Angiographic evolution of intracoronary thrombus and dissection following percutaneous transluminal coronary angioplasty (the Thrombolysis and Angioplasty in Unstable Angina [TAUSA] trial).

The evolution and progression of thrombus and dissection after percutaneous transluminal coronary angioplasty (PTCA) are unknown. As part of the protocol of the Thrombolysis and Angioplasty in Unstable Angina (TAUSA) trial, 1 and 15 minutes post-PTCA angiograms were routinely performed and evaluated by the core laboratory for the presence of thrombus and either minor or major dissection. Thrombus was present at 1 minute in 4.4% of culprit lesions. This increased to 16% at 15 minutes (p < 0.005) and was equally seen in patients receiving both urokinase and placebo. Any dissection was noted in 25.2% at 1 minute versus 30.5% at 15 minutes (p < 0.08), and this trend was mainly related to an increase in major dissection with urokinase at 15 minutes versus 1 minute (10.1% vs 5.9%, respectively, p = 0.10). The in-hospital clinical outcome of patients with lesions that did or did not have thrombus or major dissection at 1 and 15 minutes was retrospectively assessed in the placebo group. The presence of either thrombus or major dissection at 1 minute was associated with a subsequent incidence of acute closure of 14% and an incidence of emergency bypass surgery of 11% (p < 0.01 compared with no thrombus or major dissection at 1 minute). The absence of thrombus and major dissection at 15 minutes (n = 173) was associated with no subsequent acute closure or emergency bypass surgery, (p < 0.05 for acute closure vs thrombus or major dissection at 15 minutes). Thrombus evolves progressively over 15 minutes after PTCA in unstable angina, whereas dissection is usually present immediately after PTCA. The absence of thrombus and major dissection at 15 minutes is associated with very low-acute in-hospital complications. Delayed angiograms following standard balloon angioplasty for unstable angina may be predictive of low complications and our study suggests a possible role for their use.

Angioplasty of complex lesions in ischemic rest angina: results of the Thrombolysis and Angioplasty in Unstable Angina (TAUSA) trial.

OBJECTIVES: This study sought to analyze the role of complex lesion morphology on the acute results of angioplasty. BACKGROUND: Acute complications of angioplasty are higher in unstable than in stable angina. The unstable culprit lesion is usually complex, indicative of plaque disruption and thrombus formation. Previous nonrandomized studies have shown that the presence of intracoronary thombus increases morbidity after coronary angioplasty. The role of complex morphology in coronary angioplasty outcome was studied in a prespecified subgroup analysis of a large multicenter coronary angioplasty trial. METHODS: The results of coronary angioplasty from the Thrombolysis and Angioplasty in Unstable Angina (TAUSA) trial were analyzed. This large trial randomized 469 patients in double-blinded manner to receive either intracoronary urokinase or placebo during coronary angioplasty of the culprit lesion in ischemic rest angina with or without recent infarction. The study presented here analyzes in detail the results of coronary angioplasty in complex versus simple lesions in the urokinase and placebo groups. Complex lesions were defined before angioplasty by a core laboratory as having one or more of the following: irregular borders, overhanging edges, ulcerations or intraluminal filling defects proximal or distal to the lesion. RESULTS: Of the 469 patients, 458 had identifiable culprit lesions, of which 245 were complex and 213 were simple. Complex lesions were associated with a higher abrupt closure rate than simple lesions (10.6% vs. 3.3%, respectively, p < 0.003). Patients with complex lesions also had higher recurrent in-hospital angina (p < 0.02) and emergent bypass surgery (p < 0.02). Further analysis of complex lesions revealed that abrupt closure was particularly high in the urokinase group (15.0% vs 5.9% for the placebo group, p < 0.03), and most abrupt closures were thrombotic. Composite clinical end points were also significantly higher with complex lesions and urokinase. In the placebo group, complex lesions had a higher abrupt closure rate as well as postcoronary angioplasty filling defects, but clinical end points were not significantly different. CONCLUSIONS: Complex lesions before coronary angioplasty increase acute complication rates after coronary angioplasty. Urokinase as administered in the TAUSA trial had significant adverse effects, especially in complex lesions. However, even in the placebo arm, complex lesions were associated with higher complication rates than simple lesions. Newer antithrombotic measures that particularly target the platelet may eventually decrease complication rates in these lesions.

Adjunctive thrombolytic therapy during angioplasty for ischemic rest angina. Results of the TAUSA Trial. TAUSA Investigators. Thrombolysis and Angioplasty in Unstable Angina trial.

BACKGROUND: Acute closure is increased after angioplasty in unstable angina, and adjunctive intracoronary thrombolytic therapy has been used successfully to increase angiographic success. The role of prophylactic thrombolytic therapy during angioplasty in unstable angina is unknown. METHODS AND RESULTS: Four hundred sixty-nine patients with ischemic rest pain with or without a recent (< 1 month) infarction were randomized in double-blind fashion to intracoronary urokinase or placebo. Randomization was carried out in two sequential phases. In phase I, 257 patients were randomized to 250,000 U of urokinase or placebo given in divided doses at the time of angioplasty. In phase II, 212 patients were randomized to 500,000 U of urokinase or placebo in divided doses. All patients were pretreated with aspirin, and activated clotting times were followed to maintain them at > 300 seconds during angioplasty. Angiographic end points of thrombus after angioplasty were insignificantly decreased by urokinase (30 [13.8%] versus 41 [18.0%] with placebo; P = NS). Acute closure, on the other hand, was increased with urokinase (23 [10.2%] versus 10 [4.3%] with placebo; P < .02). The difference in acute closure between urokinase and placebo was more striking at the higher dose of urokinase (P < .04) than in phase I at the lower urokinase dose (P = NS). Adverse in-hospital clinical end points (ischemia, infarction, or emergency coronary artery bypass surgery) were also increased with urokinase versus placebo (30 [12.9%] versus 15 [6.3%], respectively; P < .02). Angiographic and clinical end points were worse with urokinase in unstable angina without recent infarction than with angioplasty after a recent infarction. CONCLUSIONS: Adjunctive urokinase given prophylactically during angioplasty for ischemic rest angina as administered in this trial is associated with adverse angiographic and clinical events. These detrimental effects may be related to hemorrhagic dissection, lack of intimal sealing, or procoagulant or platelet-activating effects of urokinase.