A. Aggarwal

Adverse Cerebral Outcomes after Coronary Bypass Surgery

Background Acute changes in cerebral function after elective coronary bypass surgery are a difficult clinical problem. We carried out a multicenter study to determine the incidence and predictors of — and the use of resources associated with — perioperative adverse neurologic events, including cerebral injury. Methods In a prospective study, we evaluated 2108 patients from 24 U.S. institutions for two general categories of neurologic outcome: type I (focal injury, or stupor or coma at discharge) and type II (deterioration in intellectual function, memory deficit, or seizures). Results Adverse cerebral outcomes occurred in 129 patients (6.1 percent). A total of 3.1 percent had type I neurologic outcomes (8 died of cerebral injury, 55 had nonfatal strokes, 2 had transient ischemic attacks, and 1 had stupor), and 3.0 percent had type II outcomes (55 had deterioration of intellectual function and 8 had seizures). Patients with adverse cerebral outcomes had higher in-hospital mortality (21 percent of patients ...

Cerebral Injury After Cardiac Surgery Identification of a Group at Extraordinary Risk

BACKGROUND AND PURPOSE Cerebral injury after cardiac surgery is now recognized as a serious and costly healthcare problem mandating immediate attention. To effect solution, those subgroups of patients at greatest risk must be identified, thereby allowing efficient implementation of new clinical strategies. No such subgroup has been identified; however, patients undergoing intracardiac surgery are thought to be at high risk, but comprehensive data regarding specific risk, impact on cost, and discharge disposition are not available. METHODS We prospectively studied 273 patients enrolled from 24 diverse US medical centers, who were undergoing intracardiac and coronary artery surgery. Patient data were collected using standardized methods and included clinical, historical, specialized testing, neurological outcome and autopsy data, and measures of resource utilization. Adverse outcomes were defined a priori and determined after database closure by a blinded independent panel. Stepwise logistic regression models were developed to estimate the relative risks associated with clinical history and intraoperative and postoperative events. RESULTS Adverse cerebral outcomes occurred in 16% of patients (43/273), being nearly equally divided between type I outcomes (8.4%; 5 cerebral deaths, 16 nonfatal strokes, and 2 new TIAs) and type II outcomes (7.3%; 17 new intellectual deterioration persisting at hospital discharge and 3 newly diagnosed seizures). Associated resource utilization was significantly increased--prolonging median intensive care unit stay from 3 days (no adverse cerebral outcome) to 8 days (type I; P<0.001) and from 3 to 6 days (type II; P<0.001), and increasing hospitalization by 50% (type II, P=0.04) to 100% (type I, P<0.001). Furthermore, specialized care after hospital discharge was frequently necessary in those with type I outcomes, in that only 31% returned home compared with 85% of patients without cerebral complications (P<0.001). Significant risk factors for type I outcomes related primarily to embolic phenomena, including proximal aortic atherosclerosis, intracardiac thrombus, and intermittent clamping of the aorta during surgery. For type II outcomes, risk factors again included proximal aortic atherosclerosis, as well as a preoperative history of endocarditis, alcohol abuse, perioperative dysrhythmia or poorly controlled hypertension, and the development of a low-output state after cardiopulmonary bypass. CONCLUSIONS These prospective multicenter findings demonstrate that patients undergoing intracardiac surgery combined with coronary revascularization are at formidable risk, in that 1 in 6 will develop cerebral complications that are frequently costly and devastating. Thus, new strategies for perioperative management--including technical and pharmacological interventions--are now mandated for this subgroup of cardiac surgery patients.

Electrocardiographic and hemodynamic changes and their association with myocardial infarction during coronary artery bypass surgery : A multicenter study

Background Electrocardiographic (ECG) changes during coronary artery bypass graft surgery have not been described in detail in a large multicenter population. The authors describe these ECG changes and evaluate them, along with demographic and clinical characteristics and intraoperative hemodynamic alterations, as predictors of myocardial infarction (MI) as defined by two sets of criteria. Methods Data from 566 patients at 20 clinical sites, collected as part of a clinical trial to evaluate the efficacy of acadesine for reducing MI, were analyzed at core laboratories. Perioperative ECG changes were identified using continuous three‐lead Holter ECG. Systolic blood pressure, diastolic blood pressure, and heart rate were recorded each minute during operation. The occurrence of MI by Q wave or myocardial fraction of creatine kinase (CK‐MB) or autopsy criteria, and by (Q wave and CK‐MB) or autopsy criteria was determined. Results During perioperative Holter monitoring, episodes of ST segment deviation, major cardiac conduction changes greater or equal to 30 min, or use of ventricular pacing greater or equal to 30 min occurred in 58% patients, primarily in the first 8 h after release of aortic occlusion. Of the 25% patients who met the Q wave or CK‐MB or autopsy criteria for MI, 19% had increased CK‐MB as well as ECG changes. (Q wave and CK‐MB) or autopsy criteria for MI were met by 4% of patients. The CK‐MB concentration generally peaked by 16 h after release of aortic occlusion. In patients with (n = 187) and without a perioperative episode of ST segment deviation, the incidence of MI was 36% and 19%, respectively (P < 0.01), by Q wave or CK‐MB or autopsy criteria, and 6% and 3%, respectively (P = 0.055), by (Q wave and CK‐MB) or autopsy criteria. Multiple logistic regression analysis showed that intraoperative ST segment deviation, intraventricular conduction defect, left bundle branch block, duration of hypotension (systolic blood pressure < 90 mmHg) after cardiopulmonary bypass, and duration of cardiopulmonary bypass are independent predictors of Q wave or CK‐MB or autopsy MI. The independent predictors of (Q wave and CK‐MB) or autopsy MI are intraoperative ST segment deviation and duration of aortic occlusion. Conclusions Major ECG changes occurred in 58% of patients during coronary artery bypass graft surgery, primarily within 8 h after release of aortic occlusion. Multicenter data collection revealed a substantial variation in the incidence of MI and an overall incidence of up to 25%, with most MI occurring within 16 h after release of aortic occlusion. Intraoperative monitoring of ECG and hemodynamics has incremental value for predicting MI.

