Angioplasty For Unstable Angina Research Articles

Editorial: Managing Coronary Thrombus in the Cath Lab During PCI

The last two articles specifically address the question of therapeutic maneuvers for dealing with intracoronary thrombus during PCI. Either the thrombus is removed by aspiration or manual thrombectomy or embolic protection devices are deployed to prevent downstream embolization. Are there any other methods in selected cases? No one in the symposium has considered thrombolytic therapy as a method for dissolving thrombus during PCI. In 1994, our group published the Thrombolyisis and Angioplasty in UnStable Angina (TAUSA) trial which found that routine intra coronary thrombolytic therapy immediately before and after balloon angioplasty for unstable angina was detrimental [1]. However, that was prior to stenting. Other studies indicated that in selected cases, an infusion of IC thrombolytics could be effective for dissolving large intracoronary thrombi albeit at the risk of increasing bleeding complications [2, 3]. In the following case done in 2012, a patient with an ectatic, tortuous right coronary artery with an intra coronary thrombus distal to a severe complex lesion underwent intervention after a NSTEMI. The wire could not cross the lesion, so mechanical and aspiration thrombectomy were not an option. The patient was treated with IV integrilin overnight and 15milligrams of tissue plasminogen activator (t-PA) were infused into the ostium of the right coronary artery over 20 minutes. The sheath was left in place and the patient returned the next day. At that time, a Kinetics-Plus wire was successfully placed across the lesion and a 5.0mm bare metal stenting was deployed with excellent results. The t-PA/integrilin combination had dissolved the thrombus distal to the lesion (Fig. ​11-​-33). The patient tolerated the procedure without significant bleeding. Fig. (1) Right coronary artery in the LAO position showing the severe lesion at the crux with post lesion thrombus (arrows) pre IC thrombolytic and IV integrilin. Fig. (3) Post stenting and post balloon dilatation showing excellent result. These results underscore the possibility in very selected cases of utilizing this combination approach for large intra coronary thrombi in an open artery when other approaches are not possible. Whether integrilin alone with an anti thrombin would have produced the same results is unknown but this thrombus was likely fibrin rich and these are quite sensitive to small doses (10 to 15mgs) of a locally delivered thrombolytic.

Effect of early statin and selective cyclooxygenase-2 inhibitor therapy on C-reactive protein level after percutaneous coronary angioplasty in unstable angina.

We evaluated the effect of cyclooxygenase-2 inhibitor rofecoxib added to atorvastatin, initiated immediately after percutaneous coronary angioplasty (PCI), on C-reactive protein (CRP) and interleukin-6 (IL-6) in patients with unstable angina (UA). Sixty patients were prospectively randomized to receive: (A) 10 mg atorvastatin or (B) 40mg atorvastatin or (C) atorvastatin 40 mg plus rofecoxib 12.5 mg. Treatment was continued for 6 months. CRP and IL-6 levels increased within 48 hours after PCI in all groups, in comparison with A and B, a more pronounced decrease in CRP (mg/l) and IL-6 (pg/ml) levels at 3- and 6-month follow-up was present in C: CRP at 6 months: 0.76 vs. 1.92 vs. 0.11, p<0.05; IL-6 at 6 months: 0.02 vs. 0.04 vs. 0.01, p<0.05. At 6-month follow-up the reduction in CRP level occurred in 70% of subjects with CRP higher than median (3.6mg/l) at baseline vs. 15% of patients with CRP lower than median (p<0.041). After PCI in UA, cyclooxygenase-2 inhibitor rofecoxib added to atorvastatin reduced CRP and IL-6 levels more profoundly than atorvastatin alone at 3- and 6-month after intervention. In the group receiving combined therapy, reduction in CRP levels was more frequently observed in patients with higher CRP at baseline.

Coronary stenting versus balloon angioplasty for unstable angina

Coronary stenting versus balloon angioplasty for unstable angina

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.

Results of percutaneous transluminal coronary angioplasty in unstable angina and non-Q-wave myocardial infarction. Observations from the TIMI IIIB Trial.

