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NN Intervals (nn + interval)

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Medical Sciences	100%

Selected Abstracts

Heart Rate Variability Declines with Increasing Age and CTG Repeat Length in Patients with Myotonic Dystrophy Type 1

ANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 3 2003
Bradley A. Hardin
Background: Cardiac myopathy manifesting as arrhythmias is common in the neurological disease, myotonic dystrophy type 1 (DM1). The purpose of the present study was to evaluate heart rate variability (HRV) in patients with DM1. Methods: In a multicenter study, history, ECG, and genetic testing were performed in DM1 patients. Results: In 289 patients in whom the diagnosis of DM1 was confirmed by a prolonged cytosine-thymine-guanine (CTG) repeat length the most common ambulatory ECG abnormality was frequent ventricular ectopy (16.3%). The 24-hour time domain parameters of SDNN (SD of the NN interval) and SDANN (SD of the mean NN, 5-minute interval) declined as age and CTG repeat length increased (SDNN: ,8.5 ms per decade, 95% confidence intervals [CI],12.9, ,4.2, ,8.7 ms per 500 CTG repeats, CI ,15.7, ,1.8, r = 0.24, P < 0.001; SDANN: ,8.1 ms per decade, CI ,12.4, ,3.8, ,8.8 ms per 500 CTG repeats, CI ,15.7, ,1.9, r = 0.23, P < 0.001). Short-term frequency domain parameters declined with age only (total power: ,658 ms2 per decade, CI: ,984, ,331, r = 0.23, P < 0.001; low frequency (LF) power ,287 ms2 per decade, CI: ,397, ,178, r = 0.30, P < 0.001; high frequency (HF) power: ,267 ms2 per decade, CI: ,386, ,144, r = 0.25, P < 0.001). The LF/HF ratio increased as the patient aged (0.5 per decade, CI: 0.1, 0.9, r = 0.13, P = 0.03). Conclusions: In DM1 patients a decline in HRV is observed as the patient ages and CTG repeat length increases. A.N.E. 2003; 8(3):227-232 [source]

Circadian Profile of Cardiac Autonomic Nervous Modulation in Healthy Subjects:

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 8 2003
Differing Effects of Aging, Gender on Heart Rate Variability
Introduction: Although heart rate variability (HRV) has been established as a tool to study cardiac autonomic activity, almost no data are available on the circadian patterns of HRV in healthy subjects aged 20 to 70 years. Methods and Results: We investigated 166 healthy volunteers (81 women and 85 men; age 42 ± 15 years, range 20,70) without evidence of cardiac disease. Time-domain HRV parameters were determined from 24-hour Holter monitoring and calculated as hourly mean values and mean 24-hour values. All volunteers were fully mobile, awoke around 7 A.M., and had 6 to 8 hours of sleep. Circadian profiles of vagus-associated HRV parameters revealed a marked day-night pattern, with a peak at nighttime and a plateau at daytime. The characteristic nocturnal peak and the day-night amplitude diminished with aging by decade. Estimates of overall HRV (geometric triangular index [TI], SD of NN intervals [SDNN]) and long-term components of HRV (SD of the averages of NN intervals for all 5-min segments [SDANN]) were low at nighttime and increased in the morning hours. There was a significant decline of 24-hour values of all HRV parameters (P < 0.001) and a strong negative correlation (P < 0.001) with increasing age. Mean 24-hour RR interval (P < 0.001), SDNN, mean SD of NN intervals for all 5-minute intervals (SDNNi), and SDANN (all P < 0.01) were significantly higher in men. Younger men also exhibited significantly higher values for vagus-associated parameters (root mean square successive difference [rMSSD], P < 0.05; SDNNi, P < 0.01); however, gender differences diminished with increasing age. Conclusion: Normal aging is associated with a constant decline of cardiac vagal modulation due to a significant decrease of nocturnal parasympathetic activity. The significant gender-related difference of HRV decreases with aging. These findings emphasize the need to determine age-, gender-, and nycthemeral-dependent normal ranges for HRV assessment. (J Cardiovasc Electrophysiol, Vol. 14, pp. 791-799, August 2003) [source]

Robust circadian rhythm in heart rate and its variability: influence of exogenous melatonin and photoperiod

