Central-peripheral neural interactions in cardiac control

      Cardiac control is achieved through a hierarchal network that may be considered in three-levels. Level 1: CNS neurons (medullary and spinal cord neurons modulated by higher centers); Level 2: Peripheral: extracardiac-intrathoracic neuronal pool; and Level 3: Peripheral: the intrinsic cardiac nervous system. The peripheral layers (Levels 2 and 3) form cardio-centric loops, while the CNS (Level 1) engages neural mechanisms for cardiac and peripheral vasculature regulation. Acting together, these hierarchical populations coordinate and regulate regional cardiac electrical and mechanical indices throughout each cardiac cycle to assure that cardiac output matches blood flow demands. To understand network interactions within and between levels 1–3, one must first understand the characteristics of its constituent parts. It is through such understanding that rational neuromodulation therapies can be devised. Autonomic dysregulation is central to the evolution of cardiac pathology. Mechanistically, this reflects reactive and adaptive responses of the cardiac neural hierarchy involving changes in sensory transduction of the diseased myocardium leading to altered neuronal network excitability. Such changes in neural processing are manifest in intrathoracic ganglia, spinal cord, brainstem and higher centers of the central nervous system. This altered neural processing leads to maladaptive responses ultimately resulting in excessive sympatho-excitation and reduced parasympathetic drive. These neural adaptations contribute to the evolution of pump failure and fatal arrhythmias. Using bioelectric methodologies applied to specific nexus points of the cardiac nervous system; one can modify processing of sensory inputs and thereby affect cardioprotection. We term this concept – Autonomic Regulatory Therapy.
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