(Circulation. 1996;94:2850-2855.)
© 1996 American Heart Association, Inc.
Articles |
Impact of Reduced Heart Rate Variability on Risk for Cardiac Events
The Framingham Heart Study
Kansai Medical University (H.T.), Osaka, Japan; Lahey Clinic Medical Center (F.J.V.), Burlington, Mass; Framingham Heart Study (H.T., M.G.L., E.S.M., J.C.E., D.L.), Framingham, Mass; National Heart, Lung, and Blood Institute (D.L.), Bethesda, Md; Brigham and Women's Hospital (C.L.F.), Boston, Mass; the Divisions of Cardiology and Clinical Epidemiology of Beth Israel Hospital (D.L.), Boston, Mass; and the Divisions of Epidemiology and Preventive Medicine of Boston University School of Medicine (D.L.), Boston, Mass.
Correspondence to Daniel Levy, MD, Framingham Heart Study, 5 Thurber St, Framingham, MA 01701.
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Abstract |
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Background Although heart rate variability (HRV) is altered in a variety of pathological conditions, the association of reduced HRV with risk for new cardiac events has not been studied in a large community-based population.
Methods and Results The first 2 hours of ambulatory ECG recordings obtained on subjects of the Framingham Heart Study who were free of clinically apparent coronary heart disease or congestive heart failure were reprocessed to assess HRV. Five frequency-domain measures and three time-domain measures were obtained. The associations between HRV measures and the incidence of new cardiac events (angina pectoris, myocardial infarction, coronary heart disease death, or congestive heart failure) were assessed with proportional hazards regression analyses. There were 2501 eligible subjects with a mean age of 53 years. During a mean follow-up of 3.5 years, cardiac events occurred in 58 subjects. After adjustment for age, sex, cigarette smoking, diabetes, left ventricular hypertrophy, and other relevant risk factors, all HRV measures except the ratio of low-frequency to high-frequency power were significantly associated with risk for a cardiac event (P=.0016 to .0496). A one–standard deviation decrement in the standard deviation of total normal RR intervals (natural log transformed) was associated with a hazard ratio of 1.47 for new cardiac events (95% confidence interval of 1.16 to 1.86).
Conclusions The estimation of HRV by ambulatory monitoring offers prognostic information beyond that provided by the evaluation of traditional cardiovascular disease risk factors.
Key Words: heart rate • electrocardiography • prognosis • epidemiology
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Introduction |
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Heart rate variability, or heart period variability, is a measure of the cyclic variations of beat-to-beat (RR) intervals that reflects cardiac autonomic function.1 Heart rate variability is influenced by various physiological and pathological conditions.2 3 4 5 6 7 8 9 10 11 12 13 For several decades, obstetricians have recognized diminished beat-to-beat variation in fetal heart rate as an indicator of distress.14 In cardiology, prior studies have documented adverse prognostic implications of reduced heart rate variability in patients after myocardial infarction15 16 17 and with other pathological conditions.18 19 20 21 Recently, we reported22 an association between reduced heart rate variability and risk for all-cause mortality in elderly original participants in the Framingham Heart Study. The relation of altered heart rate variability to risk for cardiac events has not been studied in the general population.
The present investigation was undertaken to examine the association of reduced heart rate variability with risk for cardiac events in a large population-based sample. Subjects in this study included elderly participants in the original Framingham Heart Study and younger participants in the Framingham Offspring Study. The study setting provides an opportunity to explore the prognostic implications of heart rate variability measures in a sample in which referral bias is inherently minimal.
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Methods |
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Setting
The Framingham Heart Study began in 1948, enrolling 5209 residents of Framingham, Mass, who were between the ages of 28 and 62 years in a prospective epidemiological study. In 1971, 5124 subjects (offspring of the original cohort and spouses of these offspring) were entered into a second prospective study. Selection criteria and study design have been reported previously.23 24 25 From 1983 to 1987, ambulatory ECG recordings were obtained routinely on original Framingham Heart Study subjects undergoing their 18th biennial examination and Framingham Offspring Study subjects attending their 3rd examination.
Processing of Ambulatory Recordings
All ambulatory recordings included two channels of ECG information and were obtained on standard four-track cassette tapes with the use of either a Cardiodata PR2 or PR3 pace recorder (Cardiodata Corp). The tape speed was 1 mm/s, and one channel was used to record a 32-Hz crystal-controlled timing track. For heart rate variability analysis, tapes were played back at 120 times real time on a Cardiodata/Mortara Mk5 Holter analysis system (Mortara Instrument Co) that sampled each ECG channel at 180 samples/s. The playback incorporated a phase-locked loop that used the recorded timing track to compensate for errors in recorder speed control. Because clinic examinations typically lasted 2 to 3 hours, only the first 2 hours of data were analyzed for heart rate variability by use of recently described methods.22 Briefly, the fast Fourier transform was calculated on 100-s blocks of RR interval data. The power density spectrum was estimated by taking the sum of the squares of the magnitude of the fast Fourier transform performed on all usable 100-s blocks.26 The resulting 100-s power spectra were corrected for attenuation. We computed power spectral densities on all usable 100-s blocks and calculated five frequency-domain measures: (1) very-low-frequency power (0.01 to 0.04 Hz), (2) low-frequency power (0.04 to 0.15 Hz), (3) high-frequency power (0.15 to 0.40 Hz), (4) total power (0.01 to 0.40 Hz), and (5) the ratio of low-frequency to high-frequency power.3 In addition, we computed three time-domain measures: (1) the SD of normal RR intervals (2-hour SDNN), (2) the percentage of differences between adjacent normal RR intervals exceeding 50 ms (pNN50), and (3) the square root of the mean of the squared differences between adjacent normal RR intervals (r-MSSD).
