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Ann Thorac Surg 2001;72:137-142
© 2001 The Society of Thoracic Surgeons

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Original article: cardiovascular

Magnetic resonance imaging findings and postoperative neurologic dysfunction in elderly patients undergoing coronary artery bypass grafting

Accepted for publication March 27, 2001.

Address reprint requests to Dr Goto, Department of Anesthesiology, Kumamoto Chuo Hospital, 1-5-1 Tainoshima, Kumamoto 862-0965, Japan
e-mail: togoto{at}bronze.ocn.ne.jp

	Abstract

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
Background. Small cerebral infarctions are common in elderly patients, but the association between the magnetic resonance imaging finding and neurologic dysfunction after coronary artery bypass grafting has not been evaluated.

Methods. We determined, prospectively, whether varying degrees of abnormal findings on magnetic resonance images of the brain increased the incidence of preoperative cognitive decline, postoperative neuropsychological dysfunction, and stroke in 421 elderly patients ( 60 years) undergoing coronary artery bypass grafting.

Results. Control patients (almost normal or leukoaraiosis, n = 212) had rates of postoperative neuropsychological dysfunction (7%) and stroke (1.4%); the small infarctions group (some small infarctions, n = 126) had rates of 13% and 5.6%, respectively; whereas patients with multiple infarctions (multiple small infarctions or broad infarctions, n = 83) had rates of 20% and 8.4%, respectively (p = 0.004, p = 0.013). In the group with multiple infarctions, 49 patients (59%) were asymptomatic and 21 patients (25%) had cognitive decline. Stepwise logistic regression analysis demonstrated that the significant predictors of multiple small infarctions or large infarctions were history of cerebrovascular disease, renal insufficiency, cognitive decline, and cerebral arteriosclerosis.

Conclusions. Multiple infarctions significantly increase the risk of neurologic dysfunction after coronary artery bypass grafting. Routine screening for preoperative cognitive decline should be performed to detect underlying ischemic cerebral disease in elderly patients.

	Introduction

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Advanced age is often associated with increased systemic arteriosclerosis and a major risk of neurologic dysfunction after coronary artery bypass grafting (CABG) [1, 2]. Several studies have shown multiple risk factors of neurologic dysfunction after CABG [3, 4]. Recently, we have demonstrated that the incidence of neurologic dysfunction after CABG increased in patients who had a higher total atherosclerotic score in the brain, carotid arteries, and aorta [5]. In addition, our previous study revealed that small cerebral infarctions were common in elderly patients undergoing CABG [6]. Most patients with multiple small infarctions were asymptomatic with no manifest clinical signs. However, the Hisayama study showed that asymptomatic small infarctions were an important factor in the development of vascular dementia in a 7-year follow-up study of normal elderly residents of Hisayama [7]. Neuropsychological (NP) tests, such as the 7-minute screen, are believed to reflect an early stage of cognitive dysfunction in patients with Alzheimer’s disease [8]. Preoperative identification and preventive operative strategies can potentially reduce the incidence of NP dysfunction and stroke after CABG in high-risk patients. Cerebral magnetic resonance imaging (MRI) and cervical magnetic resonance angiography (MRA) allow for noninvasive observation of asymptomatic cerebral ischemic change and carotid stenosis. However, few prospective studies have investigated the association between MRI findings in the brain and neurologic dysfunction after CABG in elderly patients.

The purpose of this study was to further elucidate the relation between MRI findings and neurologic dysfunction after CABG and to identify predictors of multiple infarctions and broad infarctions. We determined prospectively whether varying degrees of MRI findings were associated with increased preoperative cognitive decline, systemic arteriosclerosis, postoperative NP dysfunction, and stroke in elderly patients undergoing CABG.

