The incidence of neurocognitive impairment after coronary artery bypass graft surgery varies noticeably between studies.3–5,16
This is because of variations in the tests used, the time points of assessment, the definition of impairment, and the statistical methods used for comparing groups.16
We found significantly less neurocognitive impairment 1 week and 10 weeks after off-pump coronary artery bypass graft surgery for patients with triple vessel disease. Previous studies have shown equivocal results. One prospective randomised study found increased concentrations of S100 protein, a marker of neurological injury, in the on-pump group, but no difference in neurocognitive impairment.11
The definition of neurocognitive impairment was, however, unclear. More than 60% of patients recruited in that study had single or double vessel disease. Another study found a higher concentration of serum S100 protein, a higher number of high intensive transient signals picked up by transcranial Doppler, and an increased incidence of neurocognitive impairment in the on-pump than off-pump group.9
This was a randomised study including 40 patients. The neuropsychological assessment was limited to the preoperative period and 1 week postoperatively, and the tests used did not conform to the consensus statement.14
In one randomised controlled trial, neurocognitive outcome was assessed in 281 patients, using 10 neuropsychometric tests.6
Improved cognitive outcomes were found in the off-pump group at 3 months, but the effects were limited and became negligible at 12 months. A significant proportion of the patients in this study had single and double vessel disease (76%); only 24% had triple vessel disease. Anaesthetic management differed between the groups: 99% of patients in the on-pump group received total intravenous anaesthesia including high dose opioids, and 54% of patients in the off-pump group received thoracic epidural anaesthesia.
Strengths of study
Overall, we included 91% of eligible patients in our trial. The operations were performed by a single surgeon (VZ). We standardised anaesthetic and surgical factors that might lead to cerebral injury. Both groups underwent the same surgical procedure, including the use of the same conduits and the same technique for proximal grafting. We included only patients with triple vessel disease. Previous studies have included a significant proportion of patients with single or double vessel disease.6,9–11
No cross over occurred. None of the patients in the off-pump group required conversion to on-pump surgery. Follow up was 100% at 10 weeks. Our prospective randomised trial produced two similar groups (table ). We are thus confident that cardiopulmonary bypass was the only major difference between our study groups.
Limitations of study
One limitation of our study is that a single surgeon operating in a single hospital, with standardisation of the anaesthetic and surgical techniques allows reproducibility of findings, but generalisability is affected. Our findings need to be tested in a multicentric study with different surgeons and hospitals. Aortic atherosclerosis is an important factor in neurological and neurocognitive outcomes. We did not use epiaortic scanning or transoesophageal echocardiography to detect aortic atherosclerosis. Our patients were assessed only at 1 week and 10 weeks postoperatively. Although outcomes at 10 weeks may reflect more important longer term outcomes, they may not necessarily reflect any permanent sequelae. The incidence of neurocognitive outcome decreased from 1 to 10 weeks; future studies need to incorporate longer term follow up.
Cardiopulmonary bypass has been implicated in the pathogenesis of neurocognitive impairment. Various mechanisms are responsible, including hypoperfusion during cardiopulmonary bypass, venous hypertension due to manipulation of the heart during surgery, emboli originating from the cardiopulmonary bypass circuit and the ascending aorta, and systemic inflammatory response syndrome leading to cerebral swelling and an increase in the permeability of the blood-brain barrier.17–22
Neuropsychometric testing and the measurement of serum levels of biochemical markers (S100β and neurone specific enolase) are two ways of measuring neurological injury. Neuropsychometric tests assess specific domains of the brain, whereas the serum markers assess global injury. Two studies showed an association between neurocognitive impairment and S100β and neurone specific enolase levels.14,15
Others have found no such association.11,23
Administering a comprehensive battery of neuropsychometric tests is time consuming. Development of a serum marker or a computerised objective test that could be administered in less time and that correlated well with the severity of neuropsychometric impairment would improve the work of future researchers. At present, comprehensive neuropsychometric tests need to be administered to assess neurocognitive impairment.
We found one notable difference between our patient population and those in other studies. The average IQ of our patients was 115, higher (107 and 108) than in other studies.10,20
It is possible that the slightly higher incidence of neurocognitive impairment in our patients could be related to a higher premorbid IQ. One study found a higher composite neurocognitive score at baseline to be a significant predictor of change in the composite cognitive index.7