Normal QRS complexes and arrhythmias were diagnosed under constant visual monitoring. Supraventricular premature beats were differentiated from sinus arrhythmia on the basis of P-wave morphology and cyclic changes in RR intervals.
Clinical Covariates
Risk factors possibly predisposing to coronary heart disease were recorded at each examination.23 Additional variables that might be associated with autonomic function also were considered, including coffee and alcohol consumption.
Systolic and diastolic blood pressures were measured twice on seated subjects by the examining physician using a mercury column sphygmomanometer positioned near eye level. The averages of repeated measures were used for analysis. Diabetes was defined, with the use of current and historical data, as a nonfasting blood glucose level 
200 mg/dL (11.10 mmol/L) or the use of insulin or an oral hypoglycemic agent. The diagnosis of left ventricular hypertrophy on the 12-lead ECG was made on the basis of fulfillment of at least one of the following voltage criteria with associated ST-T repolarization abnormalities: R wave >1.1 mV in aVL, R wave 2.5 mV in left precordial leads, S wave 2.5 mV in right precordium, sum of precordial SV1 or SV2 plus RV5 or RV6 3.5 mV, or sum of limb lead RI plus SIII 2.5 mV. Current cigarette smoking status and use of cardioactive medications were recorded. For Offspring Study subjects, total and HDL cholesterol data were obtained at the index examination. Because total and HDL cholesterol data were not obtained at the 18th biennial examination of the original cohort subjects, levels obtained at a prior examination cycle 6 years earlier were used. Mean heart rate was calculated from the same ambulatory monitoring recording processed for the analysis of heart rate variability. The number of ventricular premature beats per hour was analyzed as a continuous variable, but supraventricular premature beats were categorized into three groups as follows: <120 per hour, 120 to 240 per hour, and >240 per hour. Average reported alcohol consumption was converted to ounces of alcohol per week on the basis of a published algorithm.27
Sample Selection
At baseline, all study subjects had to be free of clinically apparent coronary heart disease and congestive heart failure by history and clinical examination. We required that they have 60 minutes of analyzable data16 17 on the ambulatory recording, at least 50% time processed, and premature beats <10% of total beats.28 Subjects were excluded if they had no follow-up contact after the index examination.
Outcome Events
At each follow-up examination, interim cardiovascular events were assessed with the help of medical history, physical examination, and 12-lead ECG. Medical records were obtained for all participants, including those who did not attend an examination, and these were evaluated for evidence of interim heart disease. All suspected interim events were reviewed by a committee of three physicians who evaluated pertinent medical records, hospitalization records, and pathology reports. All deaths were evaluated by a committee of three physicians who determined probable cause after review of hospital records, autopsy findings, death certificates, and interviews with family members. A death that occurred within 1 hour of the onset of symptoms suggestive of coronary heart disease was classified as a sudden death attributable to coronary heart disease. A death that occurred >1 hour after the onset of symptoms suggestive of myocardial ischemia was classified as a nonsudden death of coronary heart disease.
The primary end point in the present study was time to onset of coronary heart disease or congestive heart failure. Coronary heart disease comprised angina pectoris, coronary insufficiency (unstable angina with transient ischemic ECG changes), myocardial infarction (clinically recognized at time of occurrence or unrecognized), and sudden or nonsudden death attributed to coronary heart disease. Criteria for the cardiovascular disease events have been reported.29
Statistical Methods
Measures of heart rate variability were transformed by natural logarithm because their distributions were skewed. Proportional hazards regression procedures30 were used to assess heart rate variability measures as predictors of cardiac events. All proportional hazards regression analyses were stratified by sex with age as a covariate, and all were performed with the use of the Statistical Analysis System version 6.09 procedure PHREG31 on a Sun Sparc 2 workstation.
Measures of heart rate variability were studied first without, then with adjustment for several pertinent clinical variables that may be associated with heart rate variability and/or subsequent cardiac events. These clinical variables included frequent supraventricular premature beats (<120/h versus 120/h), systolic blood pressure (in mm Hg), left ventricular hypertrophy on ECG (no versus yes), diabetes (no versus yes), diuretic use (no versus yes), ß-blocker use (no versus yes), other cardiac medication use (no versus yes), and cigarette smoking (no versus yes). These covariates were chosen by use of a stepwise procedure (selection criterion P<.20) from a list that also included the following variables that were not selected (P.20): coffee consumption, alcohol consumption, diastolic blood pressure, starting time of day of recording, and ventricular premature beats. Mean heart rate was considered separately both because it had an inverse association with heart rate variability measures22 and because mean heart rate reflects autonomic balance. Additional multivariate analyses were performed with the use of total cholesterol and the ratio of total to HDL cholesterol levels.
Separate analyses were performed for each measure of heart rate variability to assess its relations to the incidence of cardiac events. Events rates, expressed per 1000 person-years of follow-up, were computed for sex-specific tertiles of each heart rate variability measure. In addition, because the risk was assumed to be smooth and monotonic, risk was assessed as a function of continuous values for each heart rate variability measure. Hazard ratios and 95% CIs were computed for each heart rate variability measure, and the statistical significance level was P=.05 (two-sided) for each significance test. As expressed, the hazards ratios represent the proportional increase in risk that is associated with having measured heart rate variability lower, by 1 SD, relative to an individual of the same sex with otherwise identical risk factors.
