A comprehensive meta-analytic review of the neurophysiological properties of the heartbeat evoked potential in health and disease.
The heartbeat evoked potential (HEP) is an electrophysiological indicator of cortical processing of cardiac signals and a putative neural index of cardiac interoception. Various clinical conditions are associated with disrupted heart-brain communication, raising the possibility that the HEP could serve as a valid biomarker of disrupted cardiac interoception. Yet there is limited understanding about how the HEP signal, and its various parameters, is associated with different health conditions.
We synthesised the current evidence for HEP amplitude as a biomarker across all available clinical subpopulations using a random-effects multilevel meta-analysis. Secondly, we systematically characterised and quantitatively evaluated key HEP parameters, such as latency windows, reference electrodes, and scalp topographies across HEP studies (OSF Doi: 10.17605/OSF.IO/TMQ3W).
Subgroup analyses for each condition showed no difference in HEP amplitude between clinical conditions relative to healthy comparisons; however, large negative effect estimates were found in neurological and cardiovascular diseases, though these were based on a small number of studies and should be interpreted with caution. In subsequent multivariate analysis, clinical category partially explained the global variability in HEP parameters.
Based on these results, no firm conclusions can be drawn regarding the utility of HEP amplitude as a clinical biomarker. Substantial heterogeneity and widespread methodological inconsistencies across studies preclude definitive interpretations, and rigorous, standardised research is needed before the clinical value of HEP can be established.
We synthesised the current evidence for HEP amplitude as a biomarker across all available clinical subpopulations using a random-effects multilevel meta-analysis. Secondly, we systematically characterised and quantitatively evaluated key HEP parameters, such as latency windows, reference electrodes, and scalp topographies across HEP studies (OSF Doi: 10.17605/OSF.IO/TMQ3W).
Subgroup analyses for each condition showed no difference in HEP amplitude between clinical conditions relative to healthy comparisons; however, large negative effect estimates were found in neurological and cardiovascular diseases, though these were based on a small number of studies and should be interpreted with caution. In subsequent multivariate analysis, clinical category partially explained the global variability in HEP parameters.
Based on these results, no firm conclusions can be drawn regarding the utility of HEP amplitude as a clinical biomarker. Substantial heterogeneity and widespread methodological inconsistencies across studies preclude definitive interpretations, and rigorous, standardised research is needed before the clinical value of HEP can be established.
Authors
Wilkinson Wilkinson, Jones Jones, Kohler Kohler, Khalsa Khalsa, Moseley Moseley, Berryman Berryman
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