Thrombotic Occlusion of the Left Main Coronary Artery During Coronary Angiography

A. Javier Sanz, MD, Felipe Hern√°ndez, MD, Jua
A. Javier Sanz, MD, Felipe Hern√°ndez, MD, Jua
Cardiac catheterization and coronary angiography (CA) carry a small but definite risk of complications. In a review of different series, mortality rates ranged from 0.02–3.70% and myocardial infarction rates ranged from 0.0–7.4%.1,2 In recent series, both complications occurred in approximately 0.1% of cases. Abrupt vessel closure during CA is an infrequent complication, which was described more frequently in early reports with an estimated incidence of 1%.3 More recently, it has been reported in approximately 0.1% of CA.4 The rate is higher when intervention is performed, ranging from 2.0–8.3%.5 We present a case of left main coronary artery (LMCA) occlusion due to thrombus during the performance of a diagnostic CA. Case Report. A 69-year-old female with a personal history of severe mitral stenosis of rheumatic origin and a previous episode of pulmonary edema was referred to our center for a percutaneous mitral balloon valvuloplasty (PMV). Her functional class was New York Heart Association grade II and she was being treated with diuretics and potassium supplements, as well as digoxin and coumadin because of chronic atrial fibrillation. She had no history or known risk factors for coronary artery disease apart from her advanced age. Seven days prior to the procedure, a transthoracic (TTE) and transesophageal echocardiogram (TEE) was carried out. It confirmed the presence of severe mitral stenosis, favorable anatomic features for PMV and absence of thrombus in the left atrium (including the left appendage). Ten days before the procedure, coumadin was discontinued and unfractionated intravenous heparin infusion was initiated. Infusion was stopped approximately three hours before catheterization. Platelet count was normal and aPPT prior to the procedure was 60 seconds (1.8 times control). First, a right and left heart catheterization was performed in order to confirm the diagnosis. An 8 French (Fr) sheath (Input.S, Medtronic® AVE, AVE Ireland Limited, Galway, Ireland) was inserted through the right femoral vein and a 6 Fr sheath was inserted through the left femoral artery using the Seldinger technique. Both sheaths were flushed with saline solution with 10 units of heparin per milliliter immediately after insertion. Pressure measurements were obtained by means of a 7 Fr Swan-Ganz catheter and a 6 Fr “pigtail” catheter. All catheters employed were also flushed with heparin solution before use. The pigtail catheter was inserted over a guidewire, which was then removed and carefully washed with saline plus heparin solution. A left ventriculography was carried out using non-ionic contrast (Ioversol; Optiray 350®, Mallinckrodt Medical Imaging, Damastown, Dublin, Ireland), during which patency of both coronary arteries could be seen. Subsequently, we performed a CA, as we routinely do for patients over age 60. The pigtail catheter was removed directly and a 6 Fr left Judkins catheter was inserted over the guidewire. The sheath was not flushed again before the catheter was introduced. After the catheter reached the ascending aorta and the guidewire was removed, we found that no pressure transmission was obtained; the catheter was removed and a large thrombus in the distal end was visualized. A new catheter was inserted, and we checked that pressure was correctly transmitted and blood easily aspirated through the catheter while it was placed in the ascending aorta. After catheterization of the LMCA, an initial test injection of contrast was made and total occlusion of the vessel was observed (Figure 1). The patient developed chest pain and ST-segment elevation in a few seconds. The catheter was removed and exchanged for a 6 Fr angioplasty guide catheter. A 0.014´´ guidewire was advanced through the occlusion although no blood flow beyond it was achieved. Rapid hemodynamic deterioration took place, followed by cardiac arrest secondary to ventricular fibrillation, so resuscitation maneuvers were initiated. Multiple high-energy defibrillation attempts, endotracheal intubation, vasoactive drugs and temporary transvenous pacing were required. A 2.5 mm AVE balloon catheter was inserted and inflated in the LMCA. After this, lumen recanalization and distal TIMI I flow were achieved, and it was possible to observe a large thrombus in the LMCA (Figure 2). Subsequently, a 3 x 16 mm AVE stent was implanted, resulting in angiographic TIMI II flow. After an intraaortic counterpulsation balloon was inserted, TIMI III flow was obtained. Total occlusion lasted 21 minutes. As