	Material and methods

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Data were prospectively collected on 421 Japanese patients older than 60 years who underwent elective CABG by a single surgeon at Kumamoto Chuo Hospital between January 1995 and June 1999. There were 351 asymptomatic patients who had no history of stroke or transient ischemic attack, and 71 with a history of stroke or transient ischemic attack. Patients who underwent cardiac valve replacement or ventricular aneurysmectomy were excluded to eliminate the effects of intracardiac air embolism and left ventricular thrombus. We excluded 3 patients who could not be evaluated for the outcomes of NP dysfunction and stroke, 1 patient who died in the immediate postoperative period, and 1 patient each with pulmonary complication or multiorgan system failure. Demographic and historic data were defined as follows: age, sex, history of hypertension requiring treatment with antihypertensive medication, history of diabetes mellitus (insulin or oral hypoglycemic therapy or a carbohydrate-restricted diet), hyperlipidemia (total cholesterol 240 mg/dL or triglyceride 150 mg/dL or antihyperlipidemic therapy), renal insufficiency (creatinine 1.9 mg/dL), history of peripheral vascular disease, and history of cerebrovascular disease (CVD) with strokes or transient ischemic attack. Informed consent was obtained from all participants, and the study was approved by the medical ethics committees and the institutional review board.

Cerebral and neurologic evaluation
Preoperative cerebrovascular evaluation was performed by cerebral MRI, cerebral MRA, and cervical MRA (0.5-T Superconductive MR unit, Philips, Amsterdam, The Netherlands, 1995 to 1997, and 1.5-T Superconductive MR unit, Toshiba, Tokyo, Japan, 1998 to 1999) as described previously [6]. The scatter representing ischemic changes or infarctions in the brain on MRI were classified as 0 (almost normal); 1 (leukoaraiosis, small and high signal spots on T2 high-weighted images); 2 (some small infarctions on T1 low- and T2 high-weighted images with a diameter < 15 mm); or 3 (multiple small infarctions or broad infarctions). The degree of stenosis in the intracranial arteries was graded bilaterally by MRA as 0 (almost normal); 1 (moderate narrowing of > 50%); or 2 (occluded) [9]. The degree of stenosis in the carotid arteries was graded by MRA as 0 (almost normal); 1 (mild narrowing of < 50%); 2 (moderate narrowing of 50% to 75%); or 3 (severe narrowing > 75% or obstruction). The lesions on MRI and MRA were independently evaluated by two radiologists who were blinded from preoperative risk factors and symptoms. Reliability was excellent, with interobserver correlation coefficients for MRI and MRA of 0.81 and 0.87, respectively, and intraobserver coefficients of 0.89 and 0.99, respectively.

Cognitive status was measured using the Hasegawa dementia score (HDS, score 0 to 30, with 30 best), a modification of the Mini-Mental State Examination. Scores less than 24 on the HDS are indicative of cognitive decline (equivalent to 24 on the Mini-Mental State Examination). All patients received neurologic and NP examinations before operation by one of three investigators (T.G., T.B., Y.S.) and on the seventh postoperative day by the same investigator (T.B.). Neuropsychological examiners were blinded to patients’ preoperative neurologic findings and atherosclerotic score. Postoperative NP dysfunction was defined as a decrease in performance from baseline of at least 4 (equal to two standard deviations from baseline). Postoperative MRI or computed tomography were performed only on patients with neurologic deficits lasting more than 24 hours or with a decrement of HDS from baseline of at least 8 on postoperative day 7. Patients with new postoperative neurologic symptoms and positive findings on postoperative MRI or computed tomography of the brain were examined by a staff neurologist to confirm intraoperative and postoperative stroke. Total stroke was the sum of intraoperative stroke and postoperative stroke. For stroke subtype, we used a diagnostic algorithm that classified patients as having infarction caused by embolism, infarction caused by hypoperfusion (watershed infarctions or diffuse hypoxia), or infarction from thrombosis caused by large-vessel arteriosclerosis (atherothrombotic stroke).