This report describes the results of percutaneous transluminal coronary angioplasty (PTCA) in the Thrombolysis in Myocardial Ischemia (TIMI) IIIB Investigation. PTCA was performed before hospital discharge in 444 of 1473 patients with either unstable angina pectoris or non-Q-wave myocardial infarction (NQWMI) enrolled in TIMI IIIB. Angiographic success was observed in 96.1% of patients. For the entire cohort, the cumulative incidences of death and infarction at 1 year were 2.0% and 8.2%, respectively. The periprocedural incidence of myocardial infarction was 2.7%; emergency coronary bypass surgery, 1.4%; and death, 0.5%. By 1 year of follow-up, 122 patients (28.0%, Kaplan-Meier) had an additional revascularization procedure, 75 (61.5%) had PTCA only, 30 (24.6%) had coronary bypass surgery only, and 17 (13.9%) had both procedures. The results of PTCA were not improved by routine pretreatment with intravenous tissue plasminogen activator (TPA). Periprocedural myocardial infarction was more common among patients receiving TPA than placebo (odds ratio [OR], 2.19; P = .03) and among those with unstable angina than those with NQWMI (OR, 15.5; P = .007). No difference in outcome was observed when patients were analyzed according to age (OR, 1.06; P = .092) or sex (OR, 1.54; P = .51). Variables predictive of poor outcome were PTCA within the first 24 hours of enrollment, PTCA site being the left anterior descending coronary artery, and unsuccessful angiography. In TIMI IIIB, PTCA was performed for patients with unstable angina and NQWMI with a very high rate of angiographic success and a low incidence of complications. By 1 year, repeat revascularization was performed in 28.0% of patients. Routine pretreatment with thrombolysis did not enhance outcome.

Angioplasty of complex lesions in ischemic rest angina: Results of the Thrombolysis and Angioplasty in Unstable Angina (TAUSA) Trial

This study sought to analyze the role of complex lesion morphology on the acute results of angioplasty. 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. 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. 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. 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.

Antiplatelet, antithrombotic, and lytic therapy for unstable angina, and the appropriate role of revascularization.

The management of unstable angina continues to be a challenge for the clinician. Evidence is accumulating that inflammation plays an important role in plaque rupture and thrombosis. Thrombolytic treatment is not indicated in unstable angina, and in fact may even be harmful. The use of new platelet glycoprotein IIb/IIIa receptor antagonists and direct thrombin inhibitors offers great potential in the management of unstable angina. Balloon angioplasty for unstable angina is associated with a high major complication rate, which can be reduced by the use of these novel agents. New techniques such as directional atherectomy do not appear to be safer than balloon angioplasty.

Urokinase helpful for angioplasty in unstable angina

Urokinase helpful for angioplasty in unstable angina

Adjunctive thrombolytic therapy for angioplasty in ischemic rest angina: Results of a double-blind randomized pilot study

Objectives. A multicenter pilot study was instituted to assess the role of intracoronary thromholytic therapy during angioplasty for ischemic ress angina.Background. Acute thrombotic coronary occlusion is increased during angioplasty for unstable angina, and intracoronary thrombolytic agents have been used to maintain patency. Prophylactic use of intracoronary thrombolytic agents has been advocated in certain high risk subgroups, although no studies have randomized therapy.Methods. Ninety-three patients with either unstable angina and pain at rest (trial A, 66 patients) or postinfarction pain at rest (trial B, 27 patients) were randomized in double-blind fashion to administration of either intracoronary urokinase, 150,000 U, or saline solution placebo given immediately before angioplasty. Cineangiograms of the culprit lesion were recorded and analyzed in blinded fashion by a core laboratory for definite or possible (haziness) filling defects 15 min after angioplasty or after acute closure.Results. Urokinase decreased filling defects at 15 min after angioplasty in comparison, with placebo (14% vs. 29%, respectively, p = 0.08). Four patients in each treatment group developed acute vessel closure. However, although urokinase significantly reduced the incidence of filling defects in trial A (3% vs. 23%, p = 0.03), the drug had no effect at the selected dose in trial B (42% vs. 43%, respectively). Acute vessel closure occurrred significantly more frequently in trial B than in trial A, and urokinase at the selected dose also had no effect. Ischemic events after angioplasty appeared to be related more to dissection than to thrombosis, although redilation, which was more frequent after placebo administration, may have reduced their incidence as well as that of acute closure.Conclusions. These data suggest a possible role for intracoronary urokinase during angioplasty for unstable angina. The lack of effect after infarction may represent a greater thrombus burden or degree of plaque disruption. A trial utilizing higher doses of urokinase in a larger patient group is in progress.

Aggressive clinical pattern of angina at restenosis following coronary angioplasty in unstable angina

The frequency, clinical pattern, and timing of recurrent angina following successful single-lesion percutaneous transluminal coronary angioplasty (PTCA) was assessed in a consecutive group of 104 patients with stable angina and in 85 with unstable angina. In addition, the relationship between lesion morphology and angiographic features and the pattern of recurrent angina was determined. Restenosis, defined as recurrence of symptoms with >50% stenosis at the site of PTCA, occurred in 25 (24%) of the stable group and in 23 (27%) of the unstable group ( p = NS). The pattern of angina at repeat presentation was aggressive in nature in 8% of the stable group and in 48% of the unstable group ( p = 0.002). The time interval between the recurrence of symptoms and repeat coronary angiogram or PTCA was longer in the nonaggressive group than in the aggressive group, 16 ± 12.1 and 5 ± 6.8 weeks, respectively ( p < 0.003). The key factors predicting the recurrent angina pattern identified by multiple logistic regression analysis were the angina status pre-PTCA ( p = 0.001) and the presence of double-vessel disease ( p = 0.01). An aggressive pattern of angina at the time of restenosis is frequent in patients with unstable angina at the time of PTCA, and close post-PTCA surveillance is necessary in these patients.

