Key result
Biofeedback training reversed cellular and molecular markers of heart failure, demonstrating biological changes in response to a psychophysiologic intervention.
Why the study?
Autonomic imbalance is a therapeutic target in heart failure, and noninvasive biofeedback training may improve autonomic function and remodel the failing heart.
Should not yet change heart failure practice; hypothesis-generating for psychophysiologic effects on cellular markers.
Autonomic imbalance is a therapeutic target in heart failure patients. Overactivation of the sympathetic branch of the autonomic nervous system has for years been treated with beta-adrenergic blocking drugs, although it cannot be long before invasive therapies such as renal sympathetic denervation, currently being tested for resistant hypertension, make their way to the heart failure arena. Insufficient parasympathetic input to the heart is already being augmented with implanted vagal nerve stimulators. It is our contention that biofeedback training could provide much of the same benefit as these more invasive therapies in improving autonomic imbalance, with the added advantage of increasing patient self-efficacy. This article describes a pilot study of biofeedback training in patients with end-stage heart failure awaiting heart transplantation. It was our goal to show not only that patients would appreciate this training and benefit from it but also that patient-controlled autonomic modulation could actually reverse the cellular and molecular markers of heart failure, or remodel the failing heart, similar to what we had previously shown for other types of heart failure therapy such as the left ventricular assist device. To our knowledge, this is the first study to demonstrate changes in the biology of the failing heart in response to a psychophysiologic intervention.
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Moravec et al. (2013) studied end-stage heart failure. Biofeedback training was evaluated on Changes in cellular and molecular markers of heart failure. Biofeedback training reversed cellular and molecular markers of heart failure, demonstrating biological changes in response to a psychophysiologic intervention.
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