it was now evident that the cause of the occlusion was clot and not a dissection, an intravenous bolus of abciximab was administered, followed by continuous infusion. The patient was then transferred to the Coronary Care Unit, where she could be extubated 8 hours later. The peak creatine kinase value was 974 IU/L and it was reached approximately 24 hours after the procedure. No Q-waves appeared on the electrocardiogram. Abciximab infusion was administered concomitantly with intravenous unfractionated heparin and double oral anti-aggregation with aspirin and clopidogrel. Both abciximab and heparin were discontinued four hours after the procedure because of mild upper gastrointestinal bleeding. No further complications developed and intraaortic counterpulsation could be stopped after 24 hours. Ten days later, during which the patient was treated with intravenous heparin, oral aspirin and clopidogrel, cardiac catheterization was repeated. Stent patency was confirmed and PMV was successfully performed using a 26 mm Inoue Balloon. Both a contrast ventriculography and a post-valvuloplasty TTE ruled out any abnormalities in left ventricular wall motion and systolic function. The patient was discharged 3 days after PMV, on double oral anti-aggregation (clopidogrel and aspirin). Three months later, we performed a follow-up CA. The patient was asymptomatic, the stent remained patent (Figure 3) and left ventricular function was preserved. Clopidogrel had been stopped and oral anticoagulation was reinitiated. Discussion. The most common causes of abrupt vessel closure are medial dissection and/or intracoronary thrombosis. Other possible mechanisms, such as severe spasm or coronary embolism, occur more infrequently.3,5 In our patient, angiographic findings were typical of clot; there was a globular filling defect with contrast “staining”, which became more evident after lumen patency restoration. There are several possible origins. Intracardiac thrombus situated either in the left atrium or ventricle might have been dislodged during left ventriculography, thus causing coronary embolism. We believe this is rather improbable since a TEE was performed prior to the procedure and no intracardiac thrombi had been detected. A left ventriculography was also performed before the development of coronary occlusion and it did not show any intraventricular filling defects or images suggestive of thrombus. Another possibility is that debris or thrombotic material originating from any aortic atherosclerotic plaques might have become detached by the tip of the catheter, carried into the coronary ostium and introduced after the first contrast injection. Complex aortic plaques have been related to embolic events and mobile fragments of potentially thromboembolic material have been described.6,7 Nevertheless, this is quite improbable since the patient had no significant risk factors for atherosclerosis and there were no data from her personal history, physical examination, TEE or CA suggestive of extensive atherosclerotic disease. Another possible mechanism is intracoronary formation of thrombus. This might have occurred because of endothelial disruption due to impact of the catheter tip. However, thrombus was detected in the first Judkins catheter employed before clinical deterioration, so this possibility is very small. We believe that the thrombotic material most likely formed on the catheter or guidewire surface. Deposition of platelets and fibrin on catheters and guidewires takes place quickly when they are introduced into the bloodstream, even in heparinized patients.8,9 As the catheter is removed, such material may be stripped from the surface of the catheter by the tip of the sheath or the arterial wall, particularly if exchanges are made over the wire. When another catheter is inserted, it may “pick up” this thrombus, not necessarily occluding, and carry it upstream as the catheter is advanced. Thus, the thrombotic material can be deposited and embolized into the coronary artery, either spontaneously or when contrast is injected.3 In this patient, clot most likely formed on the surface of the pigtail catheter or the wire inside it. These catheters may be particularly prone to deposition of thrombus distally to the lateral holes, where flow is stagnant.3 Subsequently, despite the fact that we did not exchange catheters over the guidewire, the material might have been stripped off at the tip of the sheath and picked up by the first Judkins catheter, where it caused obstruction and was observed at withdrawal. Some thrombus fragments might have remained adhered to the sheath, which was not flushed again. Thus, the second catheter would have picked up