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Ann Thorac Surg 1998;65:1656-1659
© 1998 The Society of Thoracic Surgeons

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Original articles: cardiovascular

Posterior Distribution of Infarcts in Strokes Related to Cardiac Operations

^a Departments of Neurology, Radiology, Cardiothoracic Anesthesiology, and Cardiothoracic Surgery, Cornell University Medical College, New York, New York, USA

Accepted for publication January 29, 1998.

Address reprint requests to Dr Barbut, Starr-607, 520 E 70th St, New York, NY 10021

	Abstract

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
Background. Stroke complicates cardiac surgical procedures in a substantial number of patients. The mechanism of stroke is predominantly embolic, although hypoperfusion may play a role. The aim of this study was to determine whether radiologic appearances in this population were consistent with an embolic cause.

Methods. We reviewed computed tomographic scans and medical records in 24 patients who suffered stroke after cardiac operation. Stroke was evident at 24 hours in 19 patients (79%). Infarcts were multiple in 16 and single in 3 patients (group 1). The remaining 5 patients suffered stroke beyond 24 hours and had single infarcts on computed tomographic scan (group 2).

Results. In group 1, 15 patients (79%) had bilateral cerebellar infarcts, 4 (74%) had posterior cerebral artery infarcts, 10 (53%) had posterior watershed infarcts, and 11 patients (58%) had middle cerebral artery branch infarcts. The mean number of vascular territories involved was 5.1 (range, 1 to 10). Mobile atheromatous plaque was present in the ascending aorta or arch in 5 of 9 patients (56%) in group 1. In group 2, stroke occurred in close association with atrial or ventricular fibrillation in 3 of 5 patients (60%).

Conclusions. In patients with radiologic evidence of infarction, perioperative strokes after cardiac operation are typically multiple, and involve the posterior parts of the brain, consistent with atheroembolization. Delayed strokes may be attributable to cardiogenic embolism.

	Introduction

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Cardiac operations are associated with neurologic deficits in a substantial number of patients [1]. Stroke complicates the outcome in 5% of patients undergoing coronary artery bypass grafting and is increasing in proportion to the number of elderly patients undergoing the procedure [1, 2]. The incidence of stroke is substantially higher among patients undergoing valve grafting or combined cardiac procedures [3, 4].

The etiology of this dysfunction is multifactorial and includes embolization [5, 6], and hypoperfusion [7]. In patients undergoing coronary artery bypass grafting, embolization of atheromatous material from the aorta is considered to be the single most important risk factor for stroke [8]. In open surgical procedures, calcific material from valves and larger volumes of air compound the neurologic injury caused by atheroembolism.

With transcranial Doppler echography, emboli have been detected in most patients during operation [6, 9], and numbers of emboli have been shown to correlate with neurologic outcome [10, 11]. Consistent with a higher incidence of stroke after combined surgical procedures [3, 4], numbers of emboli are much higher during combined procedures than during isolated coronary artery bypass grafting.

Radiologic appearances associated with embolization include distal artery branch infarcts in multiple arterial territories. The purpose of this study was to evaluate radiologic findings in patients sustaining stroke after a cardiac operation and to establish whether the pattern of infarction was consistent with embolization.

	Material and methods

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Patient selection
We retrospectively reviewed computed tomographic (CT) scans and medical records in 24 patients who suffered stroke after undergoing cardiac operation during a 4-year period. The protocol was approved by our Institutional Review Board. Patients were excluded if CT scans were not obtained at the time of stroke (4 patients), if CT scans were negative (15 patients), or if relevant information was incomplete (6 patients). Preoperative CT scans were not available in any of the patients.

Thirteen patients were male, and the mean age was 74 years (range, 61 to 88 years). Thirteen patients underwent isolated coronary artery bypass grafting, 10 patients underwent coronary bypass grafting combined with open cardiac procedures (aortic aneurysm repair in 3, left ventricular aneurysm repair in 1, mitral valve repair in 2, and aortic valve repair in 4) and 1 patient underwent isolated tricuspid valve repair.

Stroke was defined as fixed focal neurologic deficit with CT evidence of infarction, or coma not attributable to metabolic causes and associated with CT evidence of infarction. The CT scans were reviewed independently by two neuroradiologists and classified according to infarct distribution. Territorial infarcts were distinguished from border zone infarcts. The neuroradiologists concurred in all cases.