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Results |
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There were 5698 subjects who attended the index examination. A total of 2278 subjects did not have ambulatory ECG data (did not have an examination in the Framingham Heart Study clinic, ambulatory recording not obtained, poor quality recording, no available data, or missing tape). Among 3420 tapes analyzed, a total of 919 subjects were excluded for reasons listed in Table 1
; arrhythmia or excessive artifact were the major reasons (n=666) for exclusion. Compared with ineligible subjects, the eligible subjects were younger, had lower blood pressure, and had more favorable clinical risk factors. The eligible sample of 2501 subjects comprised 1101 men and 1400 women. Their clinical characteristics are shown in Table 2. The mean age was 52 years for men and 54 years for women. Women had higher HDL cholesterol levels, a lower ratio of total to HDL cholesterol, lower diastolic blood pressure, and higher mean heart rate than men.
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Heart Rate Variability and Cardiac Events
Table 3 shows mean values (±SD) for eight heart rate variability measures separately for men and women. The mean duration of processed time for analyses was 94 minutes (range, 33 to 120 minutes), corresponding to 56 100-s blocks.
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During a mean follow-up of 3.5 years (range, 4 days to 6.4 years), there were 58 new cardiac events. The initial event was angina pectoris in 22 subjects, coronary insufficiency in 1, recognized myocardial infarction in 20, unrecognized myocardial infarction in 2, death of coronary heart disease in 5, and congestive heart failure in 8.
Rates for cardiac events according to tertiles of each heart rate variability measure are presented in Table 4. Two-hour SDNN, very-low-frequency power, low-frequency power, and total power demonstrated strikingly higher event rates among subjects in the lowest tertile. Approximately two thirds of cardiac events occurred in subjects in the bottom tertile, whereas only 
10% of the outcomes occurred in subjects in the top tertile.
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Table 5 lists hazard ratios for subsequent cardiac events per 1-SD decrement of all eight heart rate variability measures analyzed separately. In age- and sex-adjusted analyses, 2-hour SDNN, very-low-frequency power, low-frequency power, and total power were significantly associated with increased risk for cardiac events; each had a hazard ratio of 1.4.
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In the stepwise analyses to determine relevant clinical risk factors, frequent supraventricular premature beats (120/h), smoking, diabetes, systolic blood pressure, left ventricular hypertrophy on ECG, diuretic use, ß-blocker use, other cardiac medication use, and mean heart rate were each associated with subsequent cardiac events. Therefore, they were included in multivariate proportional hazards models. All heart rate variability measures except the ratio of low-frequency to high-frequency power revealed significant associations with subsequent cardiac events after adjustment for the clinical risk factors. The highest hazard ratio was 1.47 for 2-hour SDNN.
Additional multivariate analyses were performed incorporating total cholesterol and the ratio of total to HDL cholesterol; these analyses were based on 560 original subjects and 1828 Offspring Study participants. Hazard ratios for cardiac events per 1-SD increment of each heart rate variability measure are shown in the bottom third of Table 4
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Mean heart rate was significantly associated with risk for cardiac events after adjustment for age, sex, and clinical risk factors (P=.04). Because it was correlated with heart rate variability measures22 and is a simple measure of autonomic balance, mean heart rate subsequently was added to the multivariate models along with sex, age, and clinical risk factors. After we adjusted for mean heart rate and clinical variables, 2-hour SDNN was the only heart rate variability measure significantly related to risk for cardiac events; a 1-SD decrement in 2-hour SDNN was associated with a hazard ratio of 1.41 (95% CI of 1.05 to 1.89; P=.0216).
Because there was less objective evidence to substantiate diagnoses of angina and unrecognized myocardial infarction, we performed secondary analyses of "hard" end points (coronary insufficiency, recognized myocardial infarction, deaths from coronary heart disease, and congestive heart failure [n=40]). These analyses revealed that the hazard ratios of all eight heart rate variability measures, adjusted for age and sex, were higher than their corresponding associations in the primary analyses. The highest hazard ratio was 1.65 for 2-hour SDNN with a 95% CI of 1.28 to 2.12 (P=.0001).
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Discussion |
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In this study of 2501 men and women who were free of clinically apparent heart disease, reduced heart rate variability predicted increased risk for subsequent cardiac events. These findings may provide insight into the prognostic implications of altered heart rate variability.
We previously demonstrated that reduced heart rate variability predicted increased risk for all-cause mortality.22 The present investigation differs from our earlier study in several key aspects. Our earlier report22 was based on 736 subjects (mean age, 72 years) from the original Framingham Heart Study cohort, whereas the current report is based on 2501 subjects (mean age, 53 years) from the original Framingham Heart Study cohort and from the Framingham Offspring Study. Fewer than 30% of subjects in the current report were included in the earlier investigation. The end points were different in the two reports; the prior study only examined all-cause mortality (only 18 of 74 deaths were due to coronary heart disease). In the present investigation, the end point was coronary disease or congestive heart failure (n=58); there were only 5 fatal end points. In addition, subjects in the current investigation were excluded if they had evidence of prior coronary disease or congestive heart failure.
