Acute coronary occlusion during coronary angiography in two cases. Treatment by transluminal disobliteration.

Acute coronary obstruction occurred in two patients during coronary angiography. In one case the obstruction was in the left main coronary artery; in the other it was close to the origin of the left anterior descending artery. In both cases acute cardiac ischaemia ensued, with electromechanical dissociation and collapse, which was not reversible by resuscitation. Rapid disobliteration of the occluded coronary artery was done with a guide-wire pushed through the obstruction via the coronary catheter. The recanalisation was completed by an intracoronary perfusion of streptokinase in one case. In both cases recovery was rapid and spectacular. The occurrence of acute ischaemia during coronary angiography should suggest accidental coronary occlusion. If a thromboembolic origin is suspected, transluminal disobliteration should be attempted. It is simple and can reverse a dangerous condition.     

Acute coronary occlusion during percutaneous transluminal coronary angioplasty.

Two hundred and forty percutaneous transluminal coronary angioplasty procedures were performed in three centres over a two year period. Acute occlusion of the vessel undergoing angioplasty was seen on 20 (8%) occasions. The cause of occlusion was determined angiographically and in some cases confirmed at the time of emergency open heart surgery. The mechanism of coronary occlusion was arterial dissection in six cases, persisting coronary arterial spasm in seven, and coronary thrombosis in four. In three patients the mechanism could not be determined. Immediate reintroduction of a balloon dilatation catheter was attempted in 10 patients and resulted in restoration of adequate coronary flow in six. The remaining 14 patients underwent open heart surgery as an emergency procedure.     

Acute coronary occlusion during percutaneous transluminal coronary angioplasty

Two hundred and forty percutaneous transluminal coronary angioplasty procedures were performed in three centres over a two year period. Acute occlusion of the vessel undergoing angioplasty was seen on 20 (8%) occasions. The cause of occlusion was determined angiographically and in some cases confirmed at the time of emergency open heart surgery. The mechanism of coronary occlusion was arterial dissection in six cases, persisting coronary arterial spasm in seven, and coronary thrombosis in four. In three patients the mechanism could not be determined. Immediate reintroduction of a balloon dilatation catheter was attempted in 10 patients and resulted in restoration of adequate coronary flow in six. The remaining 14 patients underwent open heart surgery as an emergency procedure.     

Acute coronary occlusion during transluminal angioplasty: role of coronary thrombosis

We here report on 2 patients treated by transluminal coronary angioplasty, who presented baseline angiographic aspects of an intracoronary thrombus upon vessel stenosis. In both cases mechanical dilatation was successful in increasing vessel diameter, but was complicated by activation of the thrombotic process with clot proliferation--as shown by multiple coarse filling defects irregularly stained by contrast material--and vessel occlusion. The intracoronary injection of streptokinase achieved partial slowing of the thrombotic process, but did not succeed in inhibiting it completely or in restoring vessel patency. As clinical conditions were stable, the patients were not sent to emergency surgery, but were treated conservatively with anticoagulants and platelet inhibitors: in only one patient the procedure was followed by moderate myocardial enzyme release. In both cases the coronary artery was patent at short term angiographic control. These 2 cases confirm that in the outset of transluminal angioplasty an acute coronary occlusion can be managed conservatively by thrombolytic treatment when thrombus formation can be clearly identified the cause of vessel occlusion: the activation of spontaneous lytic systems can completely restore vessel patency. If coronary occlusion was of short duration or collateral supply was adequate, myocardial infarction may not occur and emergency coronary surgery will not be necessary.     

Coronary occlusion during coronary angiography.

Between January 1, 1970, and December 31, 1974, 2981 patients underwent coronary arteriography. Twelve acute coronary dissections or embolizations occurred, an incidence of 0.4%. The incidences of acute occlusions for the Sones and Judkins techniques were 0.19% (4/2077 studies) and 0.88% (8/940), respectively. No instance of acute occlusion has occurred during the past 490 studies performed by the Judkins technique. Eight patients with right coronary artery dissections or circumflex emboli were treated medically. All survived, but in seven a myocardial infarction evolved. Four patients underwent emergency saphenous venous bypass grafting because of refractory ventricular fibrillation (two patients) or because large amounts of myocardium were thought jeopardized (two patients). All patients in this group had interruption of flow supplying the left anterior descending coronary artery. Despite surgical intervention in less than three hours in all patients, survivors all sustained transmural myocardial infarctions. Three patients survived surgery and were discharged home.     

