Objectives . We designed a randomized trial to evaluate the effects of heparin administration in conjunction with anistreplase (anisoylated plasminogen streptokinase activator complex [AFSACD on arterial patency and clinical end points. Background. The role of conjunctive intravenous heparin therapy with APSAC has not been tested despite the recommen-dations that intravenous heparin should be used. Methods Four hours after APSAC administration, 2,50 patients with acute myocardial infarction were randomly assigned to receive 325 mg of either aspirin alone or aspirin and a continuous infusion of hemdn (15 IU&g boody weight per h) . Clinical ischemic events and bleeding complications were monitored . On hospital day 5, coronary arteriography and left ventriculography were performed. Results. The primary end point of the trial (the combined outcome of death, reinfarction, recurrent ischemia and occlusion of the infarct-related artery) occurred in 42% of the heparin-treated group versus 43% of the group treated without heparin (p = 0.94). A patent artery was present in 80% of the patients treated with heparin and in 73% of those treated without heparin (p = 0.26). Left ventricular function, as measured by ejection fraction, was well preserved in both groups (52% vs. 50.5%, respectively, p = 0.29). The overall bleeding rate was higher in patients with (32%) than without (17 .2%) heparin (p = 0.006). after APSAC in acute myocardial infarction does not reduce the combined incidence of death, reinfarction, recurrent ischemia and xcluslon the infarct-related artery . Furthermore, withholding intravenous heparin therapy is associated with a 46% reduction in bleeding complications do not support the addition of intravenous heparin after APSAC therapy, as currently recommended, and suggest that a strategy of withholding heparin is simpler and safer and does not place the

We determined the timing of ischemic complications within 30 days after percutaneous coronary intervention (PCI) in patients enrolled in the Enhanced Suppression of the Platelet IIb/IIIa Receptor with Integrilin Therapy (ESPRIT) trial. Complications (death, myocardial infarction [MI], target vessel revascularization) occurred in 178 of 2064 patients (8.6%) within 30 days. More than 85% of complications occurred within the 24 hours following randomization, with the greatest risk hazard at 12-18 hours. Unexpectedly, 31% of patients who ultimately met criteria for an endpoint MI within 24 hours of PCI had completely normal CK-MB concentrations at the first 6-hour measurement. There was no rebound increase in events after cessation of eptifibatide. Treatment benefit persisted to 30 days. Post-procedural MI is often not detected until greater than or equal to 12 hours after PCI. Treatment with a glycoprotein IIb/IIIa inhibitor is the only modifiable parameter that reduces the risk for early ischemic complications.

Background Although aspirin is beneficial in patients with unstable angina, it is a relatively weak inhibitor of platelet aggregation. The effect of Integrelin, which inhibits the platelet fibrinogen receptor glycoprotein (GP) IIb/IIIa, on the frequency and duration of Holter ischemia was evaluated in 227 patients with unstable angina. Methods and Results Patients received intravenous heparin and standard anti-ischemic therapy and were randomized to receive oral aspirin and placebo Integrelin; placebo aspirin and low-dose Integrelin, 45 μg/kg bolus followed by a 0.5-μg·kg −1 ·min −1 continuous infusion; or placebo aspirin and high-dose Integrelin, 90 μg/kg bolus followed by a 1.0-μg·kg −1 ·min −1 constant infusion. Study drug was continued for 24 to 72 hours, and Holter monitoring was performed. Patients randomized to high-dose Integrelin experienced 0.24±0.11 ischemic episodes (mean±SEM) on Holter lasting 8.41±5.29 minutes over 24 hours of study drug infusion. Patients randomized to aspirin experienced a greater number (1.0±0.33, P P =.01) of ischemic episodes than the high-dose Integrelin group. There was no evidence of rebound ischemia after withdrawal of study drug. In 46 patients, platelet aggregation was rapidly inhibited by Integrelin in a dose-dependent fashion. The number of clinical events was small, and there were no bleeding differences in the three treatment arms. Conclusions Intravenous Integrelin is well tolerated, is a potent reversible inhibitor of platelet aggregation, and added to full-dose heparin reduces the number and duration of Holter ischemic events in patients with unstable angina compared with aspirin.