The biological mechanism explaining our present results remains unknown. Heart rate variability is a marker of sympathetic and parasympathetic influences on the modulations of heart rate.32 In patients with heart disease, increased sympathetic tone and/or decreased parasympathetic tone, which predispose to ventricular fibrillation, have been proposed as mechanisms explaining the associations of reduced heart rate variability with increased mortality.15 16 However, our subjects were free of clinically apparent cardiac disease at baseline, and the vast majority of our outcomes were not arrhythmic (eg, sudden death); hence, it is difficult to attribute our results to autonomic imbalance precipitating fatal arrhythmic events. Rather, other factors such as cardiac chronotropic responsiveness may play an important role. In this sense, reduced heart rate variability may reflect subclinical cardiac disease. Alternatively, autonomic imbalance or other factors related to heart rate variability, such as the renin-angiotensin system,1 33 may contribute to the pathogenesis of coronary heart disease,34 but this hypothesis requires additional support.
Mean heart rate reflects autonomic balance and correlates inversely with all eight heart rate variability measures.22 Although adjustment for mean heart rate may reduce the inherent predictive value of heart rate variability as an indicator of autonomic tone, 2-hour SDNN remained predictive of prognosis even after adjustment for mean heart rate. Two reasons for this can be considered. First, heart rate variability is a more sensitive tool for detecting autonomic balance than mean heart rate. Second, heart rate variability reflects additional information beyond autonomic imbalance.
This report is based on use of daytime 2-hour ambulatory ECG recordings for heart rate variability. Recordings were obtained during an active clinic visit; the results of basal, resting recordings likely would be different. Although the short-term nature of the recordings may have influenced heart rate variability measures, Bigger and coworkers35 reported that frequency-domain analyses computed from 2- to 15-minute segments were not meaningfully different from those calculated for 24 hours, and they remained predictive of mortality regardless of the time of day. On the other hand, the SD of normal RR intervals increases as a function of the recording duration.36 The SD of normal RR intervals from 24-hour recordings is predictive of mortality15 and strongly correlates with low-frequency power, very-low-frequency power, and ultralow-frequency power,22 37 which are predictors of mortality in frequency-domain analyses.16 17 19 The SD of normal RR intervals is a simple measure of heart rate variability. On the basis of the present study, it would appear that the SD of normal RR intervals calculated from 2 hours of ambulatory recording may suffice to assess risk for clinical outcomes, and it was the superior predictor of outcome among the eight heart rate variability measures studied.
A few limitations of the present study should be addressed. First, the number of outcomes was too small to assess the relations of heart rate variability measures to individual cardiac end points. Nevertheless, secondary analyses of hard cardiac outcomes demonstrated higher hazard ratios for all eight heart rate variability measures than in primary analyses, thereby suggesting a stronger association of heart rate variability with risk for more rigorously defined and objective end points. Second, this investigation was based on a relatively healthy sample because of the exclusion of subjects with frequent arrhythmias, a history of coronary heart disease or congestive heart failure, and those who did not attend the index examination. Third, because of the 100-s block method we used, the lower limit of the frequency-domain variables was 0.01 Hz. Additionally, the time-domain analyses were based on 2 hours of data; the values obtained from short-term recordings will differ from those based on longer periods of observation. Last, the ability to predict future cardiac events by use of only heart rate variability measures is limited; a 1-SD decrement in 2-hour SDNN reflects an 50% increase in risk of cardiac events over the next 3.5 years. In the present study, this equates to the same risk increase estimated for an 8-year age increment, or approximately one half the increase associated with diabetes or smoking.
This is the first prospective study to identify an association between heart rate variability and heart disease risk in a community-based population. The estimation of heart rate variability by ambulatory ECG monitoring offers prognostic information beyond that provided by the evaluation of traditional cardiovascular risk factors.
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Acknowledgments |
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This study was supported by grants from the Eleanor Naylor Dana Foundation and Cardiodata/Mortara Inc.
Received April 20, 1996; revision received June 18, 1996; accepted July 11, 1996.
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References |
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|---|
1. Akselrod S, Gordon D, Ubel FA, Shannon DC, Barger AC, Cohen RJ. Power spectrum analysis of heart rate fluctuation: a quantitative probe of beat-to-beat cardiovascular control. Science. 1981;213:220-222.
2.
Pomeranz B, Macaulay RJB, Caudill MA, Kutz I, Adam D, Gordon D, Kilborn KM, Barger AC, Shannon DC, Cohen RJ, Benson H. Assessment of autonomic function in humans by heart rate spectral analysis. Am J Physiol. 1985;248:H151-H153.
3.
Pagani M, Lombardi F, Guzzetti S, Rimoldi O, Furlan R, Pizzinelli P, Sandrone G, Malfatto G, Dell'Orto S, Piccaluga E, Turiel M, Baselli G, Cerutti S, Malliani A. Power spectral analysis of heart rate and arterial pressure variabilities as a marker of sympatho-vagal interaction in man and conscious dog. Circ Res. 1986;59:178-193.
4.
Shannon DC, Carley DW, Benson H. Aging of modulation of heart rate. Am J Physiol. 1987;253:H874-H877.
5.
Malpas SC, Purdie GL. Circadian variation of heart rate variability. Cardiovasc Res. 1990;24:210-213.
