Abstract
INTRODUCTION: Enhanced External Counterpulsation (EECP) has been described to help Long Covid related cardiovascular (e.g. chest pain, fatigue) and neurocognitive (e.g. brain fog) symptoms. We sought to determine whether EECP improves cognitive function. Methods: A retrospective evaluation of a contemporary consecutive patient cohort referred to Flow Therapy for management of Long Covid. All patients subjectively reporting brain fog were assessed using the BrainCheck tool to determine degree of cognitive impairment pre- and post EECP therapy. BrainCheck is an FDA-approved, web-based battery of standardized neuropsychological tests that includes the Trail Making Test (Trails A, Trails B) for assessing executive function (cognitive flexibility), the Digit Symbol Substitution Test (DSST) for assessing attention and processing speed, the Stroop Test for assessing executive function (response inhibition), and the List Learning Test for immediate/delayed verbal memory evaluation. BrainCheck scores have a normative mean of 100±15 with a clinically meaningful change ranging from 12-21 depending on age. Change from baseline to post-EECP were assessed using the paired student’s t-test. Results: A total of 51 Long Covid patients were included (49.3±11.0 years, 60.8% female, 22% had CAD) with the average duration since Covid diagnosis being 9.9±6.1months. No patients were excluded. All patients completed 25-35 sessions of EECP. Baseline BrainCheck composite score was 88.0±22.1 which significantly improved to 100.1±16.4 post-EECP (+11.9±18.7, p<0.001). When limiting to baseline score under 85 (n=20; baseline average 66.7±17.6) the improvement was +26.0±20.9 (p<0.001). EECP therapy improved the patients’ performance across cognitive domains, as indicated by significant enhancements in scores from baseline in Trails A (+6.1±19.7), Trails B (+5.0±11.8), DSST (+12.9±24.1) and Stroop Test (+11.2±19.1) (all p-values<0.05). Conclusion: This is the first evaluation showing significant improvement in Long Covid related cognitive impairment post-EECP therapy. Further study is needed to determine if the mechanistic basis may include EECP induced improved cerebral perfusion, change in endothelial function, or a yet unelucidated pathway.
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