Key result
Low cardiac autonomic regulation (low sympathetic and parasympathetic control) predicted the occurrence of myocardial infarction and neuroinflammatory consequences of cardiac arrest.
Why the study?
The historical view of reciprocal control of autonomic branches is limited, and assessing sympathovagal balance does not adequately capture the autonomic patterns relevant to myocardial infarction and cardiac arrest.
A coactive model of cardiac autonomic regulation better predicts myocardial infarction and post-arrest neuroinflammation than traditional reciprocal sympathovagal balance models.
Supports coactive autonomic models over reciprocal balance for MI risk; hypothesis-generating, requires prospective validation before practice change.
Understanding psychosomatic relations, and their implications for heath, is importantly dependent on our conceptual and measurement models. The historical view of reciprocal control of the autonomic branches is applicable in some contexts, but not others. Control of the autonomic branches can vary reciprocally, independently, and even coactively. Assessment of sympathovagal balance, based on a reciprocal model of regulation of the autonomic branches, may have applications in orthostatic contexts and in insulin resistance in diabetes. However, it does not adequately capture the pattern of autonomic control that is relevant for myocardial infarction (MI; in humans) and experimental cardiac arrest (in mice). A measure of sympathovagal balance (cardiac autonomic balance) was predictive and informative of the autonomic contributions to diabetes but was blind to autonomic contributions to cardiac arrest and its sequelae. However, a metric designed to capture the coactivity dimension of cardiac autonomic regulation (CAR) was predictive of MI and its sequelae. Both human and animal model studies revealed that low CAR (low sympathetic and especially low parasympathetic control) predicted the occurrence of MI and the neuroinflammatory consequences of cardiac arrest. These effects were importantly modulated by social support in both humans and animals, via an apparent oxytocinergic pathway that impacts parasympathetic cardiac control and CAR, and thus neuroinflammation. Results indicate the importance of a physiologically meaningful model of autonomic control in understanding health implications of the modes of autonomic control.
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Gary G. Berntson (2018) conducted an editorial in Myocardial infarction, cardiac arrest, diabetes. Cardiac autonomic regulation (CAR) assessment vs. Sympathovagal balance assessment was evaluated. Low cardiac autonomic regulation (low sympathetic and parasympathetic control) predicted the occurrence of myocardial infarction and neuroinflammatory consequences of cardiac arrest.
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