6. Saul JP, Arai Y, Berger RD, Lilly LS, Colucci WS, Cohen RJ. Assessment of autonomic regulation in chronic congestive heart failure by heart rate spectral analysis. Am J Cardiol. 1988;61:1292-1299.[Medline] [Order article via Infotrieve]
7.
Airaksinen KE, Ikaheimo MJ, Linnaluoto MK, Niemela M, Takkunen JT. Impaired vagal heart rate control in coronary artery disease. Br Heart J. 1987;58:592-597.
8. Ewing DJ, Borsey DQ, Bellavere F, Clarke BF. Cardiac autonomic neuropathy in diabetes: comparison of measures of R-R interval variation. Diabetologia. 1981;21:18-24.[Medline] [Order article via Infotrieve]
9. Counihan PJ, Fei L, Bashir Y, Farrel TG, Haywood GA, McKenna WJ. Assessment of heart rate variability in hypertrophic cardiomyopathy: association with clinical and prognostic features. Circulation. 1993;88[pt 1]:1682-1690.
10. Ajiki K, Murakawa Y, Yanagisawa-Miwa A, Usui M, Yamashita T, Oikawa N, Inoue H. Autonomic nervous system activity in idiopathic dilated cardiomyopathy and in hypertrophic cardiomyopathy. Am J Cardiol. 1993;71:1316-1320.[Medline] [Order article via Infotrieve]
11.
van Ravenswaaij-Arts CMA, Kollee LAA, Hopman JCW, Stoelinga GBA, van Geijn HP. Heart rate variability. Ann Intern Med. 1993;118:436-447.
12. Malik M, Camm AJ. Heart rate variability: from facts to fancies. J Am Coll Cardiol. 1993;22:566-568.[Medline] [Order article via Infotrieve]
13.
Mandawat MK, Wallbridge DR, Pringle SD, Riyami AAS, Latif S, Macfarlane PW, Ross Lorimer A, Cobbe SM. Heart rate variability in left ventricular hypertrophy. Br Heart J. 1995;73:139-144.
14. Hon EH, Lee ST. Electronic evaluation of the fetal heart rate patterns preceding fetal death, further observations. Am J Obstet Gynecol. 1965;87:814-826.
15. Kleiger RE, Miller JP, Bigger JT Jr, Moss AJ, and the Multicenter Post-Infarction Research Group. Decreased heart rate variability and its association with increased mortality after acute myocardial infarction. Am J Cardiol. 1987;59:256-262.[Medline] [Order article via Infotrieve]
16.
Bigger JT Jr, Fleiss JL, Steinman RC, Rolnitzky LM, Kleiger RE, Rottman JN. Frequency domain measures of heart period variability and mortality after myocardial infarction. Circulation. 1992;85:164-171.
17. Bigger JT Jr, Fleiss JL, Rolnitzky LM, Steinman RC. Frequency domain measures of heart period variability to assess risk late after myocardial infarction. J Am Coll Cardiol. 1993;21:729-736.[Abstract]
18.
Hrushesky WJM, Fader DJ, Berestka JS, Sommer M, Hayes J, Cope FO. Diminishment of respiratory sinus arrhythmia foreshadows doxorubicin-induced cardiomyopathy. Circulation. 1991;84:697-707.
19.
Stein KM, Borer JS, Hochreiter C, Okin PM, Herrold EM, Devereux RB, Kligfield P. Prognostic value and physiological correlates of heart rate variability in chronic severe mitral regurgitation. Circulation. 1993;88:127-135.
20.
Mortara A, La Rovere MT, Signorini MG, Pantaleo P, Pinna G, Martinelli L, Ceconi C, Cerutti S, Tavazzi L. Can power spectral analysis of heart rate variability identify a high risk subgroup of congestive heart failure patients with excessive sympathetic activation? A pilot study before and after heart transplantation. Br Heart J. 1994;71:422-430.
21.
Nakagawa M, Saikawa T. Progressive reduction of heart rate variability with eventual sudden death in two patients. Br Heart J. 1994;71:87-88.
22.
Tsuji H, Venditti FJ Jr, Manders ES, Evans JC, Larson MG, Feldman CL, Levy D. Reduced heart rate variability and mortality risk in an elderly cohort: the Framingham Heart Study. Circulation. 1994;90:878-883.
23. Dawber TR, Meadors GF, Moore FE. Epidemiologic approaches to heart disease: the Framingham Study. Am J Public Health. 1951;41:279-286.
24. Dawber TR, Kannel WB, Lyell LP. An approach to longitudinal studies in a community: the Framingham Study. Ann N Y Acad Sci. 1963;107:539-556.
25. Gordon T, Moore TE, Shurtleff D, Dawber TR. Some methodologic problems in the long-term study of cardiovascular disease: observations on the Framingham Study. J Chronic Dis. 1959;10:186-206.
26. Feldman CL, Hubelbank M, Shook TL, Polan BA, MacCallum G, Stone PH, and the ASIS Study Group. Circadian variations in heart rate spectrum. In: Proceedings of Computers in Cardiology. Venice, Italy; September 1991:253-256.
27. Hjortland MC, Feinleib M. Epidemiologic relationships of alcohol intake and coronary heart disease: results from NHLBI programs. In: Avogaro P, Sirtori CR, Tremoli E, eds. Metabolic Effects of Alcohol. New York, NY/Amsterdam, Netherlands: Elsevier/North-Holland Biomedical Press; 1979:393-403.
