title: Angiographic evolution of intracoronary thrombus and dissection following percutaneous transluminal coronary angioplasty (the Thrombolysis and Angioplasty in Unstable Angina [TAUSA] trial).
abstract: 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.
authors.affiliation: Department of Medicine, Mount Sinai Hospital, New York, New York, USA.
authors.forename: J A
authors.initials: JA
authors.lastname: Ambrose
authors.forename: O D
authors.initials: OD
authors.lastname: Almeida
authors.forename: S K
authors.initials: SK
authors.lastname: Sharma
authors.forename: G
authors.initials: G
authors.lastname: Dangas
authors.forename: D E
authors.initials: DE
authors.lastname: Ratner
mesh_terms: D000208:Acute Disease; D000784:Aortic Dissection / Q000000981:diagnostic imaging / Q000209:etiology*; D000789:Angina, Unstable / Q000188:drug therapy / Q000628:therapy*; D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects; D003323:Coronary Aneurysm / Q000000981:diagnostic imaging / Q000209:etiology*; D017023:Coronary Angiography; D001026:Coronary Artery Bypass; D003327:Coronary Disease / Q000209:etiology; D003328:Coronary Thrombosis / Q000000981:diagnostic imaging / Q000209:etiology*; D018450:Disease Progression; D005343:Fibrinolytic Agents / Q000627:therapeutic use; D005544:Forecasting; D006801:Humans; D015994:Incidence; D017202:Myocardial Ischemia / Q000209:etiology; D010919:Placebos; D012189:Retrospective Studies; D015912:Thrombolytic Therapy; D013997:Time Factors; D016896:Treatment Outcome; D014568:Urokinase-Type Plasminogen Activator / Q000627:therapeutic use
chemical_list: D005343:Fibrinolytic Agents; D010919:Placebos; D014568:Urokinase-Type Plasminogen Activator