Patient management and evaluation of arteriosclerosis in the aorta
Diazepam and fentanyl were used for induction and maintenance of anesthesia. The perfusion apparatus consisted of a membrane oxygenator (Baxter, Irvine, CA; Mera, Tokyo, Japan; and Dideco, Mirandola, MO, Italy) that included a 40-µm filter in the arterial line. The cardiopulmonary bypass (CPB) flow rate was maintained at 2.0 to 2.4 L · min^-1 · m^-2 and mean arterial pressure between 50 and 70 mm Hg and more than 70 mm Hg in patients with multiple infarctions or severe carotid stenosis. Prostaglandin E₁ or norepinephrine was used as needed. The rectal temperature was kept between 28°C and 34°C. Distal coronary anastomoses and proximal anastomoses were performed during a single aortic cross-clamp. To limit release of atherosclerotic emboli from the ascending aorta, we changed the standard site for clamp and cannulation, and performed proximal anastomosis on ventricular fibrillation or circulatory arrest when there was at least a 3-mm intimal thickening of the aorta. We evaluated atherosclerotic lesions in the ascending aorta by echocardiography (Sonolayer SSA-260A, Toshiba, Tokyo, Japan) using an epiaortic probe (linear, 7.5 MHz, IOE 702V). Grading of the degree of arteriosclerosis in the ascending aorta was performed according to the modified method of Wareing and coworkers [10]: 0 (almost normal); 1 (mild, < 3 mm intimal thickening); 2 (moderate, 3 mm intimal thickening involving one segment of the ascending aorta); or 3 (severe or diffuse, 3 mm intimal thickening involving two or all three segments).

Statistical analyses
To relate MRI findings to postoperative NP dysfunction and stroke, the 421 patients were divided into three groups according to MRI findings: control—normal or leukoaraiosis (n = 212); small infarctions—some small infarctions (n = 126); and multiple infarctions—multiple small infarctions or broad infarctions (n = 83). Statistical comparisons among the three groups were performed using the ² test and one-way analysis of variance. Spearman rank correlation coefficients were used to examine the association between MRI grade and atherosclerotic diseases in the ascending aorta, carotid arteries, age (decade), preoperative HDS, cognitive decline, and risk factors. All probabilities are two-tailed, with a p value less than 0.05 regarded as significant. To assess the predictors of multiple small infarctions or broad infarctions, we examined all variables by stepwise logistic regression analysis. Odds ratios were calculated for each factor in the presence of the others in the final model. Goodness of fit was assessed by Hosmer-Lemeshow statistic. All statistical analyses were completed using the SAS Institute, Inc. statistical package (version 6.12, Cary, NC).

	Results

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Of the 421 patients studied, 126 patients (30%) had small infarctions, and 83 (20%) had multiple infarctions; of the latter, 72 had multiple small infarctions, and 11 had broad infarctions. There was an increase in infarctions with age compared with control patients (p = 0.052). Preoperative and intraoperative characteristics for all patients are summarized in Table 1. In general, the patients with multiple infarctions had more atherosclerotic risk factors than the patients in the other two groups. Of 73 patients with severe or diffuse arteriosclerosis in the ascending aorta, 25 patients underwent CABG without aortic clamp: 13 with hypothermic circulatory arrest and 12 with beating heart techniques. The arterial cannulation site was changed in 73 patients: 41 at an alternate site on the ascending aorta identified by ultrasonography, 17 with femoral artery, 15 with subclavian artery. No stroke occurred among 8 patients who underwent CABG when alternative techniques were used to avoid manipulation or clamping of the ascending aorta.

View larger version (18K): [in this window] [in a new window]   Fig 1. Preoperative Hasegawa dementia scale (HDS) by magnetic resonance imaging findings among three groups. Each point represents the mean HDS of subjects in a given age decade. Error bars indicate standard deviation.

	Comment

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

Small cerebral infarctions are common in elderly patients undergoing CABG [6]. Of 83 patients with multiple small infarctions or broad infarctions, 49 patients (59%) were asymptomatic. Schmid and associates [11] also noted that 58% of their patients with coronary disease had coincident silent ischemic damage. The characteristics of small infarctions were noted chiefly in the basal ganglia or cerebral white matter and were usually smaller than 1 cm. Those lesions often do not produce neurologic symptoms. Yoshitake and colleagues [7] showed that asymptomatic small infarctions were an important factor in the development of vascular dementia in a 7-year follow-up study of normal elderly residents of Hisayama town. In our study, preoperative HDS was lower in patients with multiple small infarctions or broad infarctions than in the other two groups. In addition, cognitive decline appeared to predict the development of asymptomatic multiple infarctions. Because NP tests, such as the HDS or Mini-Mental State Examination, are considered to reflect an early stage of cognitive impairment, they may be useful for identifying asymptomatic small infarctions in the elderly patients undergoing CABG.