28. Vybiral T, Bryg RJ, Maddens MA. Impact of arrhythmias on heart rate variability: strategies to deal with imperfect clinical data. Trans Computers Cardiol. 1990;16:251-254.
29. Shurtleff D. Some characteristics related to the incidence of cardiovascular disease and death: Framingham Heart Study 18-year follow-up. In: Kannel WB, Gordon T, eds. The Framingham Study. Section 30. Washington, DC: US Government Printing Office; 1974:17-25. US Dept of Health, Education, and Welfare publication NIH 74-599.
30. Cox DR. Regression models and life tables (with discussion). J R Stat Soc. 1972;34(series B):187-220.
31. SAS Institute Inc. SAS Technical Report P-217, SAS/STAT Software: The PHREG Procedure, Version 6. Cary, NC: SAS Institute Inc; 1991:63.
32. Malik M, Camm AJ. Components of heart rate variability: what they really mean and what they really measure. Am J Cardiol. 1993;72:821-822.[Medline] [Order article via Infotrieve]
33.
Bonaduce D, Marciano F, Petretta M, Migaux ML, Morgano G, Bianchi V, Salemme L, Valva G, Condorelli M. Effect of converting enzyme inhibition on heart period variability in patients with acute myocardial infarction. Circulation. 1994;90:108-113.
34.
Hayano J, Sakakibara Y, Yamada M, Ohte N, Fujinami T, Yokoyama K, Watanabe Y, Takata K. Decreased magnitude of heart rate spectral components in coronary artery disease: its relation to angiographic severity. Circulation. 1990;81:1217-1224.
35.
Bigger JT Jr, Fleiss JL, Rolnitzky LM, Steinman RC. The ability of several short-term measures of RR variability to predict mortality after myocardial infarction. Circulation. 1993;88:927-934.
36. Tsuji H, Venditti FJ Jr, Manders ES, Evans JC, Larson MG, Feldman CL, Levy D. Determinants of heart rate variability in an elderly cohort: the Framingham Heart Study. Circulation. 1993;88(suppl I):I-115. Abstract.
37. Bigger JT Jr, Fleiss JL, Steinman RC, Rolnitzky LM, Kleiger RE, Rottman JN. Correlations among time and frequency domain measures of heart period variability two weeks after myocardial infarction. Am J Cardiol. 1992;69:891-898.[Medline] [Order article via Infotrieve]
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 S. K. Park, K. L Tucker, M. S O'Neill, D. Sparrow, P. S Vokonas, H. Hu, and J. Schwartz Fruit, vegetable, and fish consumption and heart rate variability: the Veterans Administration Normative Aging Study Am. J. Clinical Nutrition, March 1, 2009; 89(3): 778 - 786. [Abstract] [Full Text] [PDF]
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 S.-X. Zhou, J. Lei, C. Fang, Y.-L. Zhang, and J.-F. Wang Ventricular electrophysiology in congestive heart failure and its correlation with heart rate variability and baroreflex sensitivity: a canine model study Europace, February 1, 2009; 11(2): 245 - 251. [Abstract] [Full Text] [PDF]
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P. L.S. Ljungman, N. Berglind, C. Holmgren, F. Gadler, N. Edvardsson, G. Pershagen, M. Rosenqvist, B. Sjogren, and T. Bellander Rapid effects of air pollution on ventricular arrhythmias Eur. Heart J., December 1, 2008; 29(23): 2894 - 2901. [Abstract] [Full Text] [PDF]
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 C. M. M. Licht, E. J. C. de Geus, F. G. Zitman, W. J. G. Hoogendijk, R. van Dyck, and B. W. J. H. Penninx Association Between Major Depressive Disorder and Heart Rate Variability in the Netherlands Study of Depression and Anxiety (NESDA) Arch Gen Psychiatry, December 1, 2008; 65(12): 1358 - 1367. [Abstract] [Full Text] [PDF]
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 M. Kikuya, T. Ohkubo, H. Metoki, K. Asayama, A. Hara, T. Obara, R. Inoue, H. Hoshi, J. Hashimoto, K. Totsune, et al. Day-by-Day Variability of Blood Pressure and Heart Rate at Home as a Novel Predictor of Prognosis: The Ohasama Study Hypertension, December 1, 2008; 52(6): 1045 - 1050. [Abstract] [Full Text] [PDF]
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 K. L. Teff Visceral Nerves: Vagal and Sympathetic Innervation JPEN J Parenter Enteral Nutr, September 1, 2008; 32(5): 569 - 571. [Abstract] [Full Text] [PDF]
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 L Bosquet, S Merkari, D Arvisais, and A E Aubert Is heart rate a convenient tool to monitor over-reaching? A systematic review of the literature Br. J. Sports Med., September 1, 2008; 42(9): 709 - 714. [Abstract] [Full Text] [PDF]
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 B. Z. Simkhovich, M. T. Kleinman, and R. A. Kloner Air Pollution and Cardiovascular Injury: Epidemiology, Toxicology, and Mechanisms J. Am. Coll. Cardiol., August 26, 2008; 52(9): 719 - 726. [Abstract] [Full Text] [PDF]
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 C. Langelotz, M. Scharfenberg, O. Haase, and W. Schwenk Stress and Heart Rate Variability in Surgeons During a 24-Hour Shift Arch Surg, August 1, 2008; 143(8): 751 - 755. [Abstract] [Full Text] [PDF]
