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Letter by Meinel et al Regarding Article, "Perioperative Cerebral Microbleeds After Adult Cardiac Surgery".

To the Editor: We congratulate Patel et al for their important work to elucidate the occurrence and significance of susceptibility weighted imaging (SWI) lesions in patients with prior cardiac surgery. We recently performed a retrospective analysis in 155 patients with artificial heart valves and can confirm that cardiopulmonary bypass (CPB) time was a significant factor on multivariable logistic regression related to postoperative SWI lesion count (per 10 minutes CPB: β=0.498; 95% CI, 0.116–0.880; P=0.011, in preparation). However, we are missing important aspects of the authors’ project. First, in patients with mechanical heart valves, the presence of cerebral SWI lesions suspected to be caused by small metallic emboli by degenerative metallic abrasion rather than true cerebral microbleeds has been described years ago and is frequently referred to in clinical practice as “valve abrasion” in radiological reports. However, the scientific basis for this hypothesis is very poor. In our cohort, we found no difference of SWI lesions between biological and mechanical heart valves. We wonder how many of the 49 patients receiving valve surgery in the study by Patel et al received a mechanical and how many a biological heart valve implantation and if the valve type (biological vs mechanical) affected SWI lesion count irrespective of CPB time? If no difference was observed, this might further weaken the hypothesis of degenerative metallic abrasion as a reason for SWI lesions seen in patients with artificial heart valves and spotlight CPB or other peri-interventional factors as the true reason for SWI occurrence. Autopsy studies are warranted to identify the true pathophysiological etiology of SWI lesions in patients with CPB exposure. Second, the authors reported on how many patients fulfilled the modified Boston criteria for cerebral amyloid angiopathy (CAA) before surgery, but not after surgery. Their findings suggest, however, that the SWI lesions seen with cardiac surgery can mimic CAA in a relevant proportion of patients. This might interfere with anticoagulation prescription because of fear of intracerebral hemorrhage, for example, in a patient with a biological heart valve and atrial fibrillation. In our cohort, postoperatively 23.9% of patients fulfilled the criteria of possible or probable CAA according to the modified Boston criteria, although only 16% of those patients had superficial siderosis. We therefore wonder how many of the 9 patients with preoperative probable CAA had superficial siderosis on the preoperative magnetic resonance imaging scan? Furthermore, if any of the patients had a prior CPB exposure maybe explaining the SWI lesions? And lastly and most importantly, how many patients postoperatively fulfilled the criteria of possible or probable CAA and if superficial siderosis was present in any of those? We plead for further research to differentiate CAAand CPBassociated lesions by using size, distribution, and shape of SWI lesions to optimize secondary prevention in those patients. In our cohort, we could show that SWI lesion count remains relatively stable in medium-term follow-up. As SWI lesions are increasingly considered in guiding treatment decisions for intravenous thrombolysis or anticoagulation, we hence question whether the SWI lesions seen with CPB share the same pathophysiological features and long-term bleeding risk as true cerebral microbleeds seen with CAA or classical vascular risk factors. We propose, that in a patient with CPB exposure—until clinical suspicion for CAA is high or superficial siderosis present—SWI lesions should not be a reason to withhold intravenous thrombolysis or long-term anticoagulation. Third, we wonder if any of the patients had other diagnoses that might lead to confounding SWI lesions including infectious endocarditis or cardiac myxoma as an indication for cardiac surgery? Last, there are some patients without SWI lesions despite CPB exposure. We wonder if further CPB parameters like coagulation parameters during implantation (maximal anti-Xa-activity) or specific CPB components were available and were analyzed by the authors?