the material, this time without occluding, and carried it to the coronary ostium, where the first dye injection dislodged it. Bonafede et al.10 describe a similar case; they concluded that the most plausible explanation was formation of thrombus within the arterial sheath, probably in relation to prolonged procedure duration. This was certainly not the case with our patient, since the complication appeared shortly after initiating catheterization. Thrombus formation might have been accelerated by other factors in our patient. We routinely use a non-ionic contrast medium, because a higher incidence of adverse effects, arrhythmias and hemodynamic instability has been associated with the use of ionic media.11,12 Nevertheless, while the latter possess an inhibitory effect both on platelet aggregation and thrombus formation, the former may induce platelet degranulation and activation, have fewer anticoagulant properties, and have caused concern over a possible association with thrombotic complications.1,4,12–15 Adherence of platelets to catheters and guidewires is also greater with non-ionic contrast media.16 Thus, the use of a non-ionic contrast might have contributed to clot formation in this patient. In the same way, this may be facilitated in the case of a thrombotic state after discontinuation of oral anticoagulants, which seems to be particularly pronounced about one week after withdrawal.17 In our patient, this should have been offset by the concomitant administration of intravenous heparin. Nevertheless, a transient hypercoagulable state after interruption of heparin infusion, at least in the context of unstable angina and angioplasty, has also been described.18,19 We cannot rule out the potential role of these coagulation disarrangements in thrombotic complications during CA. Different measures have been recommended to prevent this complication,1,3,10,15 such as shortening procedure time as much as possible, avoiding guidewires for catheter exchanges, performing left ventriculography as the last procedure, flushing catheters away from the coronary ostia, not allowing contrast and blood to remain stagnant together in catheters and syringes, and flushing the side arm of the arterial sheath before any new catheter is inserted. Some have advocated the use of systemic heparinization during this procedure, but this has not been shown to reduce the incidence of thrombotic complications.1,15,20 Laboratories currently use heparin in less than 50% of procedures,2 and we follow this common practice. We also routinely delay administration of heparin during PMV until successful atrial septal puncture has been confirmed. We continue to do this because we are concerned about the risk of cardiac tamponade in the case of unsuccessful puncture. We treated the patient with urgent balloon angioplasty plus stent implantation. Stenting has proven an effective option in the management of abrupt closure during coronary intervention.5,21 There is also evidence that stents can be safely and successfully implanted in the LMCA, both in elective and emergency situations.22–24 The possibility of thrombus aspiration and/or thrombectomy devices is to be considered, although because it takes a longer time to set them for use, we proceeded to perform a conventional balloon angioplasty plus stent implantation in this emergency situation. Intra-aortic counterpulsation had an immediate favorable effect in TIMI grade blood flow, and its use in the setting of high-risk angioplasty and cardiogenic shock has also been recommended, particularly in the setting of myocardial infarction.25–27 Because of the angiographic features of clot, we administered abciximab, a potent antiplatelet agent that has also proven effective in this context.28,29 PTCA and anti-aggregation are superior to thrombolytics (either intravenous or intracoronary) in the setting of abrupt vessel closure. We do not currently use intracoronary thrombolytic therapy; a randomized study showed no benefit over heparin as an adjunct to angioplasty.30 Conclusion. Thrombotic vessel closure still occurs during conventional CA. Although several factors may have an influence on the development of this complication, the formation of clot on catheter surfaces probably plays an outstanding role. Because of this, particular attention must be paid to adequate and meticulous management of vascular sheaths and catheters, as well as a number of different preventive measures. When vessel closure including the LMCA takes place, it can be successfully relieved with the use of balloon angioplasty, stent implantation, and immediate anti-aggregation with abciximab.
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