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Ann Thorac Surg 2001;72:1933-1938
© 2001 The Society of Thoracic Surgeons

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Original article: cardiovascular

Safety and efficacy of intraarterial thrombolysis for perioperative stroke after cardiac operation

^a Department of Thoracic and Cardiovascular Surgery, The Cleveland Clinic Foundation, Cleveland, Ohio, USA
^b Department of Neurology, The Cleveland Clinic Foundation, Cleveland, Ohio, USA

* Address reprint requests to Dr Smedira, Department of Thoracic and Cardiovascular Surgery, The Cleveland Clinic Foundation, 9500 Euclid Ave, Desk F25, Cleveland, OH 44195, USA
e-mail: smedirn{at}ccf.org

Presented at the Thirty-seventh Annual Meeting of The Society of Thoracic Surgeons, New Orleans, LA, Jan 29–31, 2001.

	Abstract

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Background. Acute ischemic stroke after cardiac operations is a devastating complication with limited therapeutic options. As clinical trials of thrombolysis for acute ischemic stroke exclude patients with recent major surgery, the safety of intraarterial thrombolysis in this setting is unknown.

Methods. Thirteen patients with acute ischemic stroke within 12 days of cardiac operation underwent intraarterial thrombolysis within 6 hours of stroke symptom onset. The National Institutes of Health Stroke Scale was used to assess neurologic recovery.

Results. The mean age was 69 years (standard deviation ±5 years) and 62% were men. Cardiac procedures included valve operations in 6 patients, coronary artery bypass grafting in 4, valve and coronary artery bypass grafting in 2, and left ventricular assist device in 1 patient. Atrial fibrillation occurred in 5 patients (38%). The mean time from operation to stroke was 4.3 days (standard deviation ± 3 days). Thrombolysis was initiated within 3.6 hours (standard deviation ±1.6 hours) of stroke symptom onset. Recanalization was complete in 1 patient, partial in 5, and 7 patients had low flow. Neurologic improvement occurred in 5 patients (38%). One patient needed a chest tube for hemothorax, 2 others were transfused for low hemoglobin. No operative intervention for bleeding was necessary.

Conclusions. In select patients with acute ischemic stroke after recent cardiac operation, intraarterial thrombolysis appears to be reasonably safe and may lead to neurologic recovery.

	Introduction

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Acute ischemic stroke is one of the most devastating complications after cardiac operation. The incidence of adverse neurologic events, many due to ischemic stroke, has been estimated to be 6% in patients undergoing elective coronary bypass grafting [1] and as high as 16% in patients undergoing valvular procedures or with preexisting cerebrovascular disease [2, 3]. Despite identification of risk factors and steps to alter surgical strategies associated with stroke [4], the incidence has remained relatively unchanged in the past decade [5].

Until recently, treatment of acute stroke has been primarily supportive. In June 1996 the US Food and Drug Administration approved the use of tissue plasminogen activator for treatment of acute ischemic stroke within 3 hours of stroke symptom onset. Multiple studies have demonstrated an increased risk of hemorrhagic complications when tissue plasminogen activator is administered intravenously after 3 hours of stroke onset but an intraarterial approach has been shown to extend the window of therapy to 6 hours from stroke onset [6]. We have used this aggressive therapy in 13 patients who suffered from a cerebral ischemic event after cardiac operation. This report summarizes our experience with direct intraarterial interventions in this highly selected group.

	Material and methods

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Patient selection
From September 1997 to December 1999, 8,538 patients underwent cardiac surgical procedures. A search in the cardiovascular database at the Cleveland Clinic Foundation identified 178 patients who had a discharge diagnosis of cerebrovascular accident, and 96 patients who had the diagnosis of transient ischemic attack. Of these, 13 patients (5%) underwent intraarterial thrombolysis and these patients are the basis of this report. Beginning in September 1997 the "stroke" team in conjunction with the cardiothoracic surgeons began considering postoperative cardiac surgical patients for intraarterial thrombolysis with the hopes of salvaging neurologic function. The database does not capture National Institutes of Health stroke scale (NIHSS) or the number of patients seen by the stroke team that failed to meet the criteria for intraarterial thrombolysis.

All patients presented with an acute neurologic deficit and were evaluated within 6 hours of stroke onset. Clinical evaluation including a NIHSS score was performed and patients with a significant deficit (more than 10), or isolated disabling symptoms were considered for treatment (Fig 1). The NIHSS more than 10 criteria was based on experience in prospective trials and identifies patients with a neurologic insult significant enough to predict poor outcome and justify the risk of administration of intraarterial thrombolytic therapy. In addition, it would exclude patients with a lacunar infarct as their scores are usually less than 10.

View larger version (48K): [in this window] [in a new window]   Fig 1. Components of the NIH Severity Score.

