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PubMed1992

An improved method for adjusting the QT interval for heart rate (the Framingham Heart Study)

Several formulas have been proposed to adjust the QT interval for heart rate, the most commonly used being the QT correction formula (QTc = QT/square root of RR) proposed in 1920 by Bazett. The QTc formula was derived from observations in only 39 young subjects. Recently, the adequacy of Bazett's formula has been questioned. To evaluate the heart rate QT association, the QT interval was measured on the initial baseline electrocardiogram of 5,018 subjects (2,239 men and 2,779 women) from the Framingham Heart Study with a mean age of 44 years (range 28 to 62). Persons with coronary artery disease were excluded. A linear regression model was developed for correcting QT according to RR cycle length. The large sample allowed for subdivision of the population into sex-specific deciles of RR intervals and for comparison of QT, Bazett's QTc and linear corrected QT (QTLC). The mean RR interval was 0.81 second (range 0.5 to 1.47) heart rate 74 beats/min (range 41 to 120), and mean QT was 0.35 second (range 0.24 to 0.49) in men and 0.36 second (range 0.26 to 0.48) in women. The linear regression model yielded a correction formula (for a reference RR interval of 1 second): QTLC = QT + 0.154 (1-RR) that applies for men and women. This equation corrects QT more reliably than the Bazett's formula, which overcorrects the QT interval at fast heart rates and undercorrects it at low heart rates. Lower and upper limits of normal QT values in relation to RR were generated.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1978

Effect of heart-rate control training on heart-rate discrimination.

4 subjects were exposed to discrimination-testing procedures before and later biofeedback training to increase and decrease their heart rates. Results indicated significant increases and decreases in heart rate, as well as a significant improvement in accuracy of discrimination. The results suggest improvements in discrimination may occur as a function of feedback training.

Biofeedback, Psychology↗
PubMed2004

Heart rate variability in patients suffering from structural heart disease and decreased AV-nodal conduction capacity. Insights into the formation of heart rate variability.

METHODS: Time and frequency domain analysis were conducted during a period of 600 s each. We performed a special protocol consisting of five different "pacing" periods: 1) recording of normal sinus rhythm (SR1); 2) atrial pacing with a rate 15% higher than the intrinsic heart rate; 3) ventricular pacing triggered by atrial activation (VAT, with a short AV-delay of 80 ms); 4) AV-sequential pacing with an atrial rate 15% higher than the intrinsic heart rate and a very short AV delay of 80 ms (DDD); 5) normal sinus rhythm (SR2). Only patients with normal AV-nodal conduction or with AV-block I degrees were included. The influence of a structural heart disease as well as a non-sustained VT on Holter ECG and a depressed EF on HRV parameters were analyzed using a multivariate analysis. All patients were lying in a supine position. Blood pressure was measured continuously and the frequency of breathing was controlled. RESULTS: No differences in HRV between the two sinus rhythm periods SR1 versus SR2 could be detected. Neither SR1 vs VAT showed a significant difference for SDNN and r-MSSD. In contrast, HRV during SR1 compared to AAI, and HRV during VAT compared to AAI were significantly different (p < 0.001). When comparing HRV during DDD, which should be zero, and AAI, we found a significantly lower SDNN and r-MSSD (1.2 ms vs 4 ms, p < 0.04). The presence of structural heart disease, a non-sustained ventricular tachycardia, a depressed ejection fraction of less than 0.50 did not reveal a significant influence on the HRV parameters (multivariate analysis). The mean Wenckebach in patients with structural heart disease tended to be greater (437 ms vs 350 ms, p = 0.05); an increase in the Wenckebach was not correlated to a change in HRV parameters (p = ns). CONCLUSION: Heart rate variability derived from consecutive RR-intervals is predominantly caused by periodicity in sinus-node impulse formation. A conduction variability of the AV-node exists, but is very low. The presence of a structural heart disease, a non-sustained ventricular tachycardia on Holter ECG, as well as a depressed ejection fraction of less than 0.50 showed no significant influence on the HRV parameters. Therefore, one can apply the calculation of heart rate variability for risk stratification in patients suffering from structural heart disease and moderate AV-nodal conduction disturbances. Attenuation of the oscillation of the heart rate, i. e. heart rate variability (HRV), is associated with an increased risk for mortality in patients with structural heart disease. Many of these patients also suffer from conduction disturbances, e. g. AV-nodal conduction delays. Whether the calculation of HRV in those patients is recommendable has not been investigated yet. Therefore, we conducted a study consisting of 20 consecutive patients in order to determine the formation of HRV, the influence of structural heart disease, the presence of a nonsustained ventricular tachycardia (VT), and a reduced ejection fraction (EF) on the HRV parameters during an elective electrophysiologic study.

