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Physiology of the Transplanted Heart

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Clinical Guide to Heart Transplantation

Abstract

The normal heart is innervated by sympathetic and parasympathetic fibers of the autonomic nervous system (ANS). The ANS exerts chronotropic and inotropic control over the heart and supplies visceral sensory fibers to the pericardium. Heart transplantation results in denervation of the donor heart by surgical dissection of postganglionic neurons. Within days, cardiac stores of norepinephrine become depleted and autonomic influence over the heart is lost.

The lack of parasympathetic tone means that heart transplant recipients have a higher average resting heart rate of 95 beats per minute (bpm) compared with 66 bpm for non-transplant cardiac patients [1]. Despite significant improvements in exercise tolerance compared with the end-stages of heart failure, patients still show a reduction in maximum achievable exertion when compared with normal individuals of the same age [2]. This is accounted for by the chronotropic incompetence of the denervated heart as well as peripheral factors that will be discussed later. The normal heart will show a rapid acceleration in HR in response to exercise that peaks during exercise and rapidly recovers. The transplanted heart shows a delayed chronotropic response to exercise due to a reliance on circulating catecholamines. Norepinephrine and epinephrine levels are either normal or elevated in the transplant recipient [3]. The lack of nervous supply and reliance on humoral mechanisms causes a shift from predominately type-1 to type-2 beta adrenergic receptors on cardiac myocytes [4].

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Kobashigawa, J., Olymbios, M. (2017). Physiology of the Transplanted Heart. In: Kobashigawa, J. (eds) Clinical Guide to Heart Transplantation. Springer, Cham. https://doi.org/10.1007/978-3-319-43773-6_8

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