Differential Effects of Halothane, Enflurane, and Isoflurane on Ca2+transients and Papillary Muscle Tension in Guinea Pigs

These studies were designed to examine the effects of inhalational anesthetics on rapid changes in myocardial intracellular Ca2+ and Ca2+ sensitivity of the contractile apparatus. The effects of halothane, enflurane, and isoflurane on rapid changes in intracellular Ca2+ (Ca2+ transients as measured with bioluminescent protein aequorin) and contractile characteristics were compared in guinea pig right ventricular papillary muscles. In addition to examination of their potencies at equianesthetic concentrations, the effects of these agents on alterations in Ca2+ sensitivity at myofilaments were also investigated. The negative inotropic effects of halothane (0.65 and 1.15%) and enflurane (1.0 and 2.2%) were dose-dependent and closely related to a decrease in Ca2+ transients. In the presence of isoflurane (0.77 and 1.6%), the contractile force decreased in a dose-dependent manner, but the decrease was significantly less as compared to that with equianesthetic concentrations of halothane and enflurane. An additional feature observed in the presence of isoflurane was a dissociation between intracellular Ca2+ availability and contractile force. Although the magnitude of the Ca2+ transients did not change when the percentage of isoflurane was increased from 0.77 to 1.6, the contractile force decreased. Because of these findings, the effects of halothane (1.2%), enflurane (2.2%), and isoflurane (1.6%) on the relationship between intracellular Ca2+ and tension developed in the papillary muscle were examined in order to assess myofibrillar responsiveness to Ca2+. The results indicate that only isoflurane slightly but significantly shifted the Ca2+/isometric tension curve toward higher intracellular Ca2+ concentrations; no differences were observed in the absence and presence of equianesthetic concentrations of halothane and enflurane.(ABSTRACT TRUNCATED AT 250 WORDS)

Additive cardiac depression by volatile anesthetics in isolated hearts after chronic amiodarone treatment.

Some patients undergoing general anesthesia may be chronically receiving the antidysrhythmic drug amiodarone.The half-life of this drug is very long and it may not be advisable or possible to discontinue its administration prior to anesthesia. We examined depressant effects of three volatile anesthetics in hearts isolated from guinea pigs chronically treated with amiodarone. Hearts were isolated and perfused retrogradely through the aorta with oxygenated Krebs-Ringer solution at 37 degrees C at constant pressure. Variables measured in 26 hearts were heart rate (HR), atrioventricular, intraatrial, and intraventricualr conduction times (AVCT, IACT, IVCT) during pacing at 240 bpm, coronary flow, and left ventricular pressure (LVP). Amiodarone (20 mg intraperitoneally) or placebo (Group 1) was given once daily for 1 (Group 2) or 4 (Group 3) wk. Cardiac tissue concentrations of amiodarone were similar (12.1 micro gram/g wet weight) in hearts in Groups 2 and 3 but serum levels were twice as high in hearts in Group 3 as in Group 2 (0.33 vs 0.17 micro gram/mL). Before anesthetic exposure, all variables for hearts in Group 2 were not significantly different from those in Group 1. Significantly, for hearts in Group 3, compared to those in Group 1, HR was slower (-14%), conduction times were longer (IACT + 5 ms, IVCT + 4 ms, AVCT + 9 ms), coronary flow was higher (+23%), and LVP was lower (-12%). After control measurements, hearts were exposed to 0.5 and 1 minimum alveolar anesthetic concentration (MAC) halothane, enflurane, and isoflurane in random order. Each anesthetic slowed HR, prolonged IACT and AVCT, and decreased LVP in a dose-dependent manner; only isoflurane increased flow in a dose-dependent manner. Enflurane depressed HR and LVP more than halothane or isoflurane, halothane decreased LVP more than isoflurane, and isoflurane increased coronary flow more than halothane or enflurane. The changes in these variables due to anesthetic effects were statistically additive to the changes due to amiodarone. Our results indicate that all three anesthetics augment cardiac depression due to chronic administration of amiodarone. This study in isolated hearts suggests that patients on chronic amiodarone therapy for dysrhythmias may exhibit pronounced impairment of conduction and contractility, especially with enflurane, and augmented coronary vasodilation, especially with isoflurane. (Anesth Analg 1995;80:917-24)