Intraoperative transesophageal echocardiography was performed in 11 patients, and carotid ultrasound results were available in 6 patients. Relevant baseline characteristics, such as vascular risk factors and ventricular ejection fractions, were noted, and intraoperative variables, such as cross-clamp time and total bypass time, were recorded. One patient had a history of "drop attacks"; the remaining 23 patients were neurologically asymptomatic.

Patients were categorized into two groups according to the timing of stroke. Group 1 (n = 19) included patients whose neurologic deficit was apparent within 24 hours of operation. Group 2 (n = 5) included patients who sustained stroke after an uneventful recovery period.

	Results

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Overall, the neurologic deficit was apparent immediately in 19 patients (79%). In the remaining 5 patients, a new deficit became apparent on days 3 (2 patients), 4, 10, and 30.

In group 1, 12 patients (63%) died, 8 as a direct consequence of the neurologic injury. Another 4 patients were slow to awaken. Evidence of cortical blindness was present in 3 of 9 patients who regained consciousness. Radiologically, cerebellar infarcts were present in 15 patients (79%) (Table 1) and involved both cerebellar hemispheres in all patients. In 9 patients, the cerebellum was studded with numerous small infarcts, giving it a salt-and-pepper appearance (Fig 1). Another patient showed radiologic evidence of cerebellar edema, without definite infarction. The posterior cerebral artery territory was involved in 14 patients (74%), and was bilateral in 9 (47%) (Fig 2). The posterior watershed territory was affected in 10 patients (53%), bilaterally in 7 (37%). Infarcts were present in a middle cerebral artery branch territory in 11 patients (58%), and involved the posterior branch in 7 patients, the anterior branch in 6 patients, and the deep branch in 3 patients. Multiple branches were affected in 5 patients (26%), and were bilateral in 2 (11%). Infarcts were present in the parasagittal watershed region in 5 patients (26%), bilaterally in all patients. Two patients (11%) had infarcts in the anterior watershed region. Overall, at least one hemispheric border zone territory was affected in 11 of 19 patients (58%). None of the patients had evidence of infarction in the anterior cerebral artery territory. The mean number of vascular territories affected was 5.1 (range, 1 to 10). Three patients had single infarcts, although 1 of these 3 died and recovery of consciousness was slow in another, with evidence of diffuse neurologic dysfunction.

View larger version (136K): [in this window] [in a new window]   Fig 1. Computed tomographic scan showing multiple cerebellar infarcts (salt and pepper cerebellum).

View larger version (125K): [in this window] [in a new window]   Fig 2. Computed tomographic scan of the same patient as in Figure 1 showing patchy infarction in the posterior cerebral artery territory bilaterally.

Intraoperative transesophageal echocardiography was performed in 11 patients. Mobile atheromatous plaque was present in any aortic segment in 6 patients (54%). Mobile plaque in the ascending aortic segment or arch was present in 5 of 9 patients (56%) in group 1, and in none of the 2 patients with transesophageal echocardiography in group 2.

Six patients had carotid Doppler examinations. High-grade carotid stenosis or occlusion was present in 3 patients and subclavian stenosis in 1 patient. One of the 3 patients with carotid stenosis had multiple small middle cerebral artery territory infarcts attributable to this lesion. In the other 2 patients and in the patient with the subclavian stenosis, infarcts were not in the corresponding vascular territory.

Mean aortic cross-clamp time was 67 minutes in group 1, and 56 minutes in group 2. Clamping was avoided altogether in 1 patient. Corresponding total cardiopulmonary bypass times were 131 minutes and 94 minutes, respectively.

A history of hypertension or diabetes was present in 12 of 19 patients (63%) in group 1 and in 3 of 5 patients (60%) in group 2. Preoperative mean left ventricular ejection fraction was 42% (range, 20% to 66%) in group 1, and 34% (range, 12% to 60%) in group 2 (p = 0.5). Mean age was 74 years in both groups.

	Comment

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In this retrospective study of patients with radiologic findings, we have shown that intraoperative strokes complicating cardiac surgical procedures are typically multiple, and affect the posterior part of the hemispheres and cerebellum in a majority of patients. The clinical picture associated with these radiologic findings was uniformly dismal; many of the patients never regained consciousness and those that did suffered permanent deficits. This group of patients, however, represents the worst extreme in the spectrum of stroke, as patients without scans and those with normal scans were excluded from analysis. Prognosis among excluded patients in that group is unlikely to have been as poor as in patients in whom infarcts were present radiologically.