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 S. K. Park, M. S. O'Neill, P. S. Vokonas, D. Sparrow, A. Spiro III, K. L. Tucker, H. Suh, H. Hu, and J. Schwartz Traffic-related Particles Are Associated with Elevated Homocysteine: The VA Normative Aging Study Am. J. Respir. Crit. Care Med., August 1, 2008; 178(3): 283 - 289. [Abstract] [Full Text] [PDF]
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V. Vaccarino, R. Lampert, J. D. Bremner, F. Lee, S. Su, C. Maisano, N. V. Murrah, L. Jones, F. Jawed, N. Afzal, et al. Depressive Symptoms and Heart Rate Variability: Evidence for a Shared Genetic Substrate in a Study of Twins Psychosom Med, July 1, 2008; 70(6): 628 - 636. [Abstract] [Full Text] [PDF]
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R. Howden, E. Liu, L. Miller-DeGraff, H. L. Keener, C. Walker, J. A. Clark, P. H. Myers, D. C. Rouse, T. Wiltshire, and S. R. Kleeberger The genetic contribution to heart rate and heart rate variability in quiescent mice Am J Physiol Heart Circ Physiol, July 1, 2008; 295(1): H59 - H68. [Abstract] [Full Text] [PDF]
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M. K. Lahiri, P. J. Kannankeril, and J. J. Goldberger Assessment of Autonomic Function in Cardiovascular Disease: Physiological Basis and Prognostic Implications J. Am. Coll. Cardiol., May 6, 2008; 51(18): 1725 - 1733. [Abstract] [Full Text] [PDF]
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 A. Baccarelli, P. A. Cassano, A. Litonjua, S. K. Park, H. Suh, D. Sparrow, P. Vokonas, and J. Schwartz Cardiac Autonomic Dysfunction: Effects From Particulate Air Pollution and Protection by Dietary Methyl Nutrients and Metabolic Polymorphisms Circulation, April 8, 2008; 117(14): 1802 - 1809. [Abstract] [Full Text] [PDF]
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M. E. Bleil, P. J. Gianaros, J. R. Jennings, J. D. Flory, and S. B. Manuck Trait Negative Affect: Toward an Integrated Model of Understanding Psychological Risk for Impairment in Cardiac Autonomic Function Psychosom Med, April 1, 2008; 70(3): 328 - 337. [Abstract] [Full Text] [PDF]
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 J. M. Golbin, V. K. Somers, and S. M. Caples Obstructive Sleep Apnea, Cardiovascular Disease, and Pulmonary Hypertension Proceedings of the ATS, February 15, 2008; 5(2): 200 - 206. [Abstract] [Full Text] [PDF]
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 B. Biondi and D. S. Cooper The Clinical Significance of Subclinical Thyroid Dysfunction Endocr. Rev., February 1, 2008; 29(1): 76 - 131. [Abstract] [Full Text] [PDF]
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T. Ohira, A. V. D. Roux, R. J. Prineas, M. A. Kizilbash, M. R. Carnethon, and A. R. Folsom Associations of Psychosocial Factors With Heart Rate and Its Short-Term Variability: Multi-Ethnic Study of Atherosclerosis Psychosom Med, February 1, 2008; 70(2): 141 - 146. [Abstract] [Full Text] [PDF]
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 F. Galetta, F. Franzoni, P. Fallahi, L. Tocchini, L. Braccini, G. Santoro, and A. Antonelli Changes in heart rate variability and QT dispersion in patients with overt hypothyroidism Eur. J. Endocrinol., January 1, 2008; 158(1): 85 - 90. [Abstract] [Full Text] [PDF]
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 A. Perciaccante, A. Fiorentini, R. Valente, M. Granata, and L. Tubani Migraine and Heart Rate Variability Arch Intern Med, November 12, 2007; 167(20): 2264 - 2264. [Full Text] [PDF]
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K. S. Heffernan, C. A. Fahs, K. K. Shinsako, S. Y. Jae, and B. Fernhall Heart rate recovery and heart rate complexity following resistance exercise training and detraining in young men Am J Physiol Heart Circ Physiol, November 1, 2007; 293(5): H3180 - H3186. [Abstract] [Full Text] [PDF]
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A. L. Marsland, P. J. Gianaros, A. A. Prather, J. R. Jennings, S. A. Neumann, and S. B. Manuck Stimulated Production of Proinflammatory Cytokines Covaries Inversely With Heart Rate Variability Psychosom Med, October 1, 2007; 69(8): 709 - 716. [Abstract] [Full Text] [PDF]
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 D. Felber Dietrich, J. Schwartz, C. Schindler, J.-M. Gaspoz, J.-C. Barthelemy, J.-M. Tschopp, F. Roche, A. von Eckardstein, O. Brandli, P. Leuenberger, et al. Effects of passive smoking on heart rate variability, heart rate and blood pressure: an observational study Int. J. Epidemiol., August 1, 2007; 36(4): 834 - 840. [Abstract] [Full Text] [PDF]
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M. Buchheit, Y. Papelier, P. B. Laursen, and S. Ahmaidi Noninvasive assessment of cardiac parasympathetic function: postexercise heart rate recovery or heart rate variability? Am J Physiol Heart Circ Physiol, July 1, 2007; 293(1): H8 - H10. [Full Text] [PDF]
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S. K. Park, M. S. O'Neill, R. O. Wright, H. Hu, P. S. Vokonas, D. Sparrow, H. Suh, and J. Schwartz HFE Genotype, Particulate Air Pollution, and Heart Rate Variability: A Gene-Environment Interaction Circulation, December 19, 2006; 114(25): 2798 - 2805. [Abstract] [Full Text] [PDF]