JOURNAL OF SLEEP RESEARCH, Issue 2 2007
GILLES VANDEWALLE
Summary Heart rate (HR) and heart rate variability (HRV) undergo marked fluctuations over the 24-h day. Although controversial, this 24-h rhythm is thought to be driven by the sleep,wake/rest,activity cycle as well as by endogenous circadian rhythmicity. We quantified the endogenous circadian rhythm of HR and HRV and investigated whether this rhythm can be shifted by repeated melatonin administration while exposed to an altered photoperiod. Eight healthy males (age 24.4 ± 4.4 years) participated in a double-blind cross-over design study. In both conditions, volunteers were scheduled to 16 h,8 h rest : wake and dark : light cycles for nine consecutive days preceded and followed by 29-h constant routines (CR) for assessment of endogenous circadian rhythmicity. Melatonin (1.5 mg) or placebo was administered at the beginning of the extended sleep opportunities. For all polysomnographically verified wakefulness periods of the CR, we calculated the high- (HF) and low- (LF) frequency bands of the power spectrum of the R,R interval, the standard deviation of the normal-to-normal (NN) intervals (SDNN) and the square root of the mean-squared difference of successive NN intervals (rMSSD). HR and HRV variables revealed robust endogenous circadian rhythms with fitted maxima, respectively, in the afternoon (16:36 hours) and in the early morning (between 05:00 and 06:59 hours). Melatonin treatment phase-advanced HR, HF, SDNN and rMSSD, and these shifts were significantly greater than after placebo treatment. We conclude that endogenous circadian rhythmicity influences autonomic control of HR and that the timing of these endogenous rhythms can be altered by extended sleep/rest episodes and associated changes in photoperiod as well as by melatonin treatment. [source]

An Approach to Measure Atrial and Ventricular Heart Rate Variability Using Pacemaker-Mediated Intracardiac Electrograms

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 12 2003
ANDREAS SCHUCHERT
Heart rate variability (HRV) measurements are usually performed from ventricular beat-to-beat intervals because of the difficulty to precisely locate the P wave fiducial point in surface ECG recordings. The aim of the study was to describe an approach to determine the atrial and ventricular HRV using pacemaker-mediated intracardiac electrograms. Twelve patients with the dual chamber pacemaker Logos were included. The atrial and ventricular intracardiac electrograms were transmitted with the high resolution telemetry channel of the pacemaker to an external recorder for 20 minutes while the patients were supine. During the measurements the patients were in sinus rhythm with intrinsic AV conduction. After computer assisted triggering of the atrial and ventricular events, the resultant intervals were used to calculate the standard deviation of all NN intervals (SDNN), the square root of the mean squared differences of successive NN intervals (RMSSD), and the percentage of successive interval differences >50 ms (pNN50). The differences between atrial and ventricular HRV-Indexes were assessed for each patient with a cut-off point of 1%. Differences >1% were analyzed in detail. A total of 15,504 heart cycles were analyzed. A manual correction due to false or not triggered atrial or ventricular events was necessary in 0.9%. The overall difference between atrial and ventricular pNN50 was ,0.5%±2.1%and differences >1% were observed in 4 patients. The NN50 events occurred in the atrial as well as in the related ventricular interval in 84%. NN50 events occurred only in the atrium in 6% and only in the ventricle in 10%. The mean differences between atrial and ventricular SDNN and RMSSD were0.4±2.1ms and ,0.1±3.5 mswith intra-individual differences <1%. The present study described a new method and demonstrated its feasibility to determine atrial as well as ventricular HRV from pacemakermediated intracardiac electrograms. The differences for pNN50 indicate that ventricular HRV did not reflect the changes of sinus node activity in all patients. (PACE 2003; 26:2272,2274) [source]

Heart Rate Variability in Arrhythmogenic Right Ventricular Cardiomyopathy Correlation with Clinical and Prognostic Features

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 9 2002
ANTONIO FRANCO FOLINO
FOLINO, A.F., et al.: Heart Rate Variability in Arrhythmogenic Right Ventricular Cardiomyopathy Correlation with Clinical and Prognostic Features. The identification of subjects with arrhythmogenic right ventricular cardiomyopathy (ARVC) at higher risk for sudden death is an unresolved issue. An influence of the autonomic activity on the genesis of ventricular arrhythmias was postulated. Heart rate variability (HRV) analysis provides a useful method to measure autonomic activity, and is a predictor of increased risk of death after myocardial infarction. For these reasons, the aim of the study was to evaluate HRV and its correlations with ventricular arrhythmias, heart function, and prognostic outcome in patients with ARVC. The study included 46 patients with ARVC who were not taking antiarrhythmic medications. The diagnosis was made by ECG, echocardiography, angiography, and endomyocardial biopsy. Exercise stress test and Holter monitoring were obtained in all patients. Time-domain analysis of HRV was expressed as the standard deviation of all normal to normal NN intervals (SDNN) detected during 24-hour Holter monitoring. Thirty healthy subjects represented a control group for HRV analysis. The mean follow-up was 10.8 ± 1.86 years. SDNN was reduced in patients with ARVC in comparison with the control group (151 ± 36 vs 176 ± 34, P = 0.00042). Moreover, there was a significant correlation of this index with the age of the patients (r =,0.59, P < 0.001), with the left (r = 0.44, P = 0.002) and right (r = 0.47, P = 0.001) ventricle ejection fraction, with the right ventricular end diastolic volume (r =,0.62, P < 0.001), and with the ventricular arrhythmias, detected during the same Holter record used for HRV analysis (patients with isolated ventricular ectopic beats < 1,000/24 hours, 184 ± 34; patients with isolated ventricular ectopic beats > 1,000/24 hours and/or couplets, 156 ± 25; patients with repetitive ventricular ectopic beats (,3) and/or ventricular tachycardia, 129 ± 25; P < 0.001). During follow-up two patients showed a transient but significant reduction of SDNN and a concomitant increase of the arrhythmic events. In eight patients an episode of sustained ventricular tachycardia occurred, but the mean SDNN of this subgroup did not differ from the mean value of the remaining patients (152 ± 15 vs 150 ± 39; P = NS). Only one subject died after heart transplantation during follow-up (case censored). Time-domain analysis of HRV seems to be a useful method to assess the autonomic influences in ARVC. A reduction of vagal influences correlates with the extent of the disease. The significant correlation between SDNN and ventricular arrhythmias confirmed the influences of autonomic activity in the modulation of the electrical instability in ARVC patients. However, SDNN was not predictive of spontaneous episodes of sustained ventricular tachycardia. [source]

