Fractal Component of Variability of Heart Rate and Systolic Blood Pressure in Congestive Heart Failure

1997 ◽  
Vol 92 (6) ◽  
pp. 543-550 ◽  
Author(s):  
Gary C. Butler ◽  
Shin-Ichi Ando ◽  
John S. Floras

1. There is a substantial non-harmonic or fractal component to the variability of both heart rate and blood pressure in normal subjects. Heart rate is the more complex of these two signals, with respect to the slope, β, of the 1/fβ relationship. In congestive heart failure, heart rate spectral power is attenuated, but the fractal and harmonic components of heart rate and systolic blood pressure variability have not been characterized. 2. Two groups, each comprising 20 men, were studied during 15 min of supine rest and spontaneous respiration: one with functional class II—IV heart failure (age 52 ± 2 years; mean ± SEM) and a second group of healthy men (age 46 ± 2 years). 3. Total spectral power for heart rate was significantly reduced in heart failure (P < 0.02), whereas total spectral power for systolic blood pressure was similar in the two groups. In both heart failure and normal subjects, 65–80% of total spectral power in these two signals displayed fractal characteristics. 4. In heart failure, the slope of the 1/fβ relationship for heart rate was significantly steeper than in normal subjects (1.40 ± 0.08 compared with 1.14 ± 0.05; P < 0.05), indicating reduced complexity of the fractal component of heart rate variability. There was no significant difference in the 1/fβ slope for systolic blood pressure variability between these two groups, but the blood pressure signals were less complex than heart rate variations in both heart failure (2.31 ± 0.15; P < 0.006) and normal subjects (2.47 ± 0.15; P < 0.0001). 5. Parasympathetic nervous system activity, as estimated from heart rate variability was reduced (P < 0.01) in patients with heart failure, whereas trends towards increased sympathetic nervous system activity and decreased non-harmonic power were not significant. 6. The non-harmonic components of cardiac frequency are reduced in heart failure. Non-harmonic power is not attenuated, but the complexity of the heart rate signal is less than in subjects with normal ventricular function. A reduction in parasympathetic modulation appears to contribute to this loss of complexity of heart rate. Consequently, the heart rate signal comes to resemble that of blood pressure. In contrast, the variability and complexity of the systolic blood pressure signal is similar in heart failure and normal subjects. This reduced complexity of heart rate variability may have adverse implications for patients with heart failure.

1994 ◽  
Vol 87 (2) ◽  
pp. 225-230 ◽  
Author(s):  
Pekka Koskinen ◽  
Juha Virolainen ◽  
Markku Kupari

1. The acute effects of a moderate dose of ethanol (1 g/kg body weight) on heart rate and blood pressure variability and baroreflex sensitivity were studied in 12 healthy male subjects in a juice-controlled experiment. Electrocardiographic and finger blood pressure data were recorded and stored in a minicomputer during 5 min of controlled breathing (15 cycles/min) and during deep breathing (5 s inpiration, 5 s expiration, four cycles) before drinking and hourly thereafter for 3 h. 2. Mean breath alcohol concentration rose to 18.9 mg/100 ml. In the time domain analysis, the root mean square difference of successive R-R interval decreased significantly with ethanol as compared with the juice experiment. The difference remained statistically significant even after adjustment for the shorter R-R interval after alcohol. In the frequency domain analysis the high-frequency (0.15-0.5 Hz) spectral power showed a significant decrease after alcohol intake. Also, the index of sensitivity of the baro-receptor reflex (square root of R-R interval power/systolic blood pressure power) decreased significantly in the high-frequency component. Ethanol did not change finger systolic blood pressure, and power spectral analysis did not show significant variability in blood pressure. 3. These data indicate that acute intake of moderate amounts of alcohol causes a significant decrease in heart rate variability owing to diminished vagal modulation of the heart rate.


