Heart failure is a progressive disease in which the heart is no longer able to pump sufficient amounts of blood to the body. Over six million Americans currently suffer from heart failure, and although pharmacological and surgical therapies continue to improve, about 50% of people with heart failure still die within five years of diagnosis.
As the human heart fails, many structural, cellular and molecular alterations occur that contribute to the decrease in heart function. It has been well-established that some of these alterations are the result of sympathetic nervous system hyperactivation, and decreasing sympathetic input with a beta blocker or left ventricular assist device improves clinical status and also reverses the cellular and molecular alterations associated with heart failure. We hypothesized that heart failure patients could be trained with biofeedback and that this method of sympathetic nervous system regulation would also produce myocardial remodeling in the direction of recovery.
To test this hypothesis, twenty end-stage heart failure patients listed for heart transplantation at the Cleveland Clinic received eight sessions of biofeedback-assisted stress management training. After biofeedback training, at the time of heart transplantation, explanted hearts were transported to the laboratory to study the heart failure phenotype. Data were compared to samples of non-failing, failing (negative control), and LVAD-supported failing (positive control) hearts.
We found that the inotropic response of left ventricular trabecular muscles to sympathetic nervous stimulation recovered in patients who received biofeedback training such that it was not significantly different from the non-failing average. Normalization of both rate of contraction and relaxation were also shown in the biofeedback group. Beta adrenergic receptor density was significantly lower in the biofeedback group relative to non-failing hearts, however significant recovery was shown in some patients. Western Blot analysis of calcium cycling proteins showed that SERCA and NCX expression in the biofeedback group was at the same level as the non-failing group, and a significant decrease in RYR expression was shown in the biofeedback hearts. These data suggest that biofeedback produces some remodeling of the heart failure phenotype, in the direction of non-failure.