[Obstetrical monitoring devices and interpretation of the data. 4. Interpretation of the fetal heart rate. 3. Fetal heart rate (FHR) baseline variability].
Explore the source record for details and available documents.
SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
BACKGROUND: Experimental data suggest that aldosterone has harmful effects promoting myocardial fibrosis and disturbing autonomic balance. There has been no evidence of these potential effects in intact man. METHODS AND RESULTS: We report the findings in 31 patients with stable chronic heart failure (CHF) who were treated with spironolactone (50-100 mg/day) or placebo in addition to diuretics and angiotensin converting enzyme (ACE) inhibition. In a controlled randomised double-blind study, we found that spironolactone treatment reduced circulating levels of procollagen type III N-terminal amino peptide, a marker of vascular collagen turnover, and in addition increased time-domain parameters of heart rate variability (n = 24). These latter parameters suggest a parasympathomimetic effect for additional spironolactone. Spironolactone significantly reduced heart rate (prolonged RR interval) particularly during the dawn hours (06.00-09.00 h). In this unbalanced study it was not possible to provide a detailed diurnal assessment of the impact of spironolactone on heart rate variability, but the preliminary data suggest that there may be an interaction with the autonomic nervous system which varies in time. CONCLUSIONS: These are the first human data to show that use of the aldosterone antagonist, spironolactone, can positively improve time-domain heart rate variability and reduce myocardial collagen turnover, as reflected by further reductions in serum procollagen peptide, despite concurrent ACE inhibitor treatment. Residual aldosterone after ACE inhibitor treatment may therefore have a role promoting arrhythmia and cardiac death by two mechanisms. Effects of additional spironolactone on slowing heart rate (and potentially the detrimental effect of aldosterone) were most prominent between 6 a.m. and 10 a.m. when cardiac death is also known to be most prominent.
Patients with congestive heart failure (CHF) are characterized by an imbalance of the autonomic nervous system, which may contribute to the progression of circulatory failure and influence survival. However, it is still unclear whether CHF is characterized by a suppression of the diurnal variation in autonomic tone that is observed in normal subjects. To characterize the circadian variation in autonomic tone in patients with ventricular failure, ambulatory 24-hour Holter monitor recordings were obtained in 20 patients with CHF; 4-minute epochs of data from every hour of each 24-hour recording were selected. For each epoch we calculated the mean heart rate (HR) and, by applying spectral analysis of heart rate variability (HRV), we quantified the magnitude of the total (0.02 to 0.9 Hz), sympathetically governed low frequency variability (0.02 to 0.1 Hz), and parasympathetically mediated high-frequency variability (0.1 to 0.9 Hz). These areas were also expressed as a ratio to total variability and a ratio of high to low variability. A highly significant change in the mean HR over 24 hours was observed (p = 0.0001); no changes in the measures of HRV were obtained (p < 0.3). No significant correlation was found between mean HR and any frequency domain measures. We conclude that the sustained imbalance of autonomic tone over a 24-hour period, as shown by the spectral analysis of HRV, may promote the progression of circulatory failure and predispose patients with CHF to malignant ventricular arrhythmias and sudden cardiac death.(ABSTRACT TRUNCATED AT 250 WORDS)
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Increased sympathetic drive in symptomatic menopausal women was reduced after estrogen replacement therapy for 4 months, which has a potentially beneficial effect on cardiovascular functions.