2006 ◽  
Vol 75 (1) ◽  
pp. 3-12 ◽  
Author(s):  
J. Mokrý ◽  
T. Remeňová ◽  
K. Javorka

The purpose of the study was to evaluate the changes of respiratory rate, systemic blood pressure and heart rate variability parameters (HRV) during orthostasis in anaesthetized rabbits. Furthermore, these changes were influenced by affecting the renin-angiotensin-aldosterone (RAA) system and autonomic nervous system (ANS) to study the mechanisms participating in activity of spectral frequency bands of HRV in rabbits. Ten adult rabbits (Chinchilla) were anaesthetized by ketamine and flunitrazepam. The systemic blood pressure, tidal volume and respiratory rate were measured. HRV was evaluated by microcomputer system VariaPulse TF3E. The R-R intervals were derived from the electrocardiogram signal from subcutaneous needle electrodes. The evaluation of HRV in very low (VLF; 0.01-0.05 Hz), low (LF; 0.05-0.15 Hz) and high frequency bands (HF; 0.15-2.0 Hz) was made and parameters of frequency and time analysis were calculated. The measurements were made in horizontal (supine) position, in orthostasis (the angle of 60 °) and again in supine position before and after enalapril (0.5 mg/kg b.w.), metipranolol (0.2 mg/kg b.w.), and after subsequent bilateral cervical vagotomy. The orthostasis in anaesthetized rabbits is accompanied by depression of respiratory rate reversed only by vagotomy. Furthermore, decrease of systemic blood pressure, unchanged heart rate and increased characteristics of heart rate variability were found, with predominant increase of spectral power in LF and VLF bands. This elevation can be eliminated only by complete blockade of ANS. Although the participation of ANS or RAA system in modification of individual HRV frequency bands is not as specific as in humans, we confirmed the participation of RAA system in determination of the VLF band.


2021 ◽  
Author(s):  
Rada R Veeneman ◽  
Jentien M Vermeulen ◽  
Abdel Abdellaoui ◽  
Eleanor Sanderson ◽  
Robyn E Wootton ◽  
...  

Importance: Individuals with schizophrenia have a reduced life-expectancy compared to the general population, largely due to an increased risk of cardiovascular disease (CVD). Clinical and epidemiological studies have been unable to fully unravel the nature of this relationship. Objective: Investigate genetic correlations and potential bi-directional effects between liability to schizophrenia and CVD. Design, setting, and participants: We obtained summary-data of genome-wide-association studies of schizophrenia (N=130,644), heart failure (N=977,323), coronary artery disease (N=332,477), systolic and diastolic blood pressure (N=757,601), heart rate variability (N=46,952), QT interval (N=103,331), early repolarization and dilated cardiomyopathy ECG patterns (N=63,700). We computed genetic correlations with linkage disequilibrium score regression and conducted bi-directional Mendelian randomization (MR). With multivariable MR, we investigated whether associations were mediated by smoking, body mass index, physical activity, lipid levels, or type 2 diabetes. To ensure robustness, we applied a range of sensitivity methods. Main outcomes and measures: Schizophrenia, heart failure, coronary artery disease, systolic blood pressure, diastolic blood pressure, heart rate variability, QT interval, early repolarization, dilated cardiomyopathy. Results: Genetic correlations between liability to schizophrenia and CVD were close to zero (-0.02 to 0.04). With MR, we found robust evidence that liability to schizophrenia increases heart failure risk. This effect remained consistent with multivariable MR. There was also evidence that liability to schizophrenia increases early repolarization risk, largely mediated by BMI and lipid levels. Finally, there was evidence that liability to schizophrenia increases heart rate variability, a direction of effect contrasting previous studies. In the other direction, there was weak evidence that higher systolic, but not diastolic, blood pressure increases schizophrenia risk. Conclusions and relevance: Our findings indicate that liability to schizophrenia increases the risk of heart failure, and that this is not mediated by key health behaviours. This is consistent with the notion that schizophrenia is characterised by a systemic dysregulation of the body (including inflammation and oxidative stress) with detrimental effects on the heart. To decrease cardiovascular mortality among schizophrenia patients, priority should lie with optimal treatment and interventions in early stages of psychoses. We also identified early repolarization, currently understudied, as a potential CVD marker among patients with schizophrenia.


