The disability that results from acute infarction is easier to recognize and treat when the patient presents with clear physical sequela of stroke. The impact of subclinical infarction is an understudied area and thus the treating physician lacks clear guidance. Neurologists are all too familiar with ordering head imaging and discovering evidence of prior ischemic insult with the patient denying history of an acute event. What is the physician to do with this information? As our population ages, one can expect that this will become a more common occurrence. More procedures, such as cardiac surgery are also being performed in the latter years. This provides an excellent backdrop upon which to investigate the sequela of accumulating new subclinical infarcts post procedure in those with pre-existing cerebrovascular disease. 

Patel et al. used rapidly evolving technology, the 3T MRI, to assess for new lesions following cardiac surgery, quantified against levels of pre-existing cerebrovascular disease, and also compared neuropsychological testing conducted at identical time intervals. Patients undergoing either a CABG and/or valve surgery at the University of Leicester were eligible for inclusion. Only those who had contraindication to MRI or were not native English speakers were excluded. 3mm 3T MRI images were obtained at intervals 1-2 weeks prior to surgery as well as 6-8 weeks postoperatively. Neuropsychological evaluation with standard battery assessments occurred at the same time intervals. Acute or chronic ischemic change was determined by comparing the DWI and FLAIR sequences by a blinded neuroradiologist. Chronic ischemic change was characterized using a computer program which looked at location and volume of the lesions. Patient cognitive improvement or decline was indicated by a change in the Z score which incorporated the mean and standard deviation from a healthy population.

77 of the 103 patients enrolled successfully completed pre/post-operative MRI and cognitive assessments. FLAIR signal change was found in 49 patients pre procedure. New FLAIR lesions were identified in 24 patients (9 with >1) post procedure with the majority occurring in the MCA territory. There were no baseline characteristics that differed between those with new lesions after cardiac surgery and those without. 22/24 with new lesions had evidence of prior FLAIR signal change. Volume comparison suggested that the accumulation of lesions following surgery is relatively minor (0.004%) in comparison with pre-existing burden (0.1%) due to chronic cerebrovascular disease. Of the 35 patients who showed a decline >1SD in neuropsychological testing following surgery, the majority (24) had NO NEW postoperative lesions. The incidence of cognitive decline (46%) was therefore irrespective of presence, number or size of new lesions. 5 patients notably had acute perioperative stroke but only one patient showed decline in cognition following the procedure.

What conclusions is the practicing neurologist to draw? The good news is that lesions accumulated post cardiac procedure found on imaging appears to have no impact on a patient’s cognition. However, the authors show that patients with pre-existing lesions were ten times more likely to experience new lesions post-operatively. While we may not fully understand the impact of these subclinical lesions, it does confirm what we know to be true. There must be something about the patient population with silent ischemic disease that predisposes them to further insult making prevention all the more important.