Angiography in unstable angina

Within the last decade, it has been appreciated that the acute coronary syndromes of unstable angina, non-Q-wave, and Q-wave myocardial infarction often share a common pathogenesis based on plaque disruption and thrombosis. Such “acute” lesions frequently have a characteristic angiographic appearance with sharp overhanging edges, irregular borders, and intraluminal lucency. This review focuses on the benefits and limitations of qualitative assessment of coronary lesion morphology, with respect to the sensitivity, specificity, and prognostic significance of complex lesions and intracoronary thrombi. Angiographic findings following thrombolysis for unstable angina are discussed, as well as the possible role for thrombolytic therapy as an adjunct to angioplasty in unstable angina.

Importance of delayed angiographic views following angioplasty in unstable angina- preliminary results of tausa trial

Importance of delayed angiographic views following angioplasty in unstable angina- preliminary results of tausa trial

Desirability of immediate surgical standby for coronary angioplasty.

To assess the value of emergency surgical standby for percutaneous transluminal coronary angioplasty. Retrospective review of the major complications of coronary angioplasty in a regional cardiac centre. All angioplasties were performed in the cardiac catheterisation laboratory of Wythenshawe Hospital with surgical standby in an adjoining operating theatre. 1262 vessels were dilated in 1032 patients (mean age 53 years) between 1984 and 1989. In-hospital mortality from emergency surgical revascularisation after angioplasty; the rate of myocardial infarction and overall morbidity. Coronary angioplasty achieved primary success in 90% of cases. Thirty eight (3.7%) patients (five women (mean age 55.8) and 33 men (mean age 53.0] were referred for urgent surgical revascularisation--36 direct to operation and two within 24 hours. All patients survived surgery. Five of the 38 had had a previous angioplasty to the same vessel and one had had previous coronary artery grafts. Four of the 38 had an angioplasty for unstable angina. Eighteen had single, 13 double, and seven triple vessel coronary artery disease. The target vessel was the left anterior descending in 25, right coronary artery in nine, circumflex in three, and the left anterior descending and circumflex coronary arteries in one. Five required external cardiac massage on the way to the operating theatre; two of them had a left main stem occlusion. Four internal mammary artery and 60 reversed saphenous vein grafts were implanted (1.6 per patient). Complete revascularisation was achieved in 36 (94.7%) patients. Q wave myocardial infarction occurred in six (15.8%). The final outcome was: none dead, three patients with angina, one late death, one cerebrovascular accident, one late operation for a new left anterior descending lesion, two patients on diuretics with or without an angiotensin converting enzyme inhibitor. One orthotopic transplant was performed in a patient in whom cardiogenic shock developed after the left anterior descending coronary artery became occluded 72 hours after angioplasty. There was no surgical mortality and low morbidity among patients for whom immediate surgical cover was requested.

Coronary angioplasty in unstable angina: time for controlled clinical trials

Coronary angioplasty in unstable angina: time for controlled clinical trials

Coronary angioplasty in unstable angina and stable angina: A comparison of success and complications : Perry RA, Seth A, Hunt A, et al: Br Heart J 60:367–372, 1988

Coronary angioplasty in unstable angina and stable angina: A comparison of success and complications : Perry RA, Seth A, Hunt A, et al: Br Heart J 60:367–372, 1988

“High-risk” percutaneous transluminal coronary angioplasty

Of 6,500 percutaneous transluminal coronary angioplasty procedures performed between June 1980 and June 1987, 3,501 (1,604 single lesion and 1,897 multiple lesion) were performed in "low-risk" patients with a procedure-related mortality of 0.2 to 0.3%. In comparison, several clinical variables were identified that increased procedural risk by up to 50-fold. These factors include left main dilatation (n = 103, mortality 3.9%), left main equivalent dilatation (n = 77, mortality 2.6%), ejection fraction less than or equal to 40% (n = 664, mortality 2.7%), age greater than or equal to 70 years (n = 1,038, mortality 1.4%), dilatation of all 3 vessels (n = 305, mortality 1.3%), combined diagnostic catheterization and angioplasty for unstable angina (n = 193, mortality 1.5%), and percutaneous transluminal coronary angioplasty for acute myocardial infarction (n = 446, mortality 8.5%). Important considerations in the selection and management of these high-risk patients are discussed.

Coronary angioplasty in unstable angina and acute infarction

Coronary angioplasty in unstable angina and acute infarction

Sequential intracoronary streptokinase and transluminal angioplasty in unstable angina with evolving myocardial infarction

Sequential intracoronary streptokinase and transluminal angioplasty in unstable angina with evolving myocardial infarction