OBJECTIVES: In the present study, we aimed to evaluate the effect of adrenergic receptor polymorphisms on the response of myocardium to measured levels of cardiac adrenergic drive, and to evaluate whether polymorphisms of presynaptic adrenoceptors modified the rate of cardiac and systemic release of norepinephrine. BACKGROUND: Heightened sympathetic activity plays an important pathophysiologic role in congestive heart failure (CHF). Recently several functionally relevant polymorphisms of the alpha(2)-, beta(1)-, and beta(2)-adrenoceptors have been identified, and specific genotypes have been associated with the incidence or clinical severity of CHF. These adrenoceptors are known to be located both pre-synaptically (alpha(2) and beta(2)) and post-synaptically (beta(1) and beta(2)), raising the possibility that their association with clinical measures in CHF could be mediated either by modulation of the cardiac response to a given level of adrenergic drive or by altering norepinephrine release from sympathetic nerve terminals. METHODS: We determined the beta(1)-, beta(2)-, and alpha(2C)-adrenoceptor genotype in 60 patients with severe CHF in conjunction with measurement of cardiac and systemic sympathetic activity using the radiotracer norepinephrine spillover method. RESULTS: We showed a strong relationship (r = 0.67, p < 0.001) between heart rate and the level of cardiac adrenergic drive, and heart rate for a given level of cardiac adrenergic drive was substantially greater in patients with the Arg/Arg16 beta(2)-adrenoceptor polymorphism (p = 0.02), whereas no such relationship existed for polymorphisms of the beta(1)-adrenoceptor. The genotype of the alpha(2C)- and beta(2)-adrenoceptors showed no relationship to the rate of norepinephrine release from cardiac sympathetic nerves. CONCLUSIONS: For the first time, we show that beta(2)-adrenoceptor polymorphisms significantly influence the relationship between heart rate and cardiac adrenergic drive in CHF, but do not affect the rate of norepinephrine release from sympathetic nerve terminals.
The mechanism of the attenuated arterial baroreceptor control of heart rate in heart failure was studied in 18 unanesthetized dogs after the development of chronic right-heart failure and compared to 12 control animals. The change in heart rate and arterial pressure in response to increases in right carotid sinus pressure during isolated carotid sinus perfusion was markedly reduced in heart failure (P less than 0.05). After vagotomy the difference in heart rate responses persisted, but was less pronounced (P = 0.065). The chronotropic response to perfusion of the sinus node artery with acetylcholine in heart-failure dogs showed a selectively depressed response, when compared to norepinephrine and hypertonic saline. The ratio of the change in heart rate in heart-failure vs. control dogs was 57% for acetylcholine but was not diminished for hypertonic saline (114%). The effect of direct vagal nerve stimulation on changes in heart rate was also markedly reduced in heart-failure dogs. These studies demonstrate that the alterations in baroreceptor control of heart rate in heart failure involve both the parasympathetic and sympathetic baroreflex efferent limbs. There is, in addition, a depressed responsiveness of the sinus node to cholinergic stimuli.
Metabolic rate, heart rate and respiratory rate of three adult moose were monitored simultaneously on selected days between January 1982 and October 1983. Heart rate was successfully monitored using two types of implanted radio transmitters. Metabolic rate was significantly (P less than 0.001) correlated with heart rate for individual animals (r = 0.94-0.98). The relationship was best described by an exponential equation. A mean weighted equation predicted metabolic rate within 9% of individual equations. In adult moose cows, heart rate was a more reliable predictor of energy expenditure than respiratory rate.
