TY - JOUR
T1 - A novel heart rate control model provides insights linking LF-HRV behavior to the open-loop gain
AU - Dvir, Hila
AU - Bobrovsky, Ben Zion
AU - Gabbay, Uri
N1 - Funding Information:
Funding: This work was supported by the Elizabeth and Nicholas Slezak Super-Center for Cardiac Research and Medical Engineering, Tel Aviv Universiv, Tel Aviv, Israel.
PY - 2013/9/20
Y1 - 2013/9/20
N2 - Background: Low-frequency heart rate variability (LF-HRV) at rest has already been successfully modeled as self-sustained oscillations in a nonlinear control loop, but these models fail to simulate LF-HRV decreases either during aerobic exercise or in heart failure patients. Following control engineering practices, we assume the existence of a biological excitation (dither) within the heart rate control loop that softens the nonlinearity and studied LF-HRV behavior in a dither-embedded model. Methods: We adopted the Ottesen model with some revisions and induced a dither of high-frequency stochastic perturbations. We simulated scenarios of a healthy subject at rest and during aerobic exercise (by decreasing peripheral vascular resistance) and a heart failure patient (by decreasing stroke volume). Results: The simulations resembled physiological LF-HRV behavior, i.e., LF-HRV decreased during aerobic exercise and in the heart failure patient. The simulations exhibited LF-HRV dependency on the open-loop gain, which is related to the product of the feedback gain and the feed forward gain. Conclusions: We are the first to demonstrate that LF-HRV may be dependent on the open-loop gain. Accordingly, reduced open-loop gain results in decreased LF-HRV, and vice versa. Our findings explain a well-known but unexplained observed phenomenon of reduced LF-HRV both in heart failure patients and in healthy subjects performing aerobic exercise. These findings have implications on how changes in LF-HRV can be interpreted physiologically, a necessary step towards the clinical utilization of LF-HRV.
AB - Background: Low-frequency heart rate variability (LF-HRV) at rest has already been successfully modeled as self-sustained oscillations in a nonlinear control loop, but these models fail to simulate LF-HRV decreases either during aerobic exercise or in heart failure patients. Following control engineering practices, we assume the existence of a biological excitation (dither) within the heart rate control loop that softens the nonlinearity and studied LF-HRV behavior in a dither-embedded model. Methods: We adopted the Ottesen model with some revisions and induced a dither of high-frequency stochastic perturbations. We simulated scenarios of a healthy subject at rest and during aerobic exercise (by decreasing peripheral vascular resistance) and a heart failure patient (by decreasing stroke volume). Results: The simulations resembled physiological LF-HRV behavior, i.e., LF-HRV decreased during aerobic exercise and in the heart failure patient. The simulations exhibited LF-HRV dependency on the open-loop gain, which is related to the product of the feedback gain and the feed forward gain. Conclusions: We are the first to demonstrate that LF-HRV may be dependent on the open-loop gain. Accordingly, reduced open-loop gain results in decreased LF-HRV, and vice versa. Our findings explain a well-known but unexplained observed phenomenon of reduced LF-HRV both in heart failure patients and in healthy subjects performing aerobic exercise. These findings have implications on how changes in LF-HRV can be interpreted physiologically, a necessary step towards the clinical utilization of LF-HRV.
KW - Baro-reflex sensitivity
KW - Dither
KW - Low frequency heart rate variability (LF-HRV)
KW - Open-loop gain
KW - Peripheral vascular resistance
KW - Stroke volume
UR - http://www.scopus.com/inward/record.url?scp=84883802908&partnerID=8YFLogxK
U2 - 10.1016/j.ijcard.2012.09.073
DO - 10.1016/j.ijcard.2012.09.073
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AN - SCOPUS:84883802908
SN - 0167-5273
VL - 168
SP - 287
EP - 293
JO - International Journal of Cardiology
JF - International Journal of Cardiology
IS - 1
ER -