Baseline Heart Rate Variability Research Articles

Heart rate variability and occurrence of ventricular arrhythmias during balloon occlusion of a major coronary artery

Experimental studies suggest that autonomic mechanisms are important in the genesis of ischemia-induced malignant ventricular arrhythmias, but the role of the autonomic nervous system in human arrhythmogenesis is not well known. To assess whether heart rate variability (HRV) predicts the occurrence of ventricular arrhythmias during acute coronary artery occlusion, we performed continuous electrocardiographic, heart rate, and blood pressure recordings before and during a 2-minute balloon occlusion of a stenotic coronary artery in 252 patients with no baseline ventricular premature complexes (VPCs). The ranges of nonspecific responses in heart rate and blood pressure were determined by analyzing a control group of 19 patients with no ischemia during a 2-minute balloon inflation in a totally occluded coronary artery. Balloon occlusion of a coronary artery was stopped because of complex, i.e., bigeminal or repetitive, VPCs in 14 patients, and solitary (<5) VPCs were observed in an additional 19 patients. During coronary occlusion, HRV increased (p <0.001) and heart rate decreased (p <0.05) in patients with no VPCs, whereas an opposite tendency to reduction in HRV (p = 0.08) was observed in patients with complex VPCs. Complex VPCs were observed in 5 (42%) of the 12 patients with a significant coronary occlusion-induced decrease in HRV, in 7 (3.5%) of 200 patients with no change in HRV, but in none of the 40 patients with a significant increase in HRV (p <0.001). Baseline HRV did not predict the occurrence of VPCs during coronary occlusion. Logistic regression analysis identified the decrease in HRV (p <0.001) to be the only independent predictor of complex VPCs. In conclusion, coronary occlusion-induced increase in HRV seems to protect against occurrence of complex ventricular arrhythmias during the early phase of abrupt coronary occlusion, suggesting that vagal activation may modify the outcome of acute coronary events in patients with coronary artery disease.

Intralipid infusion combined with propranolol administration has favorable metabolic effects in elderly malnourished cancer patients

Previous studies have shown that an elevated basal metabolic rate (BMR) is present in elderly malnourished cancer patients. A possible dysfunction of the autonomic nervous system needs to be demonstrated. In aged weight-losing cancer patients (n = 40), aged non—weight-losing cancer patients (n = 30), and aged weight-losing noncancer patients (n = 18), the baseline BMR and heart rate variability were studied. Aged weight-losing cancer patients (n = 40) underwent bioimpedance analysis, ambulatory electrocardiographic monitoring with analysis of heart rate variability, and determination of the BMR. Then, the patients received infusion of Intralipid (Pharmacia, Uppsala, Sweden) without and with propranolol (6 days of 40 mg twice daily) administration. At baseline, a simple correlation between the BMR and the low-frequency component (LF) ( r = .42, P < .006) and LF to high-frequency (HF) ratio ( r = .51, P < .001) was found. After propranolol administration, the percent decline in the BMR was significantly correlated with the percent decline in the LF ( r = .39, P < .01) and LF HF ratio ( r = .53, P < .001). The percent decline in the BMR was not correlated with the HF ( r = .13, P < .34) or the plasma noradrenaline concentration ( r = .21, P < .20) at any time. With regard to the BMR and substrate oxidation, 6-day propranolol administration plus Intralipid infusion produced the strongest decline in the BMR. This study demonstrates that autonomic nervous system dysfunction occurs and is responsible for the elevated BMR in elderly cancer patients, propranolol administration rectifies the autonomic dysfunction, and Intralipid infusion combined with propranolol administration is useful for enhancing the daily caloric intake without a strong increase in energy expenditure.