The preponderance of infarcts in the posterior aspects of the brain has been noted previously [12–14]. Among 15 patients suffering stroke after coronary artery bypass grafting in whom radiologic evidence of infarction was present, Hise and colleagues [15] found infarcts in the distribution of the posterior cerebral artery, the posterior watershed territory, or the cerebellum in 60%. In a pathologic study involving 9 patients who succumbed after coronary artery bypass grafting, Malone and colleagues [12] found ischemic lesions involving the parietooccipital border zone region in all patients. They noted that in the most severe cases, ischemic changes extended anteriorly. In another study involving 11 patients who had undergone open cardiac procedures, pathologic changes were found to be confined to the parietooccipital regions and cerebellum in 10 patients. In the only patient with evidence of more diffuse cerebral injury, changes were nonetheless most marked in the parietooccipital regions [14].

The selective vulnerability of the parietooccipital regions to ischemic injury is reflected in the frequency of perceptual abnormalities in this group of patients. Gilman [13] found evidence of visual disturbances referrable to the parietooccipital region in 9 of 14 patients undergoing valvular grafting. Pathologic confirmation of parietooccipital infarction was available in 3 patients.

In this study, as in others, parietooccipital infarcts were as likely to be found in the border zone territory between the posterior and middle cerebral arteries, as they were in the posterior cerebral artery territory itself [12, 16, 17]. At autopsy, Malone and colleagues [12] found ischemic lesions along the posterior border zone regions, as well as over the occipital poles.

The multiplicity of small infarcts involving cortical branches of the middle and posterior cerebral arteries, combined with the striking number of patients with mobile aortic plaque, is highly suggestive of atheromatous embolization in patients with perioperative stroke. Although high-grade carotid stenoses were present in 4 patients, the infarcts were only attributable to this lesion in 1 patient. In the other 3 patients, infarcts occurred outside the relevant vascular territory.

The mechanism of infarction in watershed infarcts is generally held to be hypoperfusion. However, several investigators have attempted and failed to document perioperative hypotension in patients with posterior border zone infarcts occurring in the context of cardiac operation [12, 18, 19]. In the only systematic analysis of perioperative hemodynamic risk factors, Hupperts and colleagues [19] found no significant hemodynamic differences between patients with border zone infarcts and those with territorial infarcts, or no infarcts at all. They concluded that hemodynamic compromise alone could not sufficiently explain the occurrence of border zone infarction.

Atheromatous embolization may be a common cause of watershed infarctions [13, 16, 18–21]. Graeber and co-workers [16] identified 3 patients with posterior border zone infarcts, without significant carotid stenosis, in whom angiography revealed embolic occlusion of the arterial branch corresponding to the site of the infarct. Multiple, small arterial boundary zone infarcts were also the predominant necropsy finding in 1 patient with a severely atherosclerotic aorta who succumbed after coronary artery bypass grafting. Pial vessels adjacent to these infarcts were found to be occluded by large numbers of cholesterol crystals [18]. Similarly, in patients dying after valve grafting, Gilman [13] found embolic calcific material in pial vessels adjacent to both territorial and border zone infarcts.

The predilection of particulate emboli for the posterior parts of the brain has been documented experimentally. Perfusing the aorta with an antifoam solution, Cassie and colleagues [22] found the greatest number of emboli and infarcts in the cerebellum, brainstem, and occipital lobes. In addition to attracting the largest numbers of emboli, the posterior parts of the brain are also the least densely vascularized. A given embolic load would therefore occlude a larger fraction of the vasculature in this region than further anteriorly, resulting more commonly in infarction.

The mechanism of stroke in patients sustaining a new deficit days to weeks after cardiac operation appears to be different than in those with perioperative stroke. In this study, late strokes were associated with single infarcts, and occurred in close association with an episode of fibrillation in 3 of 5 patients. In this group of patients, cardiogenic embolism, rather than atheroembolism from the aorta, appears to be the mechanism responsible for stroke.

	Acknowledgments

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
This study was supported in part by grants from the Raeburn Foundation and Exor America. Additional support from Samuel and Ella Scher.

	References

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 

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