Objectives, We proposed to examine the relation between angiographic morphologic characteristics and abrupt closure after coronary angioplasty and to develop an empirically based risk stratification system.Background. Certain lesion morphologic characteristics are associated with higher rates of abrupt closure after coronary angioplasty. Previous approaches have been limited by relatively small sample sizes and an inability to combine multiple characteristics to predict risk in an individual patient.Methods. Lesion morphology was determined for 779 lesions in 658 patients undergoing an elective first angioplasty. Abrupt closure occurred in 63 lesions (8.1%). Variables associated with abrupt closure were identified by univariate and stepwise multiple logistic regression analysis, and internal validity was assessed by use of bootstrapping. An empirically based scoring system was developed by assigning different weights to each predictive characteristic and was then validated.Results. Almost all lesion characteristics previously labeled ''adverse'' were associated with an increased risk of abrupt closure, but only total occlusion, location at a branch point, increasing lesion length, evidence for thrombus and right coronary artery location were statistically significant independent predictors. Despite the large sample size, the study was under powered to detect even a 50% increase in risk with many charac teristics. Using a scoring system, we assigned each lesion a specific risk of abrupt closure. The distribution of risk was broad, with 20% of patients having less than or equal to 2.5% risk and 25% having >10% risk. Internal validation techniques revealed that when 10% of patients were randomly eliminated from the sample in multiple iterations, the risk estimates varied, again pointing to the need for a larger sample.Conclusions. Empirically based weighting of lesion characteristics could quantify the risk of abrupt closure for individual patients, but a very large sample will be required to understand the interplay of complex lesion characteristics in altering expected outcomes.

Objectives. We designed a randomized trial to evaluate the effects of heparin administration in conjunction with anistreplase (anisoylated plasminogen streptokinase activator complex [APSAC]) on arterial patency and clinical end points.Background. The role of conjunctive intravenous heparin therapy with APSAC has not been tested despite the recommendations that intravenous heparin should be used.Methods. Four hours after APSAC administration, 250 patients with acute myocardial infarction were randomly assigned to receive 325 mg of either aspirin alone or aspirin and a continuous infusion of heparin (15 IU/kg body weight per h). Clinical ischemic events and bleeding complications were monitored. On hospital day 5, coronary arteriography and left ventriculography were performed.Results. The primary end point of the trial (the combined outcome of death, reinfarction, recurrent ischemia and occlusion of the infarct-related artery) occurred in 42% of the heparin-treated group versus 43% of the group treated without heparin (p = 0.94). A patent infarct-related artery was present in 80% of the patients treated with heparin and in 73% of those treated without heparin (p = 0.26). Left ventricular function, as measured by ejection fraction, was well preserved in both groups (52% vs. 50.5%, respectively, p = 0.29). The overall bleeding rate was higher in patients with (32%) than without (17.2%) heparin (p = 0.006).Conclusions. Weight-adjusted intravenous heparin therapy after APSAC in acute myocardial infarction does not reduce the combined incidence of death, reinfarction, recurrent ischemia and occlusion of the infarct-related artery. Furthermore, withholding intravenous heparin therapy is associated with a 46 % reduction in bleeding complications. Our findings do not support the addition of intravenous heparin after APSAC therapy, as currently recommended, and suggest that a strategy of withholding heparin is simpler and safer and does not place the patient at increased risk for ischemic complications after myocardial infarction.

We report the a case of hugging balloons through an 8-French guiding catheter to stabilize an ectatic right coronary artery following failed thrombolytic therapy in the setting of acute myocardial infarction. Angiographic follow-up at 1 wk and 6 mo revealed persistent vessel patency.

There are limited data regarding percutaneous transluminal coronary angioplasty (PTCA) in patients aged >80 years, a rapidly expanding population that has a 20% prevalence of symptomatic coronary artery disease.1–3 Two studies have reported relatively low success rates, high procedural morbidity and mortality, and no data on restenosis,4,5 whereas a third reported a higher success rate, but had limited angiographic follow-up—only in symptomatic patients.6 We therefore undertook a study to assess the early and long-term outcome of octogenarian patients treated with PTCA.