Demographics
The mean age was 69 years (standard deviation ± 5 years) and 8 (62%) were men. Arteriosclerosis of the ascending aorta was minimal in all by transesophageal echocardiography obtained at the time of operation. Procedures consisted of valve repair or replacement in 6 patients (46%), isolated coronary bypass in 4 (31%), combined valve operation and coronary bypass in 2 (15%), and left ventricular assist device implantation in 1 patient. All patients had normal neurologic function in the immediate postoperative period and presented with an acute witnessed stroke from 1 to 12 days postoperatively (Table 1).

Patient monitoring
After the procedure all patients were monitored in the intensive care unit. Neurologic evaluations were performed hourly and the NIHSS was determined. Serial hemoglobin levels were measured at 4-hour to 6-hour intervals for the first 24 hours and a repeat head computed tomographic scan was obtained the following day to evaluate change in infarct size and detect hemorrhagic complications. All patients underwent repeat transesophageal echocardiography to rule out the presence of new left atrial thrombus. All common and internal carotid arteries were evaluated at the time of the intervention by four-vessel angiography.

	Results

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Time from initial presentation to angiography was a mean of 3.6 ± 1.6 hours. Occlusion was in the branches of the MCA in 9 patients (69%), the terminal carotid artery in 2 (15%), the proximal internal carotid artery in 1, and the basilar artery in 1 patient. In addition to administration of thrombolytics, 3 patients required angioplasty of the MCA and 4 required mechanical manipulation of the clot to cause dislodgement. Complete recanalization by the Thrombolysis in Myocardial Infarction (TIMI) flow categorization was achieved in 1 patient (TIMI grade 3), with 6 patients having moderate flow (TIMI grade 2), and 6 having low flow (TIMI grade 1) (Fig 2).

View larger version (13K): [in this window] [in a new window]   Fig 2. Restoration of flow after intervention. The figure shows the relationship between success at recanalization and clinical neurologic improvement. (TIMI = Thrombolysis in myocardial infarction; TIMI 3 = normal; TIMI 2 = moderate flow; TIMI 1 = low flow.)

View larger version (12K): [in this window] [in a new window]   Fig 3. Change in National Institutes of Health Stroke Scale scores before and after thrombolysis. The diagonal line divides patients into two groups: those who improved and those who were unchanged or worsened. The patients in the bottom half of the line all improved clinically.

View larger version (30K): [in this window] [in a new window]   Fig 4. Clinical outcome and distribution of the occlusion. Patients who had no clinical improvement, all had either involvement of the distal carotid or proximal middle cerebral artery. (ACA = anterior cerebral artery; ICA = internal carotid artery; MCA = middle cerebral artery with superior and inferior divisions.)

Intracranial changes on computed tomographic scan consisted of minor petechial bleeding in 2 patients, and a 0.5-cm cerebellar hemorrhage in 1 patient. Overall 3 patients (23%) died: 2 had cerebral herniation secondary to the extent of stroke and 1 died of multisystem organ failure despite improved neurologic status. The remaining 10 patients (77%) were discharged home or to a rehabilitation facility.

	Comment

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Cerebral complications after cardiac operation can be devastating. The incidence of adverse neurologic events ranges from 1.6% to 16% and negatively impacts hospital survival [1–3]. Risk factors include previous stroke, diabetes, female sex, atrial fibrillation, and aortic arteriosclerosis [7]. It is presumed that most early perioperative strokes are atheroembolic and are usually recognized in the immediate postoperative period. On the other hand, delayed strokes may have a different etiology. The time of occurrence and the composition of the occlusive lesion suggest that other mechanisms may play a role in these late strokes. Hogue and colleagues [7] examined the time of onset of stroke in 2,972 patients undergoing heart operations at Barnes-Jewish Hospital. They found that the majority of strokes occurred after an uneventful neurologic recovery from operation. They noted that earlier studies using stroke as a single end point in the postoperative period may lead to erroneous determinations of the significance of specific variables in a particular postoperative period and suggests that atheroembolism is only one of many potential causes of postoperative strokes.

In the 13 patients studied, one had complete occlusion of the internal carotid artery after off-pump coronary artery bypass grafting. After thrombolysis, a 50% lesion was identified that was likely the cause of the acute occlusion. After valve repair, 2 patients had calcified embolic occlusions. In an additional 3 patients, even after thrombolysis, residual luminal defects existed that required balloon angioplasty, suggesting that the stroke may have evolved from acute thrombosis overlying preexisting intracranial atherosclerotic disease. These findings raise the possibility that the postsurgical metabolic mileu may be an important factor contributing to the risk of stroke in patients with preexisting stable intracerebral disease. In fact, the atherosclerotic aorta may be a marker of widespread arteriosclerosis of the cerebral vessels [8].

