Neurologic injury in cardiac surgical patients with a history of stroke
ABSTRACT 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 < 0.001) 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.
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ABSTRACT: The causes of stroke following coronary-artery bypass surgery are largely unknown. To determine whether carotid bruits increase the risk of these events, we compared 54 patients with postoperative stroke or transient ischemic attacks with 54 randomly selected control patients. Both groups were drawn from 5915 consecutive patients who had coronary bypass surgery at our hospital from 1970 to 1984. Carotid bruits were noted preoperatively in 13 patients with postoperative stroke and in 4 control patients. Case-control analysis showed that the presence of carotid bruits increased the risk of stroke or transient ischemic attacks by 3.9-fold (95 percent confidence interval, 1.2 to 12.8; P less than 0.05). This increased risk remained essentially unchanged after adjustment for potentially confounding variables in a multiple logistic regression analysis. Other factors associated with a significantly increased risk (P less than 0.05) of these neurologic deficits were a history of stroke or transient ischemic attack (odds ratio, 6.0; 95 percent confidence interval, 1.6 to 22.1), a history of congestive heart failure (odds ratio, 5.3; confidence interval, 1.6 to 17.0), mitral regurgitation (odds ratio, 4.3; confidence interval, 1.4 to 12.9), postoperative atrial fibrillation (odds ratio, 3.0; confidence interval, 1.4 to 6.7), a cardiopulmonary-bypass pump time of more than two hours (odds ratio, 2.7; confidence interval, 1.1 to 6.7), and a previous myocardial infarction (odds ratio, 2.3; confidence interval, 1.1 to 5.1). We conclude that the presence of carotid bruits increases the risk of stroke after coronary-artery bypass surgery. However, the absolute magnitude of this risk, 2.9 percent, is small and comparable to the reported risk of stroke from carotid endarterectomy.New England Journal of Medicine 12/1988; 319(19):1246-50. · 51.66 Impact Factor
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ABSTRACT: To identify possible risk factors for the occurrence of stroke during coronary artery bypass grafting (CABG), the cases of 3,279 consecutive patients having isolated CABG from 1974 to 1983 were reviewed. During this period, the risk of death fell from 3.9% to 2.6%. The stroke rate, however, fell initially but then rose from 0.57% in 1979 to 2.4% in 1983. Adjustment of these data for age clearly demonstrated that the risk of stroke has increased largely because of an increase in the mean age of patients undergoing CABG procedures. A case-control study involving all 56 stroke victims and 112 control patients was used to identify those risk factors significantly associated with the development of stroke in univariate analysis: increased age (63 versus 57 years in stroke patients and controls, respectively; p less than 0.0001); preexisting cerebrovascular disease (20% versus 8%; p less than 0.03); severe atherosclerosis of the ascending aorta (14% versus 3%; p less than 0.005); protracted cardiopulmonary bypass time (122 minutes versus 105 minutes; p less than 0.005); and severe perioperative hypotension (23% versus 4%; p less than 0.0001). Other variables not found to correlate with postoperative stroke included previous myocardial infarction, hypertension, diabetes mellitus, lower extremity vascular disease, preoperative left ventricular function, and intraoperative perfusion techniques. Elderly patients who have preexisting cerebrovascular disease or severe atherosclerosis of the ascending aorta or who require extensive revascularization procedures have a significantly increased risk of postoperative stroke.The Annals of Thoracic Surgery 01/1986; 40(6):574-81. · 3.45 Impact Factor
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ABSTRACT: The primary motor cortex (MI) contains a map organized so that contralateral limb or facial movements are elicited by electrical stimulation within separate medial to lateral MI regions. Within hours of a peripheral nerve transection in adult rats, movements represented in neighboring MI areas are evoked from the cortical territory of the affected body part. One potential mechanism for reorganization is that adjacent cortical regions expand when preexisting lateral excitatory connections are unmasked by decreased intracortical inhibition. During pharmacological blockade of cortical inhibition in one part of the MI representation, movements of neighboring representations were evoked by stimulation in adjacent MI areas. These results suggest that intracortical connections form a substrate for reorganization of cortical maps and that inhibitory circuits are critically placed to maintain or readjust the form of cortical motor representations.Science 03/1991; 251(4996):944-7. · 31.03 Impact Factor