Acute coronary artery occlusion during percutaneous transluminal coronary angioplasty treated by redilation of the occluded segment

Acute occlusion of a coronary artery during percutaneous coronary angioplasty usually results in unremitting ischemia requiring emergency surgical intervention. Seven patients are described, in whom complete occlusion occurred during coronary angioplasty as a result of coronary artery dissection. Despite this, it was possible to reintroduce the balloon catheter immediately and redilate the vessel with abrupt reversal of clinical and electrocardiographic manifestations of ischemia. Six patients had no subsequent evidence of myocardial infarction. The seventh had a slight elevation of serum creatine kinase and transient electrocardiographic changes. All patients were discharged from the hospital without further intervention. Four patients had elective coronary artery bypass surgery (greater than 4 weeks after angioplasty) and three have remained asymptomatic or in improved condition since the coronary angioplasty. It is concluded that sudden occlusion of a coronary artery during coronary angioplasty can be safely treated by redilation in the acute stage.     

Acute occlusion after percutaneous transluminal coronary angioplasty--a new approach

Between July 1980 and November 1982, there were 935 coronary angioplasties attempted at Emory University Hospital. Of these patients, 20 developed acute occlusion. Of these 20, 19 presented within 3 hr of surgery or within 3 hr after stopping a continuous heparin infusion. Five patients required emergency surgery, but in 15 nitrates, nifedipine, and/or repeat angioplasty reopened the artery and the patient could be stabilized on continuous infusions of heparin and nitroglycerin. In only one case was an occluding thrombus evident on angiographic examination. The mechanism of acute occlusion is unknown, but coronary artery spasm may play a role.     

Acute coronary thrombotic occlusion following exercise testing 6 weeks after percutaneous transluminal coronary angioplasty.

Exercise stress testing is often performed following percutaneous transluminal coronary angioplasty (PTCA) in order to evaluate the efficacy of the procedure. Together with thallium-201 (Tl-201) scintigraphy, these noninvasive tests provide valuable data for predicting the recurrence of angina and restenosis. However, concerns regarding the safe timing of exercise testing post-PTCA have been raised in 3 previous case reports. Each case documents acute coronary occlusion shortly after stress testing performed within several days of successful angioplasty, leading to the recommendation that such testing be deferred up to 4 weeks following PTCA. This paper reports a patient in whom acute thrombotic occlusion of the left anterior descending coronary artery (LAD) occurred immediately after a mildly abnormal exercise Tl-201 stress test done 6 weeks after PTCA.     

Acute coronary artery occlusion during percutaneous transluminal coronary angioplasty: reopening by intracoronary streptokinase before emergency coronary artery surgery to prevent myocardial infarction

Percutaneous transluminal coronary angioplasty (PTCA) was complicated by acute coronary artery occlusion associated with ST elevation and severe chest pain in three patients. Within 10 minutes, the occluded artery was reopened by an intracoronary (i.c.) infusion of streptokinase, resulting in the disappearance of chest pain and normalization of ST segments. To keep the artery patent, i.c. streptokinase had to be continued until emergency bypass surgery was performed. In two patients, no myocardial infarction occurred, as shown by a normal postoperative left ventricular angiogram. ECG and thallium-201 scintigram. In the other patient, who was admitted with an inferior infarction and underwent PTCA after i.c. lysis, no infarct extension was observed. These results show that i.c. streptokinase rapidly opens an acute coronary artery occlusion complicating PTCA, preventing myocardial infarction.     

Acute coronary thrombotic occlusion following exercise testing 6 weeks after percutaneous transluminal coronary angioplasty

Exercise stress testing is often performed following percutaneous transluminal coronary angioplasty (PTCA) in order to evaluate the efficacy of the procedure [1]. Together with thallium-201 (T1-201) scintigraphy, these noninvasive tests provide valuable data for predicting the recurrence of angina and restenosis [2]. However, concerns regarding the safe timing of exercise testing post-PTCA have been raised in 3 previous case reports [3–5]. Each case documents acute coronary occlusion shortly after stress testing performed within several days of successful angioplasty, leading to the recommendation that such testing be deferred up to 4 weeks following PTCA. This paper reports a patient in whom acute thrombotic occlusion of the left anterior descending coronary artery (LAD) occurred immediately after a mildly abnormal exercise T1-201 stress test done 6 weeks after PTCA.     

Acute coronary artery occlusion likely due to thrombus occurring during coronary angiography: Report of a case

Twenty-five years ago, fatalities due to acute thrombotic coronary occlusion occurring during coronary angiography were reported not infrequently, but are thought to have been eliminated by changes in technique and equipment. We present a case with documentation of a normal coronary arterial tree just before the time of an abrupt occlusion, which had the angiographic features of clot. The likely source of the thrombus was the arterial sheath. Measures for prevention of this complication are discussed. Cathet. Cardiovasc. Diagn. 43:460–462, 1998. © 1998 Wiley-Liss, Inc.     