Advanced arteriosclerosis, renal insufficiency, and history of CVD were independent predictors of multiple infarctions or broad infarctions. History of CVD was demonstrated in 17% of our patients. If we excluded those with a history of CVD, our qualitative results were not altered; cognitive decline, renal insufficiency, and cerebral arteriosclerosis remained significant predictors of multiple infarctions or broad infarctions. In addition, hypertension became significantly associated with multiple infarctions. Hypertension was also one of the risk factors for silent cerebral infarction [12]. These results suggested that the progression of atherosclerotic changes in the brain was paralleled by advanced arteriosclerosis and, conversely, the evaluation of systemic arteriosclerosis could predict latent damage to the brain. In addition to cervical MRA, cerebral MRA may provide important clues about the presence of an occluded intracranial artery in cerebral infarction [13]. We found a graded association of cerebral ischemia with arteriosclerosis in the ascending aorta and carotid stenosis. Therefore, cerebral MRI and cervical and cerebral MRA may be useful for detecting underlying ischemic cerebral disease and carotid stenosis in elderly patients undergoing CABG.

Hypoperfusion is a major cause of stroke after CABG [14]. Of 83 patients in our multiple infarctions group, 2 experienced intraoperative strokes caused by hypoperfusion. One patient with watershed infarctions had bilateral severe carotid stenosis and cerebral arteriosclerosis. Another patient with diffuse hypoxia had cerebral arteriosclerosis and underwent circulatory arrest to prevent emboli from severe arteriosclerosis of the ascending aorta during proximal graft anastomosis. In addition, another 2 patients of the multiple infarctions group had atherothrombotic infarctions postoperatively. In patients with carotid stenosis and multiple infarctions, perioperative hemodynamic instability and cerebral arteriosclerosis were associated with the occurrence of stroke. Unfortunately, there are no data to define optimal mean arterial pressure during CPB in these patients. Further studies should examine whether higher mean arterial pressure may reduce the incidence of postoperative NP dysfunction and stroke after CPB in patients with multiple small infarctions and carotid stenosis.

Embolization is the most common cause of strokes developing intraoperatively and is associated with advanced arteriosclerosis in the ascending aorta [10, 15]. It is estimated that approximately 85% (11 of 13) of strokes caused by intraoperative events are embolic and 6 of 11 strokes have embolic source from arteriosclerosis in the ascending aorta. Many investigators reported that microemboli occurred during CPB, especially aortic cannulation, clamping, and unclamping [16, 17]. These data suggested that microdebris from the ascending aorta or CPB induced NP dysfunction and stroke after CPB [18, 19]. On the other hand, transcranial Doppler detects cerebral microemboli in nearly all patients undergoing CABG, but embolic load is usually not sufficient to produce neurologic dysfunction [20]. Our data suggested that microemboli from the ascending aorta or CPB may have lodged in greater numbers in the arteriolar vasculature with cerebral arteriosclerosis than in that of almost normal patients. It is conceivable that endothelial cell damage to the cerebral microvasculature is the mechanism of increased NP dysfunction and stroke in patients with multiple infarctions after CPB. These findings have important implications for the management of elderly patients undergoing CABG and should be the subject of future research. Perioperative management, diagnosis, and therapy with anticoagulant or serine protease inhibitors should be evaluated to determine whether they prevent NP dysfunction and stroke after CABG.

In summary, this study demonstrated that undiagnosed ischemic cerebral disease is common and is an increased risk for postoperative NP dysfunction and stroke in elderly patients undergoing CABG. Routine screening for preoperative cognitive decline should be performed, such as with HDS or Mini-Mental State Examination, to detect underlying ischemic cerebral disease. Preoperative assessment of cognitive decline is useful for identifying high-risk patients with multiple infarctions or broad infarctions in the elderly undergoing coronary artery surgical procedures.

	Acknowledgments

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
The authors thank Yasuhiko Matsukado, MD, for his critical comments and suggestions, and Jon Moon, MD, for his editorial assistance.

	References

Top Abstract Introduction Material and methods Results Comment Acknowledgments 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 Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Goto, T. Articles by Okuda, T. Search for Related Content PubMed PubMed Citation Articles by Goto, T. Articles by Okuda, T. Related Collections Coronary disease