Diffusion- and perfusion-weighted brain magnetic resonance imaging in patients with neurologic complications after cardiac surgery.

BACKGROUND: Neurologic complications after cardiac surgery include stroke, encephalopathy, and persistent cognitive impairments. More precise neuroimaging of patients with these complications may lead to a better understanding of the etiology and treatment of these disorders. OBJECTIVE: To study the pattern of ischemic changes on diffusion- and perfusion-weighted magnetic resonance imaging (DWI, and MRPI, respectively) in patients with neurologic complications after cardiac surgery. METHODS: All records were reviewed of our patients undergoing cardiac surgery in the previous year who also underwent postoperative DWI or MRPI. Neurologic symptoms, vascular studies, and the pattern of ischemic changes were recorded. Acute ischemic lesions were classified as having a territorial, watershed, or lacunar pattern of infarction. Patients with multiple territorial infarcts in differing vascular distributions that were not explained by occlusive vascular lesions were classified as having multiple emboli. RESULTS: Fourteen patients underwent DWI and 4 underwent MRPI. Acute infarcts were found in 10 of 14 patients by DWI as compared with 5 of 12 patients by computed tomography. Eight patients presented with encephalopathy (associated with focal neurologic deficits in 4), 4 with focal deficits alone, and 2 with either fluctuating symptoms or transient ischemic attacks. Among patients with encephalopathy, 7 of 8 had patterns of infarction suggestive of multiple emboli, including 3 of 4 patients with no focal neurologic deficits. Several patients had combined watershed and multiple embolic patterns of ischemia. Findings of MRPI studies were abnormal in 2 of 4 patients, showing diffusion-perfusion mismatch; both patients had either fluctuating deficits or transient ischemic attacks, and their conditions improved with blood pressure manipulation. CONCLUSIONS: In patients with neurologic symptoms after cardiac surgery, DWI is more sensitive to ischemic change than computed tomographic scanning and can demonstrate patterns of infarction that may help us understand etiology. The most common pattern was multiple embolic infarcts. Preliminary experience with MRPI suggests that some patients have persistent diffusion-perfusion mismatch after surgery and may benefit from therapeutic intervention.

Determinants of cognitive change after coronary artery bypass surgery: a multifactorial problem.

BACKGROUND: Several studies have investigated predictors of cognitive decline after coronary artery bypass grafting (CABG), but there is little consensus as to which specific factors are predictive of poor cognitive outcomes. METHODS: We evaluated 127 patients undergoing CABG with standardized neuropsychological tests preoperatively, at 1 month and at 1 year. The outcome measure was a continuous variable reflecting change in z-scores for eight cognitive domains over time for individual patients. Univariate analyses were performed to evaluate the association between the demographic, operative, and postoperative factors and the cognitive outcome variables. Factors that were significant were included in a multiple linear regression analysis. RESULTS: Among the medical history variables, diabetes was associated with change in executive functions and psychomotor speed. Some of the operative variables were associated with short-term changes, but none with the 1-year outcomes. For example, the surgeon's rating of degree of difficulty in selecting a cross-clamp site was associated with change in attention. Higher mean pump rate during the procedure was associated with improved performance on tests of language. The cognitive domains associated with medical variables were different from those associated with surgical variables, and the associations observed at 1-year were different from those seen at 1-month. CONCLUSIONS: Change in cognition after CABG is associated with both medical and surgical variables. The specifics of these associations depend on the choice of time points after surgery. This suggests that there are multiple etiologies for these changes, with nonspecific effects of anesthesia and prolonged surgery interacting with the more specific effects of the surgical procedure itself.

Cognitive outcome after coronary artery bypass: a one-year prospective study.

BACKGROUND: Cognitive deficits have been reported in patients after coronary artery bypass grafting, but the incidence of these deficits varies widely. We studied prospectively the incidence of cognitive change and whether the changes persisted over time. METHODS: Cognitive testing was done preoperatively and 1 month and 1 year postoperatively in 127 patients undergoing coronary artery bypass grafting. Tests were grouped into eight cognitive domains. A change of 0.5 standard deviation or more at 1 month and 1 year from patient's preoperative Z score was the outcome measure. RESULTS: We identified four main outcomes for each cognitive domain: no decline; decline and improvement; persistent decline; and late decline. Only 12% of patients showed no decline across all domains tested; 82% to 90% of patients had no decline in visual memory, psychomotor speed, motor speed, and executive function; 21% and 26% had decline and improvement in verbal memory and language; approximately 10% had persistent decline in the domains of verbal memory, visual memory, attention, and visuoconstruction; and 24% had late decline (between 1 month and 1 year) in visuoconstruction. CONCLUSIONS: This study establishes that the incidence of cognitive decline varies according to the cognitive domain studied and that some patients have persistent and late cognitive changes in specific domains after coronary artery bypass grafting.

Predictors of stroke risk in coronary artery bypass patients.