Thrombotic occlusion of the left main coronary artery during coronary angiography

A case of left main occlusion due to thrombus during coronary angiography is reported. This rare and extremely dangerous complication was successfully managed with resuscitation maneuvers, hemodynamic support, urgent balloon angioplasty plus stent implantation, anticoagulation with heparin and potent therapy directed at preventing platelet aggregation. The thrombus most likely detached from the arterial sheath, although coexisting circumstances, such as the use of non-ionic contrast or a transient hypercoagulable state, may have had an influence. A careful technique during the procedure is probably the most effective preventive measure.     

Acute coronary artery occlusion during and after percutaneous transluminal coronary angioplasty. Frequency, prediction, clinical course, management, and follow-up

BACKGROUND. Acute coronary artery occlusion after percutaneous transluminal coronary angioplasty (PTCA) continues to remain a serious complication despite significant improvement in operator performance and technological advancements. This retrospective study was performed to ascertain the frequency, predictive variables, management, and outcome of acute coronary artery occlusion. METHODS AND RESULTS. The study was based on data from 1,423 consecutive patients who underwent an elective coronary angioplasty between January 1986 and December 1988. Acute coronary artery occlusion occurred in 104 patients (7.3%). Acute occlusion developed during the dilatation procedure in 80 patients (5.6%) and within 24 hours after the procedure in 24 patients (1.7%). Four clinical and 14 angiographic variables predictive for acute coronary artery occlusion were analyzed in these 104 patients with a complicated procedure and were compared with those in 104 representative patients with successful attempts. Multivariate analysis found three independent predictive variables: unstable angina, multivessel disease, and complex lesions. The overall clinical outcome after management of acute coronary artery occlusion including immediate repeat dilatation (95 patients), use of intracoronary streptokinase (34 patients), or autoperfusion catheter (12 patients) was successful (reduction of lumen diameter to less than 50%, no death, no myocardial infarction [MI], and no emergency surgery) in 42 patients (40%), was a failure without major complication in four patients (4%), and was a failure with major complication (death, MI, and emergency surgery) in 58 patients (56%). The overall mortality rate was 6% (six patients), the overall MI rate was 36% (37 patients), and emergency bypass surgery was required in 30% of patients (31 patients). At 6 months' follow-up of 42 patients with successful management, recurrent angina pectoris due to restenosis occurred in 10 patients (24%), and a late MI occurred in one patient (3%). At 6 months' follow-up of 56 survivors with unsuccessful management (development of MI or need for emergency bypass surgery), recurrent angina occurred in nine patients (16%), and cardiac death in two patients (4%). However, the majority of patients in both groups were either symptom free or had mild angina pectoris. CONCLUSION. Acute coronary artery occlusion during PTCA is often unpredictable, but its frequency is higher in patients with unstable angina, multivessel disease, and complex lesions. Despite immediate redilatation, use of intracoronary streptokinase, and emergency bypass surgery, PTCA is associated with a high mortality and morbidity.     

Acute vascular occlusion caused by percutaneous transluminal coronary angioplasty: early and late results of repeat-PTCA

Acute vascular occlusion after percutaneous transluminal coronary angioplasty (PTCA) often necessitates a prompt aortocoronary bypass-operation (CABG). Alternatively, a re-PTCA can be attempted. In 1500 consecutive patients there was acute symptomatic occlusion due to PTCA 5 min to 16 h after the operation in 47 cases (3.1%). An immediate re-PTCA was attempted in all cases. Results: Reopening was successful in 43 of 47 cases (91%): in 15 patients (30%) within 30 min, in 36 patients (68%) within 60 min and in 42 patients (89%) within 90 min. In eight patients there was early re-occlusion 30 min to 20 h after re-PTCA, necessitating acute CABG in four patients. In 35 patients with re-PTCA the vessel remained open. Re-stenosis occurred within 1 to 10 days in 10 patients, and in additional 12 patients after 2-4 months. In most cases an additional PTCA was successful. Complications: Six patients had an emergency CABG (three with an exchange wire as a stent in the dissected coronary artery). Three patients died (one after CABG); 14 patients experienced myocardial infarction (30%) (in three of these 14 the infarct was large). Conclusion: Acute vascular occlusion after PTCA can successfully be treated by re-PTCA in four of five cases. However a rate of re-stenosis of about 60% is to be anticipated. Reperfusion with re-PTCA is fast and in these patients with transmural ischemia there are obviously less complications in comparison to emergency CABG after PTCA. 60% of the patients remain symptom free or markedly improved and without infarction or emergency CABG after 4 months.