Adult↗
PubMed1989

[Circadian behavior of blood pressure and heart rate following orthotopic heart transplantation. Studies before and during antihypertensive therapy].

The de novo hypertension, which develops in most cardiac transplant recipients within the first postoperative months, is multicausal, though toxic side-effects of cyclosporin A seem to play a key role. In order to analyze the circadian behavior of arterial blood pressure and heart rate after cardiac transplantation (HTX) and to evaluate the effect of an antihypertensive regimen on these parameters, 24-h noninvasive ambulatory blood pressure and heart rate monitoring was performed in 10 hypertensive cardiac transplant recipients on cyclosporin A (mean age 42.3 +/- 11.2 years, 14.3 +/- 8.3 months after HTX) before antihypertensive therapy and after introduction of an antihypertensive regimen with the ACE-inhibitor enalapril plus furosemide alone or combined with verapamil. The study demonstrated a complete loss of the usual nocturnal decline in blood pressure in cardiac transplant recipients (mean systolic and diastolic blood pressure 149 +/- 8 and 102 +/- 7 mm Hg during daytime and 152 +/- 8 and 104 +/- 9 mmHg at night). Antihypertensive therapy lowered the blood pressure level effectively, but did not influence the circadian pattern (mean systolic and diastolic blood pressure 121 +/- 8 and 81 +/- 4 mmHg during daytime and 121 +/- 9 and 83 +/- 3 mmHg at night, all p less than or equal to 0.001). Heart rate, in contrast, showed a significant, though in comparison to normal, a blunted decrease at night (mean heart rate 94 +/- 6 beats per min during daytime and 84 +/- 8 beats per min at night, p less than or equal to 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2003

On- and off-responses of heart rate to exercise - relations to heart rate variability.

During physical exercise, heart rate (HR) increases by parasympathetic withdrawal and increase of sympathetic activity to the heart. HR variability (HRV) in time and frequency domains provides information about autonomic control of the cardiovascular system. Non-linear analysis using the Poincaré plot method is able to reveal supplementary information about cardiac autonomic control. The aim of this study was to determine the association between HRV parameters, the initial increase of HR at the onset of exercise (on-response) and HR decrease in the recovery phase after acute exercise (off-response). HR was continuously monitored in 17 healthy male subjects (mean age: 20.3 +/- 0.2 (SEM) years) at rest (25 min supine; 5 min standing), during exercise (8 min of step test at 70% of maximal power output) and in the recovery phase (30 min supine). HRV analysis in time and frequency domains and evaluation of the Poincaré plot measures (length, widths) were performed on selected segments of HR time series. HR on- and off-responses were quantified using an exponential curve fitting technique. The time constants T(on) and T(off), representing the rate of on- and off-responses to exercise, were computed. Postexercise HRV indices and time constant of on-response - T(on) - to exercise were negatively correlated. From preexercise HRV indices, only Poincaré plot parameters were correlated with T(on). No correlation between HRV indices and parameters of off-response was found. In conclusion, preexercise HRV parameters are not closely correlated with the rate of cardioacceleration at the onset of exercise and cannot predict the rate of HR recovery. On the other hand, postexercise HRV parameters are related to the rate of initial adjustment of HR to exercise referring to the importance of rapid HR on-response for a faster recovery after exercise.

Adult↗
PubMed1999

Origins of heart rate variability: relationship of heart rate burst morphology to work duration and load.