We examined the effects of beta-blockers on the associations between heart rate and number of premature ventricular beats (PVBs) and on heart rate variability and myocardial ischemia in patients with coronary heart disease. After 2 weeks of run-in placebo treatment, 18 patients with coronary artery disease were randomized to a 7-day treatment with either propranolol (40 mg) three times a day or placebo. During run-in and after 7 days of treatment, patients underwent 24-hour Holter monitoring and exercise tests. We analyzed the 24-hour Holter recordings with customized software that computes the correlation between heart rate and occurrence of PVBs. We also computed spectral measures of heart rate variability on the same recordings. Propranolol caused a significant decrease in the log-transformed total number of PVBs recorded over 24 hours and during the day. The number of PVBs was much lower during the night than during the day both after placebo and after propranolol. There were no differences between the two treatments. During the day, there was a positive correlation between heart rate and the number of PVBs in all 18 patients. The mean correlation coefficients between heart rate and number of PVBs increased significantly after propranolol treatment both during the 24-hour monitoring (p < 0.05) and during the day (p < 0.05). The night-recorded correlation coefficients between heart rate and number of PVBs were not significantly different in the placebo versus propranolol group. Propranolol significantly increased the total power during the day. Placebo caused a significant decrease in the low-frequency band (LF) and a significant increase in the high-frequency band (HF) during the night compared with the day. During the day, propranolol significantly reduced LF power and increased HF power, with respect to placebo. After propranolol treatment, the values of LF and HF power during the day were comparable to those recorded at night. The LF/HF ratio decreased significantly after propranolol treatment with respect to placebo in the day and became similar to that recorded during sleep. Propranolol significantly reduced heart rate and systolic blood pressure at rest and at peak exercise and reduced signs of myocardial ischemia. Propranolol administration reduces PVBs in patients with coronary artery disease and severe ventricular arrhythmias possibly through an improvement of cardiac autonomic regulation and through anti-ischemic effects, antiarrhythmic effects, or both.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Two experiments focused on two information variables relevant to changes in heart rate, field dependence and the ability to perceive one's own heart rate. In Exp. I, 14 field-independent and 17 field-dependent subjects completed a heart-rate perception and a voluntary heart-rate control task. The anticipated superiority in heart-rate control by field-independent subjects was detected although no evidence was found for a relationship between the amount of biofeedback available in the situation and voluntary control of the cardiovascular system. Exp. II involved 9 field-independent and 8 field-dependent subjects in a classical conditioning paradigm involving shock sensitivity. In contrast with Exp. I, in this phase of the study heart-rate increases were correlated with the ability of the subject to discriminate heart beats, especially for the field-independent group. It was concluded that field dependence and heart-rate perception are related to classically conditioned heart-rate increase for some subjects and further that field dependence may be a potent variable operating in those situations involving the voluntary control of heart rate without exteroceptive feedback.
Forty college students were selected from a large number of introductory psychology students on the basis of high heart rate during an initial screening session. Subjects were then contacted and participated in two additional sessions during which heart rate, respiration rate, and skin conductance measures were obtained. Each session consisted of a baseline period followed by five trial periods during which subjects attempted to control their heart rate or performed a visual tracking task. Subjects were randomly assigned to one of four groups. One group served as a control and monitored a visual feedback display driven by their own heart rate but received no instructions to decrease their heart rate. In contrast, the three heart rate control groups were instructed to decrease heart rate during the trial periods by utilizing a relaxation procedure, proportional biofeedback, or proportional biofeedback plus criterion information. No group differences were present during the baseline periods. During feedback trials, however, all the training groups differed from the control in heart rate but did not differ from each other. It is suggested that feedback displays may not facilitate heart rate reduction beyond the level achieved by instructing subjects to use a general relaxation procedure.
The purpose of the present study was to determine whether readily measured blood pressure (BP) indices and, responses to autonomic reflex tests could be used as surrogates of short-term heart rate variability (HRV), which is an established marker of autonomic regulation of SA node. Therefore, we examined the correlation between short-term HRV and heart rate (HR), BP indices viz. systolic pressure, diastolic pressure, pulse pressure (PP), and rate-pressure product (RPP), during supine rest and head-up tilt in 17 young healthy normotensive subjects, aged 19.8 +/- 1 yr (mean +/- SD). Three classic autonomic indices viz. Valsalva ratio, HR response to deep breathing and pressor response to isometric handgrip were also determined. We noted two interesting and statistically significant (P < 0.05 in both cases) correlations viz. i) a positive correlation (r = 0.6) between change in RPP during tilt and change in low frequency (LF) RR spectral power expressed in normalized units (LF nu) during tilt, and ii) a negative correlation (r = -0.6) between change in PP during isometric handgrip and LF nu during tilt. The possible physiologic significance of these and other correlations is discussed in this paper. In conclusion, the presence of a statistically significant correlation between RPP, PP and spectral measures of short-term HRV supports a simplistic approach to autonomic assessment, in that, easily measurable BP indices could be used as surrogates of HRV when it is not feasible to determine HRV indices directly. However, the same have to be tested in healthy subjects belonging to various age groups and in patients with conditions known to be associated with autonomic dysregulation.