A Methodological Perspective on the Function and Assessment of Peripheral Chemoreceptors in Heart Failure: A Review of Data from Clinical Trials

Abstract

Augmented peripheral chemoreceptor sensitivity (PChS) is a common feature of many sympathetically mediated diseases, among others, and it is an important mechanism of the pathophysiology of heart failure (HF). It is related not only to the greater severity of symptoms, especially to dyspnea and lower exercise tolerance but also to a greater prevalence of complications and poor prognosis. The causes, mechanisms, and impact of the enhanced activity of peripheral chemoreceptors (PChR) in the HF population are subject to intense research. Several methodologies have been established and utilized to assess the PChR function. Each of them presents certain advantages and limitations. Furthermore, numerous factors could influence and modulate the response from PChR in studied subjects. Nevertheless, even with the impressive number of studies conducted in this field, there are still some gaps in knowledge that require further research. We performed a review of all clinical trials in HF human patients, in which the function of PChR was evaluated. This review provides an extensive synthesis of studies evaluating PChR function in the HF human population, including methods used, factors potentially influencing the results, and predictors of increased PChS.

The Long Covid-19 Syndrome the Spike Protein and Stem Cells, the Underrated Role of Retrotransposons, a Working Hypothesis

“…It is well known that persistent stress from the inflammatory spike protein may contribute to the onset of chronic kidney disease (CKD) by disrupting the RAS mechanism. It is known that in patients with chronic kidney disease anemia is a structural problem, which gives rise to a particular type of hypothermia that is often found in patients affected by Long Covid and Spike protein syndrome [95].…”

Prognostic significance and clinical determinants of residual dyspnoea at discharge in acute heart failure: a single-centre, prospective observational study

“…Residual congestion is a well-documented predictor of poor prognosis, but there are limited data available on residual dyspnoea at discharge and its clinical implications 3–7. Dyspnoea in AHF has complex and multifactorial aetiology, and therefore, its development goes far beyond ‘simple’ pulmonary congestion 8–10. In HF, several pathophysiological pathways that lead to dyspnoea sensation are activated, some may be congestion related, but most of them are congestion independent 11.…”

“…[3][4][5][6][7] Dyspnoea in AHF has complex and multifactorial aetiology, and therefore, its development goes far beyond 'simple' pulmonary congestion. [8][9][10] In HF, several pathophysiological pathways that lead to dyspnoea sensation are activated, some may be congestion related, but most of them are congestion independent. 11 The latter ones are represented by overactivity of the sympathetic nervous system that modulate the activity of the peripheral chemoreceptors located in the carotid bodies.…”