BACKGROUND: Stroke occurs after coronary artery bypass grafting with an incidence ranging between 0.8% and 5.2%. To identify factors associated with stroke, we prospectively examined a study cohort and tested findings in an independent validation sample. METHODS: The study cohort comprised 456 patients undergoing coronary artery bypass grafting only, and the validation sample comprised 1,298 patients. Stroke was detected postoperatively by the study team and confirmed by neurologic consultation and computed tomographic scanning. RESULTS: Five factors taken together were correlated with stroke: previous stroke, presence of carotid bruit, history of hypertension, increasing age, and history of diabetes mellitus. The only significant intraoperative factor was cardiopulmonary bypass time. Probabilities were calculated, and patients were placed into low, medium, and high stroke-risk groups. In the validation sample, this model was able to rank the majority of patients with stroke into the high-risk group. CONCLUSIONS: These five factors taken together can identify the risk of stroke in patients having coronary artery bypass grafting. Recognition of the high-risk group will aid studies on the mechanism and prevention of stroke by modification of surgical procedures or pharmacologic intervention.

Assessing the impact of cerebral injury after cardiac surgery: will determining the mechanism reduce this injury?

BACKGROUND: Central nervous system dysfunction continues to produce significant morbidity and associated mortality in patients undergoing cardiac surgery. Using a closed-chest canine cardiopulmonary bypass model, dogs underwent 2 h of hypothermic circulatory arrest (HCA) at 18 degrees C, followed by resuscitation and recovery for 3 days. Animals were assessed functionally by a species-specific behavioral scale, histologically for patterns of selective neuronal necrosis, biochemically by analysis of microdialysis effluent, and by receptor autoradiography for N-methyl-D-aspartate (NMDA) glutamate receptor subtype expression. RESULTS: Using a selective NMDA (glutamate) receptor antagonist (MK801) and an AMPA antagonist (NBQX), glutamate excitotoxicity in the development of HCA-induced brain injury was documented and validated. A microdialysis technique was employed to evaluate the role of nitric oxide (NO) in neuronal cell death. Arginine plus oxygen is converted to NO plus citrulline (CIT) by the action of NO synthase (nNOS). CIT recovery in the cerebrospinal fluid and from canine cortical homogenates increased during HCA and reperfusion. These studies demonstrated that neurotoxicity after HCA involves a significant and early induction of nNOS expression, and neuronal processes leading to widespread augmentation of NO production in the brain. To further investigate the production of excitatory amino acids in the brain, we hypothesized the following scenario: HCA--> increased glutamate, increased aspartate, increased glycine--> increased intracellular Ca2+--> increased NO + CIT. Using the same animal preparation, we demonstrated that HCA caused increased intracerebral glutamate and aspartate that persists up to 20 h post-HCA. HCA also resulted in CIT (NO) production, causing a continued and delayed neurologic injury. Confirmatory evidence of the role of NO was demonstrated by a further experiment using a specific nNOS inhibitor, 7-nitroindazole. Animals underwent 2 h of HCA, and then were evaluated both physiologically and for NO production. 7-Nitroindazole reduced CIT (NO) production by 58.4 +/- 28.3%. In addition, dogs treated with this drug had superior neurologic function compared with untreated HCA controls. CONCLUSIONS: These experiments have documented the role of glutamate excitotoxicity in neurologic injury and have implicated NO as a significant neurotoxin causing necrosis and apoptosis. Continued research into the pathophysiologic mechanisms involved in cerebral injury will eventually yield a safe and reliable neuroprotectant strategy. Specific interventional agents will include glutamate receptor antagonists and specific neuronal NO synthase inhibitors.

Neurologic injury in cardiac surgical patients with a history of stroke.

BACKGROUND: Controversy still exists as to whether patients with previous stroke are at increased risk for neurologic complications after heart operations. METHODS: We performed a prospective analysis of 1,000 consecutive patients undergoing cardiac operations requiring cardiopulmonary bypass, without hypothermic circulatory arrest. Of the 1,000 patients, 71 had previously documented stroke (study group); 2 control patients with no history of stroke were selected for each of these patients (control group, n = 142). There were no significant differences between the study and control patients with respect to established risk factors for neurologic complications. RESULTS: Compared with controls, study patients took longer to awaken (12.6 +/- 10.9 versus 3.5 +/- 2.1 hours; p < 0.0001) and longer to extubate (29.5 +/- 29.3 versus 9.1 +/- 5.2 hours; p < 0.001), and had a greater incidence of reintubation (7 of 71, 9.9% versus 2 of 142, 1.4%; p < 0.01) and postoperative confusion (26 of 71, 36.6% versus 7 of 142, 4.9%; p < 0.001). There was a higher incidence of focal neurologic deficit among study patients (31 of 71, 43.7% versus 2 of 142, 1.4%; p < 0.001). These deficits included new stroke (6 of 71, 8.5%) as well as the reappearance of previous deficits (19 of 71, 26.8%) or worsening of previous deficits (6 of 71, 8.5%), without new abnormalities on head computed tomography or magnetic resonance imaging. Study patients with neurologic deficit had longer cardiopulmonary bypass times than did study patients without deficit (146 +/- 48.5 versus 110 +/- 43.3 minutes; p < 0.001). The 30-day mortality rate was greater in study patients than in controls (5 of 71, 7% versus 1 of 142, 0.7%; p < 0.02), with four deaths among the 6 study patients with a new stroke (66.7%). CONCLUSION: This analysis identifies a group of patients at high risk for neurologic sequelae and confirms the vulnerability of the previously injured brain to cardiopulmonary bypass, as evidenced by reappearance or exacerbation of focal deficits in such patients.