Beside supportive measures, few options are available for treatment of acute stroke [9]. Use of thrombolytic therapy represents a novel approach to treatment of perioperative strokes and recent studies have shown the effectiveness and safety of these agents in the early postoperative period [10–12]. The National Institute of Neurologic Disorders and Stroke trial used intravenous tissue plasminogen activator in patients who presented within 3 hours of stroke onset [13]. Patients in the treatment arm had a 30% greater likelihood of having minimal or no disability at 3 months. The only randomized controlled study that has used intraarterial thrombolysis in acute ischemic stroke is The Prolyse in Acute Cerebral Thromboembolism Trial (PROACT). In PROACT II, 180 patients were randomized to receive recombinant pro-urokinase plus low-dose intravenous heparin versus low-dose heparin alone. There was a 15% absolute benefit in patients who had baseline NIHSS of 11 to 20. Recanalization rates were 66% versus 18% in the control group [14]. Risk of intracerebral hemorrhage after intraarterial therapy in this study was 10% [14].

In addition to intraarterial thrombolysis availability of soft, pliable, and steerable microcatheters in conjuction with improved imaging technology has enabled access for diagnosis and intervention in the cerebral vasculature. These developments are particularly useful in the postoperative cardiac patient in whom the etiology of stroke can be diverse. Recanalization rates with intraarterial thrombolysis averaged 70% [15]. Overall success of arterial recanalization is a reflection of the composition of the occlusion, the total thrombus load, and the distribution of the vessel. The fibrin-rich occlusions will be more amenable to lysis, whereas calcific and atheroembolic particles will not. The use of snares, suction devices, and mechanical disrupters may help in these situations. Differences in the territory involved also impact the success. In previous studies occlusions of the internal carotid artery, the carotid terminus, and the proximal segment of the MCA, have proved to be resistant to thrombolysis [6]. In addition, the proximal MCA supplies the basal ganglia and the internal capsule with end-arteries and there may be no clinical improvement even if recanalization is achieved. We had 8 patients who did not improve in their overall neurologic picture; 6 had involvement of the proximal MCA and 2 had occlusions of the carotid terminus (Fig 4). In 5 patients who improved, only 1 had involvement of the proximal MCA and others had occlusion of either the more distal branches of the MCA or the basilar artery.

In a selected group of 13 patients, we have demonstrated that immediate cerebral angiography followed by intraarterial administration of thrombolytics is reasonably safe and may produce a significant benefit. Neurologic improvement, when it occurred, was always immediate. In this group, 3 had improvement of hemiparesis, 1 had restoration of vision, and 1 had resolution of expressive aphasia, providing an overall improvement in neurologic status of 38%. Furthermore, despite concerns that recent operation is a contraindication to thrombolytic therapy (because of fear of systemic fibrinolysis of hemostatic clots), by using selective intracerebral arterial administration of low-dose urokinase or tissue plasminogen activator, we only had minor bleeding complications. Although hemopericardium after thrombolysis has been reported previously in patients with recent myocardial infarction [16, 17], we did not observe this problem in any of our patients.

In conclusion, we have demonstrated that in select patients this aggressive approach appears to be safe and may lead to clinical neurologic improvement. With further advances in this field it is hoped that our understanding of postoperative neurologic events will evolve and with it preventive and therapeutic strategies may improve. Larger trials will be necessary to prove safety and efficacy.

	Discussion

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DR DAVID A. FULLERTON (Chicago, IL): First I would like to congratulate Dr Moazami on a beautiful presentation and extend my appreciation for receipt of the manuscript ahead of the meeting.

As we all appreciate, stroke is an absolutely devastating complication, and it has a tremendous impact on the lives of our patients. Current medical therapy is largely expectant, during which time one is left to stand by helplessly hoping that the situation will improve. So I think this group needs to be heartily congratulated for taking such a provocative step as to extend some fairly controversial therapy into the arena of our specialty.

I would add, it was not intuitively obvious, to me in any case, that lytic therapy could be safely applied to patients in the early postoperative period; in fact, that is typically considered a relative contraindication. Despite that, there were no significant complications in this group of patients.

I wonder whether Dr Moazami might comment on a couple of additional points, if I could raise these. First, even with local arterial administration of lytic therapy, a systemic lytic state may follow, and I was curious as to whether or not coagulation parameters were measured and whether you might have any data in that regard.

Second, of these 13 patients, 7 actually required mechanical manipulation of the affected artery in addition to the lytic therapy. That is fairly sophisticated interventional radiology work and would lead me to conclude that this technique might be limited to centers with that sort of expertise.

My third question is: When a neurologic event occurs, it is nearly impossible at its onset to predict how much is going to resolve, and hence the traditional expectant management. In this study, 5 of these 13 patients did improve neurologically, but I think it is fair to say that we really do not know whether those 5 patients might not have improved otherwise. So I would be interested to know whether you might have another insight or a second group of patients within your own institution that might serve as a control group for us.