We are developing a lexicon of specific heart period changes, or lexons, that recur frequently and whose physiological meaning can be read into ambulatory electrocardiogram (ECG). The transient, reversible "burst" of tachycardia induced by exercise initiation can also be seen on ambulatory ECG. We hypothesized that burst morphology depended on the work that preceded it and on baroreceptor activation. Ten subjects with mean age 38 yr (range 17-69 yr) underwent two protocols of semisupine cycling in which load and duration were varied. Burst duration increased with longer cycling times (median values of 18.0, 25.5, and 23.7 s with 1, 3, and 5 s of cycling, respectively; P = 0.033). Burst shape as assessed by heart period exponential decay constant and burst magnitude did not change. To assess the impact of workload, subjects cycled for 5 s at loads of 0, 25, 50, and 75 W. No significant differences were seen in burst duration, burst magnitude, or burst shape. Tachycardia preceded hypotension by 4.6 +/- 2.2 s, which is inconsistent with baroreceptor involvement in the onset of burst tachycardia. Because burst morphology is a nearly quantal response to the initiation of exercise, the presence of a burst on an ambulatory ECG implies the onset of exercise.

Adolescent↗
PubMed2005

Outcome of first-trimester pregnancies with slow embryonic heart rate at 6-7 weeks gestation and normal heart rate by 8 weeks at US.

PURPOSE: To determine retrospectively the outcome of pregnancies in which the embryo has a slow heart rate at 6.0-7.0 weeks gestation and a normal heart rate at follow-up ultrasonography (US) by 8.0 weeks gestation. MATERIALS AND METHODS: Institutional review board approval was granted; informed consent was not required. The study was Health Insurance Portability and Accountability Act compliant. Singleton pregnancies with an embryonic heart rate measured on a 6.0-7.0-week US scan were identified. The heart rate was classified as slow if it was fewer than 90 beats per minute prior to 6.3 weeks or fewer than 110 beats/min at 6.3-7.0 weeks, normal if it was 100 or more beats/min at less than 6.3 weeks or 120 or more beats/min at 6.3-7.0 weeks, or borderline if it was 90-99 beats/min prior to 6.3 weeks or 110-119 beats/min at 6.3-7.0 weeks. Pregnancies were excluded from the analysis if they were lost to follow-up before the end of first trimester. The Fisher exact test was used for all statistical comparisons. RESULTS: The rates of first-trimester demise were 60.6% for pregnancies with slow heart rates at 6.0-7.0 weeks (188 of 310), 17.4% for those with borderline heart rates (103 of 593), and 9.1% for those with normal heart rates (186 of 2034). There were 59 pregnancies with a slow heart rate at 6.0-7.0 weeks and a normal heart rate at follow-up US by 8.0 weeks; 15 (25.4%) resulted in first-trimester demise. This rate of demise was significantly higher than that of 7.2% (28 of 390) in pregnancies with a normal heart rate at 6.0-7.0 weeks and a normal heart rate by 8.0 weeks (P <.001, Fisher exact test). Pregnancies with a borderline heart rate early in pregnancy followed by a normal heart rate had a demise rate of 7.6% (nine of 118), which is similar to those with normal heart rates early in pregnancy followed by normal heart rates at follow-up (P = .84). CONCLUSION: When a slow embryonic heart rate is detected at 6.0-7.0 weeks, the likelihood of subsequent first-trimester demise remains elevated (approximately 25%) even if the heart rate is normal at follow-up. In such pregnancies, at least one follow-up scan in late first trimester is warranted.

Female↗
PubMed1979

Antepartum fetal heart rate testing. II. Intrapartum fetal heart rate observation and newborn outcome following a positive contraction stress test.

The positive contraction stress test (CST) has been looked upon as a predictor of fetal compromise. On this basis, some reports advise routine cesarean delivery on the assumption that the compromised fetus should not tolerate labor. Other authors advocate selective cesarean delivery, based on obstetrical factors such as the inducibility of the cervix and the practicality of fetal monitoring. Finally, an attempted trial of labor may be allowed on the basis of occurrence of fetal heart rate acceleration with fetal movement, or "reactivity." The occurrence of "false positive" tests is not infrequent (20 to 45 per cent). The definition of such is unclear and little quantitative information regarding intrapartum performance is available. In this series of 27 patients, a trial of labor was undertaken in 20. Vaginal delivery occurred in 11 (55 per cent) and cesarean section in nine (45 per cent). Fetal heart rate abnormalities thought to indicate "distress" occurred in five patients (25 per cent). The "positive" window or repetitive late deceleration as equivalent to the positive CST was seen in only three patients during labor. A trial of labor should be attempted in the face of a positive CST whenever obstetric factors are favorable and careful intrapartum monitoring can be performed.