Influence of Heavy Cigarette Smoking on Heart Rate Variability and Heart Rate Turbulence Parameters

ANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 4 2009
Goksel Cagirci M.D.
Background: Cigarette smoking increases the risk of cardiovascular events related with several mechanisms. The most suggested mechanism is increased activity of sympathetic nervous system. Heart rate variability (HRV) and heart rate turbulence (HRT) has been shown to be independent and powerful predictors of mortality in a specific group of cardiac patients. The goal of this study was to assess the effect of heavy cigarette smoking on cardiac autonomic function using HRV and HRT analyses. Methods: Heavy cigarette smoking was defined as more than 20 cigarettes smoked per day. Heavy cigarette smokers, 69 subjects and nonsmokers 74 subjects (control group) were enrolled in this study. HRV and HRT analyses [turbulence onset (TO) and turbulence slope (TS)] were assessed from 24-hour Holter recordings. Results: The values of TO were significantly higher in heavy cigarette smokers than control group (,1.150 ± 4.007 vs ,2.454 ± 2.796, P = 0.025, respectively), but values of TS were not statistically different between two groups (10.352 ± 7.670 vs 9.613 ± 7.245, P = 0.555, respectively). Also, the number of patients who had abnormal TO was significantly higher in heavy cigarette smokers than control group (23 vs 10, P = 0.006). TO was correlated with the number of cigarettes smoked per day (r = 0.235, P = 0.004). While LF and LF/HF ratio were significantly higher, standard deviation of all NN intervals (SDNN), standard deviation of the 5-minute mean RR intervals (SDANN), root mean square of successive differences (RMSSD), and high-frequency (HF) values were significantly lower in heavy smokers. While, there was significant correlation between TO and SDNN, SDANN, RMSSD, LF, and high frequency (HF), only HF was correlated with TS. Conclusion: Heavy cigarette smoking has negative effect on autonomic function. HRT is an appropriate noninvasive method to evaluate the effect of cigarette on autonomic function. Simultaneous abnormal HRT and HRV values may explain increased cardiovascular event risk in heavy cigarette smokers. [source]

Clinical and demographic determinants of heart rate variability in patients post myocardial infarction: Insights from the cardiac arrhythmia suppression trial (CAST)

CLINICAL CARDIOLOGY, Issue 3 2000
Phyllis K. Stein PH.D.
Abstract Background: Clinical and demographic determinants of heart rate variability (HRV), an almost universal predictor of increased mortality, have not been systematically investigated in patients post myocardial infarction (MI). Hypothesis: The study was undertaken to evaluate the relationship between pretreatment clinical and demographic variables and HRV in the Cardiac Arrhythmia Suppression Trial (CAST). Methods: CAST patients were post MI and had , 6 ventricular premature complexes/h on pretreatment recording. Patients in this substudy (n = 769) had usable pretreatment and suppression tapes and were successfully randomized on the first antiarrhythmic treatment. Tapes were rescanned; only time domain HRV was reported because many tapes lacked the calibrated timing signal needed for accurate frequency domain analysis. Independent predictors of HRV were determined by stepwise selection. Results: Coronary artery bypass graft surgery (CABG) after the qualifying MI was the strongest determinant of HRV. The markedly decreased HRV associated with CABG was not associated with increased mortality. Ejection fraction and diabetes were also independent predictors of HRV. Other predictors for some indices of HRV included beta-blocker use, gender, time from MI to Holter, history of CABG before the qualifying MI, and systolic blood pressure. Decreased HRV did not predict mortality for the entire group. For patients without CABG or diabetes, decreased standard deviation of all NN intervals (SDANN) predicted mortality. Clinical and demographic factors accounted for 31% of the variance in the average of normal-to-normal intervals (AVGNN) and 13,26% of the variance in other HRV indices. Conclusions: Heart rate variability post MI is largely independent of clinical and demographic factors. Antecedent CABG dramatically reduces HRV. Recognition of this is necessary to prevent misclassification of risk in patients post infarct. [source]