 4860) to develop several models for risk adjustment and applied them to 38 providers performing 25 to 523 procedures in the database. Models were developed using multivariable logistic regression techniques for combinations of the end points of death, myocardial infarction, bypass surgery, and procedural success. Models were evaluated for predictive accuracy by using receiver operating characteristic (ROC) analysis, for the capacity to discriminate between superior and inferior provider outcomes, and for subjectivity and concordance. Major complications occurred in 3.6% of patients. The area under the ROC curve (with perfect discriminatory accuracy, area = 1.0; with no apparent accuracy, area = 0.5) in the validation sample, and frequency of identification of operators with outcomes outside the 95% CI for the outcome in question for the models were for death, 0.85 and 7.9%; for death, Q-wave infarction, and bypass surgery, 0.77 and 13.2%; for death, all infarction, and bypass surgery, 0.66 and 10.5%; and for procedural success, 0.76 and 23.7%. For the models as a group, identification of outliers was inversely related to provider volume (P = .05). Models evaluating non-Q-wave infarction or requiring measurement of percent diameter stenosis were identified as being most susceptible to provider manipulation.ConclusionsFor percutaneous coronary revascularization, modeling to discriminate between provider outcomes is limited by the low incidence of major adverse events, subjectivity or susceptibility to manipulation of more frequently occurring adverse events, the generally modest predictive capacity of the models, and the low volume of individual provider treatments. Modeling will be most useful in the identification of providers with extremely poor outcomes and for discrimination between providers with very large procedural volume. Until improved understanding of the biological and mechanical correlates of major complications allows the development of more predictive models, interpretation of the results of scorecarding, particularly for low-volume providers, should be made with caution. (Circulation. 1996;93:431-439.)Key Wordsangioplasty, myocardial infarction, statistics.

ISSN:0009-7322    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

BackgroundPolymorphisms of the beta fibrinogen gene have been shown to affect plasma fibrinogen levels and the risk of peripheral arterial disease. We now present the results of a detailed analysis of the beta fibrinogen gene in relation to plasma fibrinogen and to the severity of coronary artery disease (CAD) in patients with myocardial infarction (MI) in the ECTIM Study.Methods and Results50% stenosis was estimated by angiography and used as a criterion for severity of CAD. Presence of the less frequent allele of the beta Bcl I (P < .0003) and of other polymorphisms was positively associated with the severity of CAD.ConclusionsGenetic variants of the beta fibrinogen gene are associated with an increased plasma level of fibrinogen, especially in smokers. The association with CAD appears to be the consequence of an increased risk of MI in subjects with severe CAD who carry the predisposing beta fibrinogen genotypes. (Circulation. 1996;93:440-449.)Key Wordsgenetics, fibrinogen, coronary disease, myocardial infarction.

ISSN:0009-7322    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

BackgroundFew epidemiological studies have investigated the relative importance of major coronary risk factors in the two sexes within the same study population. In particular, it is not clear whether smoking carries a similar risk of coronary heart disease in men and women.Methods and ResultsThe associations between smoking, serum lipids, blood pressure, and myocardial infarction were examined in a population-based prospective study of 11 843 men and women aged 35 to 52 years at entry. During 12 years, 495 cases of first myocardial infarction among men and 103 cases among women were identified. Myocardial infarction incidence was 4.6 times higher among men. The incidence was increased sixfold in women and threefold in men who smoked at least 20 cigarettes per day compared with never-smokers, and the rate in female heavy smokers exceeded that of never-smoking men. Multivariate analysis identified current smoking as a stronger risk factor in women (relative risk, 3.3; 95% confidence interval [CI], 2.1 to 5.1) than in men (relative risk, 1.9; 95% CI, 1.6 to 2.3). Among those under 45 years old at entry, the smoking-related sex difference was more pronounced (in women: relative risk, 7.1; 95% CI, 2.6 to 19.1) (in men: relative risk, 2.3; 95% CI, 1.6 to 3.2). Serum total cholesterol, HDL cholesterol, and systolic blood pressure were also highly significant predictors in both sexes.ConclusionsSmoking was a stronger risk factor for myocardial infarction in middle-aged women than in men. Relative risks associated with serum lipids and blood pressure were similar despite large sex differences in myocardial infarction incidence rates. (Circulation. 1996;93:450-456.)Key Wordscoronary disease, smoking, blood pressure, epidemiology, lipids.

ISSN:0009-7322    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

BackgroundAccelerated coronary arteriosclerosis is the major obstacle to long-term survival after cardiac transplantation. Endothelial dysfunction is common early posttransplant. The relationship between early endothelial dysfunction and the development of allograft arteriosclerosis has not been analyzed serially with intravascular ultrasound in the same patients. We hypothesized that an early constrictor response to acetylcholine, indicative of endothelial dysfunction, may predict the development of transplant coronary arteriosclerosis.Methods and ResultsEndothelium-dependent vasomotion was assessed early posttransplant in 20 patients by serial intracoronary acetylcholine infusion, and the percent change in diameter was measured by quantitative angiography. The development of arteriosclerosis was studied by use of intravascular ultrasound in the same 20 patients by quantifying the changes in intimal index (Delta Ii) and maximal intimal thickness [Delta Mt] of 46 matched coronary segments between initial and 1-year follow-up studies. Coronary segments with endothelial dysfunction (constriction greater or equal to 5%; n = 23) demonstrated a significantly greater increase in mean Ii and Mt by 1 year posttransplant compared with segments with normal endothelial function (n = 23) (Delta Ii = 7 plus/minus 2% versus 2 plus/minus 1% [P < .05] and Delta Mt = 140 plus/minus 40 versus 50 plus/minus 20 micro meter [P < .05]). No other parameters examined predicted the development of allograft arteriosclerosis in the initial year posttransplant.ConclusionsPaired studies that used intravascular ultrasound showed that early endothelial dysfunction predicts the development of allograft arteriosclerosis during the initial year posttransplant. This early pathophysiological feature is likely an important marker that could be useful in therapeutic trials. (Circulation. 1996;93:457-462.)Key Wordsendothelium, acetylcholine, ultrasonics, transplantation, atherosclerosis.

ISSN:0009-7322    

出版商:OVID    

年代:1996

数据来源: OVID