531 The spectral characteristics of EEG and features of time perception

Heart rate variability (HRV) in individuals with autism spectrum disorders (ASD) has been investigated in some studies but the procedures and results vary. We conducted a systematic review and meta-analysis to compare HRV in individuals with and without ASD; the influence of different conditions and HRV indices is considered. Baseline HRV and HRV reactivity were analyzed in several ways: parasympathetic indices in hierarchical order (main analysis), total variability, specific parasympathetic indices and respiratory sinus arrhythmia (RSA), etc. The review covered 34 studies for quantitative analysis. Individuals with ASD had a significantly lower baseline HRV for parasympathetic indices in hierarchical order (Hedges’g=-0.5168, p < 0.0001) and RSA (g=-0.5860, p=0.0010). The reactivity of HRV in situations of social stress (g=-0.4647, p = 0.0033) and social debriefing (g=-0.5001, p = 0.0007) was also significantly lower in subjects with ASD. RSA reactivity was significantly lower in ASD group for all situations, with the largest effect size for social stress (g=-0.7246, p < 0.0001). The results support low HRV to be a potential biomarker of ASD, especially RSA reactivity under social stress.

Heart rate variability in patients with atrial fibrillation is related to vagal tone.

Analysis of heart rate variability (HRV) has thus far not been applied in patients with atrial fibrillation, probably because of the presumed absence of any form of patterning of the ventricular rhythm, particularly vagally mediated respiratory arrhythmia. However, such patterning is theoretically conceivable given the function of the atrioventricular node in atrial fibrillation and its susceptibility to autonomic influences. Sixteen patients (mean age, 56+/-4 years) with long-term atrial fibrillation on fixed doses of digoxin or verapamil were studied; 12 healthy men in sinus rhythm were used as control subjects. HRV (standard deviation of RR intervals [SD], coefficient of variance [CV], the root-mean-square of successive difference [RMSSD], and low-frequency [LF] and high-frequency power [HF]) was analyzed during 500 RR intervals at baseline, after administration of propranolol (0.2 mg/kg I.V.), and after subsequent administration of methylatropine (0.02 mg/kg I.V.). HRV at baseline and changes in HRV after methylatropine were then related to vagal tone (vagal cardiac control), quantified as the decrease in mean RR after methylatropine. Baseline HRV was higher in the atrial fibrillation group than in the control group; after propranolol, HRV increased in both groups; after methylatropine, HRV neared zero in the control group, whereas it returned to baseline values in the atrial fibrillation group. SD, RMSSD, LF, and HF at baseline were significantly (P<.05) correlated with vagal tone in the control group but also in the atrial fibrillation group (correlation coefficients of .60, .61, .57, and .64, respectively). Even stronger correlations were observed between changes in these parameters after methylatropine and vagal tone, particularly in the atrial fibrillation group (correlation coefficients of .89, .87, .72, and .90, respectively). This study shows that HRV in patients with atrial fibrillation is related to vagal tone.

96/00419 Nuclear energy in Lithuania. Present status and hopes for the future

Decreased heart rate variability (HRV) has predictive value in postinfarction as well as in ischemic stroke patients. However, it is unknown if ischemic heart disease (IHD) patients who are at high risk of stroke have different HRV profile. The goal of this study was to compare baseline HRV (traditional and novel indices) in stable IHD patients with and without stroke in long-term observation.A total of 139 consecutive patients with stable IHD scheduled for coronary angiography were enrolled. Five-minute electrocardiogram readings were taken. Traditional and novel HRV measures were calculated. After 70.06 ± 4.297 months of follow-up, baseline HRV indices in patients who had had a stroke were compared with indices in patients without the aforementioned cerebrovascular event.During follow-up, 6 patients developed stroke. Compared to patients without such a cerebrovascular event, these patients with stroke had lower values for the following HRV indices: de Hann long-term irregularity (30,521 ± 32,767 versus 46,678 ± 25,328; P < .05), Yeh interval index (.0207 ± .0208 versus .0326 ± .0157; P < .05), Organ BAND (3.0563 ± 3.328 versus 4.515 ± 2.276; P < .05), Dalton standard deviation (SD) (17,887 ± 17,636 versus 29,859 ± 16,478; P < .05), Zugaib short-term variability (.004 ± .00416 versus .00622 ± .00418; P < .05), Zugaib long-term variability (.0161 ± .0151 versus .0247 ± .0115; P < .05), standard deviation of all NN intervals (8,954 ± 8,812 versus 16,724 ± 11,594; P < .05), total power (2,616 ± 4,855 versus 4,678 ± 4,653; P < .05), w2 (.71 ± .338 versus 1.719 ± 1.08; P < .05), w3 (1.399 ± .924 versus 2.552 ± 1.609; P < .05), and w4 (1.367 ± 1.705 versus 2.824 ± 2.027; P < .05). No significant differences in other analyzed indices were observed.Patients with IHD and stroke in long-term observation have different baseline profiles of HRV indices. Further investigations are needed to assess the usefulness of HRV analysis in stroke risk assessment.

