Effects of angiotensin II (AT1) receptor blockade on cardiac vagal control in heart failure

2001 ◽  
Vol 101 (6) ◽  
pp. 559-566 ◽  
Author(s):  
J. C. VAILE ◽  
S. CHOWDHARY ◽  
F. OSMAN ◽  
H. F. ROSS ◽  
J. FLETCHER ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Heart Rate ◽  
Heart Rate Variability ◽  
Angiotensin Ii ◽  
Baroreflex Sensitivity ◽  
At1 Receptor ◽  
Receptor Blockade ◽  
Double Blind ◽  
Rr Interval

The objective of the present study was to determine the autonomic effects of angiotensin II (AT1) receptor blocker therapy in heart failure. In a randomized double-blind cross-over study, we compared the effects of candesartan and placebo on baroreflex sensitivity and on heart rate variability at rest, during stress and during 24h monitoring. Acute effects were assessed 4h after oral candesartan (8mg) and chronic effects after 4 weeks of treatment (dose titrated to 16mg daily). The study group comprised 21 patients with heart failure [mean (S.E.M.) ejection fraction 33% (1%)], in the absence of angiotensin-converting enzyme (ACE) inhibitor therapy. We found that acute candesartan was not different from placebo in its effects on blood pressure or mean RR interval. Chronic candesartan significantly reduced blood pressure [placebo, 137 (3)/82 (3)mmHg; candesartan, 121 (4)/75 (2)mmHg; P<0.001; values are mean (S.E.M.)], but had no effect on mean RR interval [placebo, 857 (25)ms; candesartan, 857 (21)ms]. Compared with placebo there were no significant effects of acute or chronic candesartan on heart rate variability in the time domain and no consistent effects in the frequency domain. Baroreflex sensitivity assessed by the phenylephrine bolus method was significantly increased after chronic candesartan [placebo, 3.5 (0.5)ms/mmHg; candesartan, 4.8 (0.7)ms/mmHg; P<0.05], although there were no changes in cross-spectral baroreflex sensitivity. Thus, in contrast with previous results with ACE inhibitors, angiotensin II receptor blockade in heart failure did not increase heart rate variability, and there was no consistent effect on baroreflex sensitivity.

scholarly journals Exploring the relationship between schizophrenia and cardiovascular disease: A genetic correlation and multivariable Mendelian randomization study

2021 ◽  
Author(s):  
Rada R Veeneman ◽  
Jentien M Vermeulen ◽  
Abdel Abdellaoui ◽  
Eleanor Sanderson ◽  
Robyn E Wootton ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Heart Rate ◽  
Heart Rate Variability ◽  
Diastolic Blood Pressure ◽  
Mendelian Randomization ◽  
Genetic Correlations ◽  
Lipid Levels ◽  
Early Repolarization ◽  
Artery Disease

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.

Sequential analysis of heart rate variability, blood pressure variability and baroreflex sensitivity in healthy pregnancy

2020 ◽  
Vol 30 (5) ◽  
pp. 433-439 ◽  
Author(s):  
Priyanka Garg ◽  
Kavita Yadav ◽  
Ashok Kumar Jaryal ◽  
Garima Kachhawa ◽  
Alka Kriplani ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heart Rate Variability ◽  
Blood Pressure Variability ◽  
Sequential Analysis ◽  
Baroreflex Sensitivity ◽  
Healthy Pregnancy

scholarly journals Preprocessing Unevenly Sampled RR Interval Signals to Enhance Estimation of Heart Rate Deceleration and Acceleration Capacities in Discriminating Chronic Heart Failure Patients from Healthy Controls

2020 ◽  
Vol 2020 ◽  
pp. 1-10 ◽  
Author(s):  
Ping Cao ◽  
Bailu Ye ◽  
Linghui Yang ◽  
Fei Lu ◽  
Luping Fang ◽  
...  
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Heart Rate Variability ◽  
Chronic Heart Failure ◽  
Characteristic Curve ◽  
Clinical Analysis ◽  
Healthy Controls ◽  
Heart Failure Patients ◽  
Rr Interval ◽  
Frequency Components

Objective. The deceleration capacity (DC) and acceleration capacity (AC) of heart rate, which are recently proposed variants to the heart rate variability, are calculated from unevenly sampled RR interval signals using phase-rectified signal averaging. Although uneven sampling of these signals compromises heart rate variability analyses, its effect on DC and AC analyses remains to be addressed. Approach. We assess preprocessing (i.e., interpolation and resampling) of RR interval signals on the diagnostic effect of DC and AC from simulation and clinical data. The simulation analysis synthesizes unevenly sampled RR interval signals with known frequency components to evaluate the preprocessing performance for frequency extraction. The clinical analysis compares the conventional DC and AC calculation with the calculation using preprocessed RR interval signals on 24-hour data acquired from normal subjects and chronic heart failure patients. Main Results. The assessment of frequency components in the RR intervals using wavelet analysis becomes more robust with preprocessing. Moreover, preprocessing improves the diagnostic ability based on DC and AC for chronic heart failure patients, with area under the receiver operating characteristic curve increasing from 0.920 to 0.942 for DC and from 0.818 to 0.923 for AC. Significance. Both the simulation and clinical analyses demonstrate that interpolation and resampling of unevenly sampled RR interval signals improve the performance of DC and AC, enabling the discrimination of CHF patients from healthy controls.

Heart Rate Variability, Blood Pressure Variability, and Baroreflex Sensitivity in Overtrained Athletes

2006 ◽  
Vol 16 (5) ◽  
pp. 412-417 ◽  
Author(s):  
Mathias Baumert ◽  
Lars Brechtel ◽  
J??rgen Lock ◽  
Mario Hermsdorf ◽  
Roland Wolff ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heart Rate Variability ◽  
Blood Pressure Variability ◽  
Baroreflex Sensitivity

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
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Heart Rate ◽  
Heart Rate Variability ◽  
Systolic Blood Pressure ◽  
Spectral Power ◽  
Normal Subjects ◽  
Total Spectral Power ◽  
Systolic Blood Pressure Variability ◽  
Harmonic Components

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.

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