Apgar Score↗
PubMed2002

Heart rate variability in infants with heart failure due to congenital heart disease: reversal of depressed heart rate variability by propranolol.

BACKGROUND: Analysis of heart rate variability (HRV) provides a noninvasive index of autonomic nervous system activity. HRV has shown to be reduced in congestive heart failure and in children with congenital heart disease (CHD). Beta-blockers improve HRV in adults with congestive heart failure, but this improvement remains to be demonstrated in children. MATERIAL/METHODS: HRV was analysed in 14 infants with severe heart failure due to CHD who received a 'standard' therapy with digoxin and diuretics ('Digoxin/Diuretics' group) and in 9 of these patients with an additional propranolol therapy ('Propranolol' group) 17 days later on average and compared with HRV of 70 healthy infants ('Healthy Control'). RESULTS: Comparing the 'Digoxin/Diuretics' group versus 'Healthy Control', we found significantly reduced HRV in the time domain and the frequency domain, that could be abolished in the 'Propranolol' group. None of the HRV parameter were significantly related to age or any hemodynamic parameter but inversely related to ejection fractions within the normal range (pNN50: r= -0.58, p=0.004; rMSSD: r= -0.42; p=0.049). HRV measurements (SDNN, r= -0.48) and plasma norepinephrine levels (r=0.7) were significantly related to clinical symptoms of heart failure, measured by the Ross Score. CONCLUSIONS: HRV represents a noninvasive parameter that is reduced in infants with congenital heart disease depending on the severity of heart failure but not on hemodynamic disturbances. Propranolol but not digoxin therapy effectively reduced the supposed autonomic imbalance in infants with severe heart failure due to CHD.

Adult↗
PubMed1993

Effects of brief rest periods upon heart rate in multiple baseline studies of heart rate reactivity.

Although there has been some discussion regarding the appropriate length of time necessary for subjects to reach true resting heart rate prior to experimentation, the relevance of conclusions from that discussion for multiple baseline studies of heart rate has not been demonstrated. To investigate this issue, data were collected from 39 males and 33 females following a standard 15-minute adaptation period and then during a series of two-minute experimental phases including stressor tasks and rest periods. Results indicated that, while the group's heart rate during brief rest periods returned to postadaptation levels, there was a substantial subgroup of subjects for whom this was not the case. Implications for the use of multiple baseline procedures in research where heart rate is the dependent variable are discussed.

Adolescent↗
PubMed1991

Autonomic control of heart rate during exercise studied by heart rate variability spectral analysis.

Spectral analysis of heart rate variability (HRV) might provide an index of relative sympathetic (SNS) and parasympathetic nervous system (PNS) activity during exercise. Eight subjects completed six 17-min submaximal exercise tests and one resting measurement in the upright sitting position. During submaximal tests, work rate (WR) was increased for the initial 3 min in a ramp fashion until it reached constant WRs of 20 W, or 30, 60, 90, 100, and 110% of the predetermined ventilatory threshold (Tvent). Ventilatory profile and alveolar gas exchange were monitored breath by breath, and beat-to-beat HRV was measured as R-R intervals of an electrocardiogram. Spectral analysis was applied to the HRV from 7 to 17 min. Low-frequency (0-0.15 Hz) and high-frequency (0.15-1.0 Hz) areas under power spectra (LO and HI, respectively) were calculated. The indicator of PNS activity (HI) decreased dramatically (P less than 0.05) when the subjects exercised compared with rest and continued to decrease until the intensity reached 60% Tvent. The indicator of SNS activity (LO/HI) remained unchanged up to 100% Tvent, whereas it increased abruptly (P less than 0.05) at 110% Tvent. The results suggested that (cardiac) PNS activity decreased progressively from rest to a WR equivalent to 60% Tvent, and SNS activity increased only when exercise intensity exceeded Tvent.

Adult↗