Neurological dysfunction following coronary artery bypass graft (CABG) surgery can manifest as stroke, encephalopathy including delirium and post-operative cognitive dysfunction. Stroke is one of the most devastating complications after CABG surgery, entailing permanent disability and a 3–6 fold increased risk of death with a case-fatality rate up to 20 %.1,2 It is also associated with incremental hospital resource consumption and a longer length of hospital stay. It has been estimated among a population of 114,233 Medicare beneficiaries that the occurrence of stroke entails an incremental cost of US$18,552 and an incremental length of hospital stay of seven days.3
The risk of stroke after CABG varies across studies ranging from 0.0 % to 5.2 %,4,5 depending on study design, patient risk profile, operative techniques and the length of study follow-up. Although advances in surgical, anaesthetic and medical management have occurred across the last 10 years, the risk of stroke after CABG has not significantly declined, likely because an older and sicker population is now deemed suitable to undergo CABG surgery.6
In addition, stroke represents a dismal point against CABG when deciding the optimal strategy of revascularisation between CABG and percutaneous coronary intervention (PCI) in patients with multivessel coronary artery disease. Specifically, in a recent meta-analysis including 19 randomised controlled trials with 10,944 patients, CABG was associated with significantly higher 30-day and one-year rates of stroke compared with PCI.7 Interestingly, the difference in the risk of stroke between the two strategies of revascularisation seemed more evident in patients with unprotected left main coronary artery disease or multivessel coronary artery disease than in patients with single vessel coronary artery disease.7 In addition, in a recently published meta-regression analysis including 20 randomised controlled trials comparing PCI versus CABG in patients with stable angina, a significant interaction between female gender and stroke risk reduction with PCI was apparent.8
Pathogenesis
The pathogenesis of stroke is multifactorial, but two variables are believed to play a major role – cerebral embolism and hypoperfusion during surgery. Some studies suggested that panvasacular inflammation may also play a role, especially in the setting of acute coronary syndromes.9 Cerebral embolism is by far the most common cause of peri-operative stroke accounting for 50–75 % of cases. Cerebral emboli arise from either the ascending aorta during surgical manipulation or from the heart due to atrial fibrillation.
The prevalence of atherosclerotic disease in the ascending aorta varies across studies, depending on the patient population, the criteria used to define the disease, and the diagnostic tool implemented to detect the disease, with case rates up to 38 % in some studies.10 This prevalence has significantly increased in recent years, likely due to better diagnostic methods and an increasing population of elderly. Peripheral vascular disease, age, hypertension and diabetes have been reported to be independent predictors of atherosclerotic disease of the ascending aorta.11
A high correlation between atherosclerosis of the ascending aorta and atheroembolism during CABG surgery has been established by several studies.5,12–14 In a prospective multicentre study including more than 2,000 patients, atherosclerosis of the ascending aorta was the strongest independent predictor of stroke associated with CABG.5 In the study by Bergman et al., extensive atherosclerotic disease of the ascending aorta was associated with a 31 % risk of post-operative stroke.12 The risk depends on the presence, location and extent of disease when the aorta is surgically manipulated.15
Embolisation of atheromatous debris from the aorta is likely to occur at the time of cannulation of the aorta for establishing cardiopulmonary bypass, when the aortic clamp is applied or released, or when proximal graft anastomoses are performed using side-biting clamp. Cerebral emboli often co-exist with intra-operative hypoperfusion, which impairs the clearance of microemboli16 and may be responsible of bilateral watershed infarcts after CABG.17 Cerebral hypoperfusion may be exacerbated by the co-existence of carotid artery stenosis, which is another important risk factor for intra-operative stroke.18
Chronic atrial fibrillation is a risk factor for cerebral embolism, and in patients undergoing CABG the peri-operative period may be at increased risk of stroke due to the necessity to modulate anticoagulant therapy. In addition, recent studies have suggested that new onset atrial fibrillation in the peri-operative period is also a risk factor for post-CABG stroke.19 Atrial fibrillation develops in 15–30 % of patients undergoing CABG,20,21 and although initial reports suggested that it was a self-limited phenomenon with no relevant clinical sequelae, a recent study including 8,058 patients undergoing CABG, suggested that new onset atrial fibrillation was associated with significantly higher rates of stroke and long-term mortality.19