1971 ◽  
Vol 33 (1) ◽  
pp. 219-226 ◽  
Author(s):  
Michael Hnatiow

Cardiac rate-variability control and an initial demonstration of systolic blood-pressure variability control using visual feedback of physiological information were examined. Continuous measures of respiration, heart rate, EXG waveform analysis, and systolic blood pressure were obtained for both experimental groups and for yoked controls who saw the same visual display as the experimental Ss. Ss successful at reducing heart-rate variability showed clear changes in the P-R wave relationships of the EKG, indicating possible direct attempts to manipulate heart rate so as to reduce variability. Ss controlling blood-pressure variability who had high heart rates were more successful in reducing variability than those with low rates, possibly because of differential feedback to Ss with high and low heart rates. In addition, apparently as a reaction to E's adjustment of the visual target range, experimental Ss showed decreases in mean blood-pressure levels.


1995 ◽  
Vol 88 (1) ◽  
pp. 95-102 ◽  
Author(s):  
Isabelle Constant ◽  
Arlette Girard ◽  
Jérôme Le Bidois ◽  
Elizabeth Villain ◽  
Dominique Laude ◽  
...  

1. The aim of the study was to examine the short-term variability in blood pressure and heart rate in 19 children who had received heart transplants and in eight normal control children. 2. Blood pressure was determined by a finger arterial pressure device. We examined the power spectra for heart rate and systolic blood pressure in the supine and tilted positions. In addition, we studied the acute changes in blood pressure and heart rate during active standing. 3. In the transplanted children we could distinguish two groups (groups A and B) in whom heart rate variability differed, although in both it was greatly reduced compared with controls (group C). In group A there were no significant fluctuations in the mid-frequency range for heart rate. The gain of the relationship between systolic blood pressure and heart rate was very low and there were virtually no heart rate changes associated with passive tilting. 4. By contrast, in group B transplant patients the heart rate variability, as assessed by standard deviation, was about half that of normal controls. The power spectra attenuation was greater in the high-frequency than in the mid-frequency bands. On passive tilting the latter became enhanced, but not the high-frequency variability. On active standing the tachycardic response was about half that of controls. The findings suggest some reinnervation involving cardiac sympathetic fibres to a greater degree than the fast-responding vagal fibres. 5. In both groups A and B the drop in systolic blood pressure observed early in active standing was about 4–6 times as great as in controls. One possible mechanism could be the loss of cardiac afferents. 6. Time since operation was a critical factor for reinnervation, since all subjects from group B were transplanted more than 44 months prior to the recording. 7. We conclude that in a proportion of children who have received heart transplantation there is a delayed reinnervation of the heart, which probably involves sympathetic effectors rather than the vagus.


2016 ◽  
Vol 16 (1) ◽  
pp. 22-29 ◽  
Author(s):  
T Vasicko ◽  
J Prindesova-Busikova ◽  
O Osina

Abstract Introduction: Heavy working conditions and many unpropitious factors influencing workers health participate in development of various health disorders, among other autonomic cardiovascular regulation malfunction. The aim of this study is to draw a comparison of autonomic nervous system functional age and heart rate variability changes between workers with and without mining occupational exposure. Material and methods: Short term HRV was measured by DiANS PF8 device in men with and without occupational mining exposure (exposure for 10 years at least) using standard orthoclinostathic protocol (each phase 300 sec or 300 heartbeats if heart rate under 60 bpm), excluding those with severe cardiovascular, metabolic, or psychiatric diseases, nicotine and other drugs abuse, as well as those, who underwent heavy stress situation during last year. Results: Evaluating 41 HRV records among miners (n=24, age 47.9 ± 6.1 years, exposure 22.5 ± 5 years) and non-miners (n=17, age 48.5 ± 6.9 years) we found significantly increased difference between functional age of ANS and calendar age in miners group (+7.2 ± 7.3 years) over against the non-miners group (−1.6 ± 6.5 years). No correlation was found between exposure duration and functional age of ANS difference. Analysis of HRV parameters show significant reduction in total spectral power, LF, HF and rMSSD in mine workers above 48 years of age. Discussion and conclusion: Our results show that influence of occupational work factors from mining exposure can clearly take part in worsening the reactivity of ANS, which can be associated with greater risk of developing mostly cardiovascular diseases. It is important to think of non-occupational factors improving or deteriorating ANS reactivity and of individual sensitivity to other external factors.


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