Prevalence of leg wound complications after coronary artery bypass grafting: determination of risk factors.

BACKGROUND: The reported prevalence of leg wound complications after coronary artery bypass grafting is 2% to 24%. Decreased length of hospital stay for patients who have this surgical procedure poses new care requirements in both acute care and community settings. OBJECTIVE: To determine the prevalence of postoperative leg wound complications in patients undergoing coronary artery bypass grafting and the risk factors associated with these complications. METHOD: In this prospective, observational study, 547 consecutive patients who had coronary artery bypass grafting alone or in combination with other cardiac surgical procedures were examined for evidence of leg wound complications each day after surgery during hospitalization. After discharge, problems were detected by home care nurses. RESULTS: The prevalence of leg wound complications was 6.8%. Factors significant by multiple logistic regression included preoperative hospitalization, use of an Ace elastic bandage in the operating room, the length of time the leg incision remained open in the operating room, and administration of nicardipine intravenously in the intensive care unit. Odds ratios were calculated for each variable. Premorbid factors such as diabetes or peripheral vascular disease were not predictive of complications. On average, most problems occurred on postoperative day 10, when many patients were at home. CONCLUSIONS: The results highlight the need to detect complications early, in both the hospital and the community settings. The determination of factors related to poor outcomes may assist clinicians in improving healthcare delivery.

Neurobehavioural sequelae of cardiopulmonary bypass.

The development of coronary artery bypass grafting (CABG) and its effect on angina is the product of a series of technical and scientific advances. Despite these advances, however, adverse neurobehavioural outcomes continue to occur. Stroke is the most serious complication of CABG, but studies that have identified demographic and medical risk factors available before surgery are an important advance. Short-term cognitive deficits are common after CABG, but may not be specific to this procedure. However, deficits in some cognitive areas such as visuoconstruction persist over time, and may reflect parieto-occipital watershed area injury secondary to hypoperfusion or embolic factors. Risk factors for cognitive decline may be time dependent, with short-term studies identifying factors that differ from those of long-term studies. Patients with depression before surgery are likely to have persistent depression afterwards. However, depression does not account for the cognitive decline after CABG. Since CABG is increasingly done in older patients with more comorbidity, the challenge is to identify patients at risk of adverse neurocognitive outcomes and to protect them by modification of the surgical procedure or by effective medical therapy.

Neuropsychologic change after cardiac surgery: a critical review.

Studies that have examined neuropsychologic change after cardiac surgery address three main issues: (1) the incidence of cognitive change; (2) the identification of factors that put patients at higher risk; and (3) the evaluation of interventions to prevent these complications. This review attempts to bring together concerns associated with various study designs and to integrate the conclusions from these studies. Thirty-five studies have been examined in this review. Some of the difficulties encountered when quantifying the degree of cognitive change are related to study design, patient sampling, and deficit definition. Additionally, changing patient populations have influenced results reported from different health care settings. Increasing age and longer cardiopulmonary bypass times have been correlated with cognitive decline in a number of studies. Filtration devices and blood gas management techniques have decreased but not eliminated the number of patients who have cognitive decline. Cognitive change exists following cardiac procedures. Identification of a subgroup of patients at high risk for cognitive change has been difficult, possibly due to issues of study design. Design of future studies, which may include intraoperative or pharmacologic interventions, is dependent on identification of this high-risk group.

Depression and cognitive decline after coronary artery bypass grafting.

BACKGROUND: Depression is commonly reported after coronary artery bypass grafting (CABG), and after cardiac surgery in general. Many earlier reports relied on non-standard assessments of depression, which may have overestimated its frequency. Cognitive decline has also been reported after CABG. We assessed the frequency of depression after CABG by a validated depression measure (Center for Epidemiological Study of Depression, CES-D), and examined the relation between depression and cognitive decline. METHODS: Patients were tested before CABG and 1 month and 1 year after surgery with a series of neuropsychological tests that assessed a range of cognitive areas. Depressed mood was measured by the CES-D scale, and defined as a score above 16. FINDINGS: 90 (73%) of the 124 patients were not depressed before surgery, and 34 were depressed at that time. Only 12 (13%) of patients not depressed before surgery were depressed at 1 month afterwards, whereas 18 (53%) of those who were depressed before surgery were depressed at 1 month (p < 0.001). 8 (9%) patients not depressed before surgery were depressed at 1 year; 16 (47%) of patients who were depressed before CABG were depressed at 1 year (p < 0.001). Statistical analysis showed only minimal correlation-or none at all-between depression and eight areas of cognitive outcome, or between changes in depressed status and cognitive scores. INTERPRETATION: Of those patients who were depressed after CABG, the large majority were depressed before surgery. There was no correlation, moreover, between depressed mood and cognitive decline after CABG, which suggests that depression alone cannot account for cognitive decline.