DR MOAZAMI: Doctor Fullerton, thank you very much for your kind comments. I will try to answer your questions in order.

You asked about whether any kind of coagulation parameters were measured in the postintervention period. Some of these patients actually were heparinized with about 8 to 10 U/kg of heparin after the intervention, once we believed that there were no bleeding complications. We then started monitoring PT/PTT. We did not look at any parameters of thrombolysis specifically, and we opted to follow the patients clinically and follow their hematocrit in an intensive care unit setting on a regular basis to determine whether there were any problems. If there was a fibrinolytic state induced, it certainly did not manifest clinically in that respect.

You also mentioned that 7 of the patients had mechanical manipulation, and that is very correct. I think that points to the diverse etiology that we generally see in this patient population. Most of the patients manifested their stroke between days 3 and 4. There clearly seems to be a separate entity that presents as delayed stroke in the postoperative period, for which nobody knows the etiology. I think one of the other interesting aspects of our study is that by acute intervention and obtaining an intracerebral angiogram, we could actually see why some of these patients had strokes. In the 7 patients who had these interventions, interestingly, 2 of them had calcified thrombus, which we presume were from the valve operations that the patients had, and these will obviously not respond to thrombolytic therapy and would require a somewhat sophisticated intervention such as snaring or suctioning or something of that nature. And you are correct in that these interventions probably have to be done at centers with neurointerventionalists who are familiar both with thrombolytic therapy as well as with these sophisticated technical details.

Finally, you asked about a control group. We only had 13 patients in this study, which was during a 3-year period, so, as you can see, it is a very selected group of patients and we did not have a control arm. Despite the fact that only about 5 of the patients improved, the purpose of the study primarily was to demonstrate that this can be done safely, that we should not be afraid of bleeding. It was not meant to necessarily demonstrate that we are truly efficacious at this. We believe that we could improve the neurologic status of the patients, and a lot of this is reflected in the neurology literature based on prospective randomized studies in patients who have presented with acute stroke and have received thrombolytic therapy. Two of these trials, one is the National Institute of Neurologic Disorders and Stroke showed a 30% improvement in these patients, and another one was the PROACT study, which demonstrated a 15% absolute benefit in these patients. Our study is too small really to make a conclusion on that.

DR IVAN KETIH CROSBY (Charlottesville, VA): Those are bold moves, Dr Moazami, and I congratulate you for them, but do you have any plans to take it up to the next level where you would investigate and treat patients who wake up with a neurological deficit after their cardiac operation?

DR MOAZAMI: We have not looked at that, although that is certainly very important. The problem with that is usually I think by the time that we figure out that the effect of anesthesia has worn off and the patient can now be assessed, we are past that 6-hour time limit. Unfortunately, the time limit for thrombolytic therapy is what will limit us. At many of these centers to be able to achieve good results, you need to be able to mobilize your team very rapidly, and in fact, in some studies, less than 3 hours is even better in terms of predicting neurologic recovery.

DR PAUL KURLANSKY (Miami Beach, FL): I think you are to be congratulated on a very courageous approach to an otherwise devastating and somewhat hopeless situation. As you bring out, these strokes were mostly on postoperative day 2 and 3, not the immediate perioperative stroke, and it raises a question about the etiology. Certainly those that responded to thrombolysis werre more primarily thrombotic rather than perhaps atherosclerotic and embolic only. I know Dr Mack has raised questions about the hypercoaguable state that occurs after off-pump bypass, and it is his area of active investigation. My question to you is, were any of these patients off-pump bypass patients or did any of them have any clinically identifiable hypercoaguable state that might be in the future used to recognize the predilection for this particular etiology of stroke? Thank you very much and I commend you once again.

DR MOAZAMI: Actually, 1 patient in this group was an off-pump coronary artery bypass grafting patient, and that was the patient who had occlusion of the proximal carotid artery. After thrombolytic therapy, there was about a 50% carotid lesion, and we believe that that was probably the culprit in this case, which may allude to the fact that, as you mentioned, probably the postoperative period established a certain metabolic milieu in which patients who may have otherwise stable carotid or intracerebral disease may be prone to an acute occlusion by thrombolysis. I think that part of the questions related to the etiology of strokes may relate to a hypercoagulable state; however, we did not look at those factors.

	References

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This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Nader Moazami Nicholas G. Smedira Patrick M. McCarthy Bruce W. Lytle Delos M. Cosgrove, III Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Moazami, N. Articles by Cosgrove, D. M. Search for Related Content PubMed PubMed Citation Articles by Moazami, N. Articles by Cosgrove, D. M., III Related Collections Cardiac - other Related Article