Heart rate variability in patients with mild to moderate heart failure: Effects of neurohormonal modulation by digoxin and ibopamine

This study assessed the effects of digoxin and ibopamine on variables of heart rate variability in relation to neurohormonal activation. Analysis of heart rate variability can be used to study the autonomic dysfunction that characterizes chronic heart failure. In the Dutch Ibopamine Multicenter Trial, patients with heart failure were found to have increased neurohormonal activation with placebo therapy but not with digoxin and ibopamine therapy. We studied 59 patients with mild to moderate heart failure (mean [+/- SEM] age 60 +/- 1 years, mean ejection fraction 0.30 +/- 0.01). Patients were randomized to double-blind treatment with digoxin (0.25 mg [n = 22]), ibopamine (100 mg three times a day [n = 19]) or placebo (n = 18); background therapy consisted of furosemide (up to 80 mg). After 3 months, plasma norepinephrine levels had increased with placebo, whereas they decreased with digoxin (+31 vs. -60 pg/ml, respectively, p < 0.01). With ibopamine, nonsignificant decrease was observed (-27 pg/ml, p = 0.10). All variables of heart rate variability showed a deterioration in the placebo group. With digoxin, the percent differences between successive RR intervals > 50 ms (pNN50) increased (+ 1.7 +/- 0.9%, p < 0.01), along with absolute and normalized high frequency power (+ 40 +/- 33 ms2, p < 0.05 and + 2.4 +/- 1.7%, p < 0.01, respectively). These changes were observed during daytime hours only and were most pronounced in patients with the most impaired baseline heart rate variability. With ibopamine, nonsignificant trends similar to the changes with digoxin were observed. In patients with early stages of heart failure, digoxin may prevent a progressive deterioration in heart rate variability, whereas ibopamine does not show statistically significant effects. The changes in heart rate variability with digoxin parallel an observed decrease in neurohormonal activation. Digoxin apparently enhances cardiac vagal tone in the setting of neuroendocrine activation.

Effect of physiologic and pharmacologic adrenergic stimulation on heart rate variability

Objectives. The aim of this study was to evaluate and compare the effects of physiologic and pharmacologic sympathetic stimulation on time and frequency domain indexes of heart rate variability.Background. Measurements of heart rate variability have been used as indexes of sympathetic tone. To date, the effects of circulating catecholamines on heart rate variability have not been evaluated.Methods. Fourteen normal subjects (eight men, six women, mean (± SD) age 28.5 ± 48 years) were evaluated. Five-minute electrocardiographic recordings were obtained in triplicate after physiologic and pharmacologic sympathetic stimulation: during upright tilt, after maximal exercise, during epinephrine and isoproterenol infusions at 50 ng/kg body weight per min, during beta-adrenergic blockade and during combined beta-adrenergic and parasympathetic blockade.Results. Beta-adrenergic stimulation resulted in a significant decrease in time domain measures of heart rate variability. The frequency domain indexes showed variable responses, depending on the individual stimulus. Tilt caused an increase in low frequency power and in the ratio of low to high frequency power. These changes were not necessarily observed with other conditions of beta-adrenergic stimulation. Double blockade suppressed baseline heart rate variability, but beta-adrenergic blockade had no significant effect. Time domain measures of heart rate variability demonstrated excellent reproducibility over the three recordings, but the frequency domain variables demonstrated fair to excellent reproducibility.Conclusions. These findings suggest that different modes of beta-adrenergic stimulation may result in divergent heart rate variability responses. Thus, current heart rate variability techniques cannot be used as general indexes of “sympthetic” tone. Studies utilizing heart rate variability to quantify sympathetic tone need to consider this.

