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• W2992606622 abstract "Heart failure (HF) has become a global pandemic with an anticipated increase in prevalence because of the ageing population worldwide. HF is a complex clinical syndrome with many aetiological causes including, among others, coronary artery disease, congenital heart disease, myocardial infarction, cardiomyopathy, myocarditis, valve insufficiency, hypertension, severe lung disease, diabetes, obesity or sleep apnoea, and is still in need of a universally accepted definition. Nonetheless, from a physiological point of view, HF can be simply defined as a clinical condition under which there is an inadequate cardiac output to meet metabolic demands. The reduced ability of the heart to pump and/or fill with blood is characteristic of HF and is the end result of wear and tear arising from aetiological causes over time. Initial management of HF generally entails medications (e.g. angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, beta blockers, diuretics or digoxin) or treatment of the underlying causes (e.g. coronary bypass surgery or valve repair or replacement). Use of devices to ensure proper heart contraction, either temporarily or permanently, is indicated for the management of persistent bradycardia and atrioventricular conduction disorder when patients are refractory to medical therapy (Kusumoto et al. 2019). With the primary purpose of maintaining adequate heart rate, the cardiac pacemaker, a medical device that generates electrical impulses to contract the heart muscles or regulate the electrical conduction system of the heart, falls into this category. It comes as no surprise that, since first reported in the late nineteenth century, cardiac pacing methods have been developed essentially to target electrical impulses to the right atrium or ventricle (single-chamber pacemaker), right atrium and ventricle (dual-chamber pacemaker), or right atrium and both ventricles (biventricular pacemaker or cardiac resynchronization therapy pacemaker) to address HF of different aetiologies. In a recent issue of The Journal of Physiology, O'Callaghan et al. (2020) propose that reestablishment of respiratory sinus arrhythmia (RSA) is worth considering as a new form of cardiac pacing for HF. RSA is a physiological cardiorespiratory phenomenon characterized by an increase in heart rate during inspiration and a fall during expiration. Since RSA is known to disappear in cardiovascular diseases, including HF, these authors tested whether enhancing RSA would improve cardiac performance in HF. The animal model used entailed induction of left ventricular dysfunction in Wistar rats by ligation of the left anterior descending coronary artery. Daily pacing for 2 weeks was delivered to conscious rats via chronic respiratory modulated heart rate (RMH) pacing using an analogue biofeedback device that can artificially augment RSA by modulating cardiac pacemaker spike frequencies in phase with electromyographic activity of the diaphragm. They found that compared to monotonic pacing (the common practice in contemporary clinical pacers), RMH pacing increased cardiac output and this was associated with an increase in stroke volume and improvement in circumferential strain that persisted beyond the pacing treatment period. The authors proposed that RSA pacing reverse-models the heart in HF. From a physiological perspective, reinstatement of RSA by RMH pacing in HF has two important implications. First, despite the controversies surrounding its functional significance (see O'Callaghan et al. 2020), RSA is basically tasked to coordinate cardiorespiratory functions to meet metabolic demands. Reestablishment of RSA therefore suitably replenishes this fundamental physiological task that is diminished in HF. Second, its popular use in biomedical research and clinical work notwithstanding, one often forgotten fact about heart rate variability is that it should be high because variations of heart beats are wide-ranging in healthy individuals. A key contribution of enhanced RSA by RMH pacing should therefore be the reversal of the reduced heart rate variability in HF. From a clinical perspective, the study by O'Callaghan et al. (2020) points to the prospect of reinstatement of RSA as a potential therapeutic target of cardiac pacing for the management of HF. Before this prospect is realized in clinical practice, there are at least three issues to ponder. First, since the 1980s (e.g. Rossi et al. 1984; Kay et al. 1989) rate-modulating pacing, in which the delivered cardiac stimulus is based on respiratory rate, has been reported to provide increases in heart rate that closely parallel physiological variables of metabolic demand during exercise in patients. Although the algorithms used in those studies to generate the cardiac stimulus are different from the breathe-to-breathe design reported by O'Callaghan et al. (2020), the clinical experiences reported in those pioneering works of more than three decades ago may still offer insights for future development of more sophisticated devices for RMH pacing in patients with HF. Second, given that the primary drive to augment RSA is respiratory rate, one foreseeable handicap is the applicability of this approach to patients with respiratory deficiencies who also require cardiac pacing. For example, it is likely that RMH pacing may not be beneficial to patients with HF and chronic obstructive pulmonary disease or sleep apnoea due to the weakness of their inspiratory muscles. Third, it is worth noting that in the study by O'Callaghan et al. (2020), RMH pacing does not result in a significant improvement of the ejection fraction of rats with left ventricular dysfunction. One potential reason is that cardiac pacing is directed primarily against reduced heart rate. In clinical practice, cardiac contractility modulation (CMM) has gained momentum as another device-based therapy for HF (Borggrefe & Mann, 2018). By applying a relatively high-voltage and long-duration biphasic electrical stimulus to the right ventricular septal wall during the absolute myocardial refractory period, CMM does not elicit a new contraction but rather influences the failing myocardium. This treatment scheme has been shown to induce an acute, mild augmentation of left ventricular contractile strength in both animal models of HF and patients with reduced ejection fraction. Perhaps a combination of RMH pacing and CMM may benefit patients whose HF results from decreases in both heart rate and ejection fraction. None declared. Sole author. Preparation of this article was not supported by any research funds." @default.
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• W2992606622 date "2020-01-15" @default.
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• W2992606622 title "Reinstatement of respiratory sinus arrhythmia as a therapeutic target of cardiac pacing for the management of heart failure" @default.
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