Background and objectives-Autonomic dysfunction seems to be involved in the progression and prognosis of severe congestive heart failure. Parasympathetic activity can still be abnormal 4-8 weeks after haemodynamic improvement by heart transplantation. To identify patients in heart failure with a more pronounced neural derangement and to analyse the changes in sympathetic and parasympathetic activity soon after heart transplantation, spectral indices of heart rate variability were assessed in 30 patients in severe heart failure and in 13 patients after heart transplantation; a group of 15 age-matched subjects served as controls. Methods and results-Heart rate variability was assessed by standard electrocardiography (ECG) in patients in heart failure and by oesophageal ECG in patients after heart transplantation. Compared with controls, the mean RR interval and total power were reduced in heart failure. The 30 patients showed two different patterns of heart rate variability: in 14 no power was detected in the low frequency band (0.03-0.15 Hz) (LF) and total power was mainly concentrated in the high frequency band (0.15-0-45 Hz) (HF), whereas in the remaining 16 patients power in the LF band was increased and power in HF band was reduced compared with the controls. Patients with undetectable LF had a lower mean RR interval and total power (745 (25) Conclusions-These data suggest that in more advanced stages of congestive heart failure, power spectral analysis of heart rate variability allows identification of a subgroup of patients with higher sympathetic activation and poorer clinical status who are at major risk of adverse events. In the short term after cardiac transplantation the spectral profile of the rhythm variability of the remnant atrium was not improved, suggesting that parasympathetic withdrawal and sympathetic hyperactivity persist, despite the restoration of ventricular function. (Br Heart J7 1994;71:422-430) Heart failure in both experimental and clinical settings is associated with considerable neurohumoral excitation, resulting in abnormal autonomic control of cardiovascular function. Increased sympathetic activity and plasma concentrations of noradrenaline.' 2 parasympathetic withdrawal,3-5 and impaired baroreflex gain68 have been reported. This excessive neurohumoral activation is involved in progression of heart failure and in prognosis.Analysis of heart rate variability is regarded a valid technique to assess non-invasively the sympathovagal balance of the heart. Frequency domain analysis of heart rate fluctuations identifies the relative influence of the two neural limbs that regulate heart rhythm. In our present study we tested the hypothesis that power spectrum analysis of heart rate variability in congestive heart failure may identify patients with a more pronounced

Data availabilitySummary statistics generated by COVID-19 Host Genetics Initiative are available online (https://www.covid19hg.org/results/r6/). The analyses described here use the freeze 6 data. The COVID-19 Host Genetics Initiative continues to regularly release new data freezes. Summary statistics for samples from individuals of non-European ancestry are not currently available owing to the small individual sample sizes of these groups, but the results for 23 loci lead variants are reported in Supplementary Table 3. Individual-level data can be requested directly from the authors of the contributing studies, listed in Supplementary Table 1.

Baroreflex sensitivity (BRS) has rapidly gained considerable attention as a result of multiple experimental and clinical reports on its prognostic value after a myocardial infarction. This article reviews the several aspects related to the use and significance of BRS. The methodology of baroreflex testing in man is described. The complex pathophysiology underlying BRS and the hypotheses proposed to explain its frequent reduction after a myocardial infarction are discussed. The section on experimental data also provides a rationale to understand the relation between increased vagal activity and reduced propensity for ventricular fibrillation. The article focuses largely on the clinical studies relating BRS and risk of cardiac mortality and also discusses the several attempts to modify this marker of reflex vagal activation.

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