Response of the premature fetus to stimulation by speech sounds

The response of the premature fetus to speech stimuli was studied in 41 healthy pregnant patients at 26–34 weeks gestation. Speech stimuli consisted of repeated syllables (‘ee’ and ‘ah’) presented externally over the maternal abdomen at either 100, 105, or 110 decibels (dB). Sound stimuli were delivered during periods of both high and low fetal heart rate variability. During periods of low FHR variability, a decrease in fetal heart rate and an increase in the standard deviation of heart rate were found. During periods of high FHR variability, no significant change in either of these measures was observed. This is the first clear demonstration of heart rate responses to speech stimuli in the premature fetus. As is the case in the term fetus, this response is dependent on baseline heart rate variability which is the primary determinant of fetal state. The clinical usefulness of this finding may be limited by the magnitude of the response.

273 THE HUMAN FETUS AND AIR TRAVEL

At artificially maintained cabin pressure in modern aircrafts, the arterial Po2 in healthy adults is close to 60 mm Hg. This relative oxygen deficiency has been discussed as a potential risk for the fetus during flight of pregnant women. In addition, there are speculations about the possible effects of acceleration and emotional stress during flight on the maternal and fetal organism. Investigations in human pregnancy have not been carried out under simulated or real flight conditions. We measured maternal respiratory and heart rate, ECG, transcutaneous blood gases, blood pressure and uterine contractions, fetal beat-to-beat heart rate and cabin pressure in 10 healthy pregnant women during 20 European continental flights. Commercially available or specially adapted instruments were used and observations were recorded on Eproms. The instrumentations were battery powered. Data were analyzed according to the various flight phases and related to the initial phase on the runway (take off, climb, maximal height, descent and landing). Maternal heart rate and blood pressure increased. Po2 decreased significantly. Maternal respiration and Pco2 remained unchanged. In the fetuses there was no instance of bradycardia, no decelerations or reduction in baseline heart rate variability. Mean fetal heart rate remained normal during all flight periods. Significant accelerations of fetal heart rate were observed in some cases.

Antepartum fetal heart rate monitoring. A semi-quantitative evaluation of the 'non-stressed' fetal heart rate.

1964 recordings (from 246 patients were analysed on the basis of a semi-quantitative evaluation of base-line heart rate variability. All the tracings were obtained in the antepartum period, between the 20th wk of pregnancy and prior to the onset of labour. None of the recordings were made during labour or after induction of uterine activity so that a 'non-stressed' fetal heart rate test was obtained in every case. The percentage of flat tracing in each recording and the presence of sinusoidal patterns were compared with the neonatal outcome. When the tracings included a more than 50% flat pattern, 81.8% of the babies were distressed at birth. When a less than 50% flat recording was present only 11.4% of the neonates were distressed. Sinusoidal patterns were more frequently associated with abnormal tracings including those with more than 50% flat recordings. The presence of sinusoidal features did not significantly influence the neonatal outcome for tracings with a less than 50% anomaly: conversely sinusoidal patterns superimposed on a more than 50% flat tracing were predictive of fetal compromise and neonatal distress in 100% of the cases. These results allow to advocate the use of 'non-stressed' antepartum fetal heart rate monitoring, as a reliable test in the management of high risk pregnancies.