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 V. L. Brooks, K. L. Freeman, and Y. Qi Time course of synergistic interaction between DOCA and salt on blood pressure: roles of vasopressin and hepatic osmoreceptors Am J Physiol Regulatory Integrative Comp Physiol, December 1, 2006; 291(6): R1825 - R1834. [Abstract] [Full Text] [PDF]
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 H. Schubiner, B. Hassunizadeh, and R. Kaczynski A controlled study of autonomic nervous system function in adults with attention-deficit/hyperactivity disorder treated with stimulant medications: results of a pilot study. J Atten Disord, November 1, 2006; 10(2): 205 - 211. [Abstract] [PDF]
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S. Shibata, R. Zhang, J. Hastings, Q. Fu, K. Okazaki, K.-i. Iwasaki, and B. D. Levine Cascade model of ventricular-arterial coupling and arterial-cardiac baroreflex function for cardiovascular variability in humans Am J Physiol Heart Circ Physiol, November 1, 2006; 291(5): H2142 - H2151. [Abstract] [Full Text] [PDF]
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Y. Zhong, K.-M. Jan, K. H. Ju, and K. H. Chon Quantifying cardiac sympathetic and parasympathetic nervous activities using principal dynamic modes analysis of heart rate variability Am J Physiol Heart Circ Physiol, September 1, 2006; 291(3): H1475 - H1483. [Abstract] [Full Text] [PDF]
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D. Felber Dietrich, C. Schindler, J. Schwartz, J.-C. Barthelemy, J.-M. Tschopp, F. Roche, A. von Eckardstein, O. Brandli, P. Leuenberger, D. R. Gold, et al. Heart rate variability in an ageing population and its association with lifestyle and cardiovascular risk factors: results of the SAPALDIA study Europace, July 1, 2006; 8(7): 521 - 529. [Abstract] [Full Text] [PDF]
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M. Buchheit and C. Gindre Cardiac parasympathetic regulation: respective associations with cardiorespiratory fitness and training load Am J Physiol Heart Circ Physiol, July 1, 2006; 291(1): H451 - H458. [Abstract] [Full Text] [PDF]
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J. J. Goldberger, F. K. Le, M. Lahiri, P. J. Kannankeril, J. Ng, and A. H. Kadish Assessment of parasympathetic reactivation after exercise Am J Physiol Heart Circ Physiol, June 1, 2006; 290(6): H2446 - H2452. [Abstract] [Full Text] [PDF]
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 M. Petrova, R. Townsend, and K. L. Teff Prolonged (48-Hour) Modest Hyperinsulinemia Decreases Nocturnal Heart Rate Variability and Attenuates the Nocturnal Decrease in Blood Pressure in Lean, Normotensive Humans J. Clin. Endocrinol. Metab., March 1, 2006; 91(3): 851 - 859. [Abstract] [Full Text] [PDF]
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M. R. Irwin, E. M. Valladares, S. Motivala, J. F. Thayer, and C. L. Ehlers Association Between Nocturnal Vagal Tone and Sleep Depth, Sleep Quality, and Fatigue in Alcohol Dependence Psychosom Med, January 1, 2006; 68(1): 159 - 166. [Abstract] [Full Text] [PDF]
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J. Schwartz, S. K. Park, M. S. O'Neill, P. S. Vokonas, D. Sparrow, S. Weiss, and K. Kelsey Glutathione-S-Transferase M1, Obesity, Statins, and Autonomic Effects of Particles: Gene-by-Drug-by-Environment Interaction Am. J. Respir. Crit. Care Med., December 15, 2005; 172(12): 1529 - 1533. [Abstract] [Full Text] [PDF]
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 |
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 S. M. Caples, A. S. Gami, and V. K. Somers Obstructive Sleep Apnea Focus, October 1, 2005; 3(4): 557 - 567. [Full Text] [PDF]
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 E Ronkainen, H Ansakorpi, H V Huikuri, V V Myllyla, J I T Isojarvi, and J T Korpelainen Suppressed circadian heart rate dynamics in temporal lobe epilepsy J. Neurol. Neurosurg. Psychiatry, October 1, 2005; 76(10): 1382 - 1386. [Abstract] [Full Text] [PDF]
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 K. Okazaki, K.-i. Iwasaki, A. Prasad, M. D. Palmer, E. R. Martini, Q. Fu, A. Arbab-Zadeh, R. Zhang, and B. D. Levine Dose-response relationship of endurance training for autonomic circulatory control in healthy seniors J Appl Physiol, September 1, 2005; 99(3): 1041 - 1049. [Abstract] [Full Text] [PDF]
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 S. Carrere, D. Yoshimoto, A. Mittmann, E. M. Woodin, A. Tabares, J. Ullman, C. Swanson, and M. Hawkins The Roles of Marriage and Anger Dysregulation in Biobehavioral Stress Responses Biol Res Nurs, July 1, 2005; 7(1): 30 - 43. [Abstract] [PDF]
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P. J. Gianaros, K. Salomon, F. Zhou, J. F. Owens, D. Edmundowicz, L. H. Kuller, and K. A. Matthews A Greater Reduction in High-Frequency Heart Rate Variability to a Psychological Stressor is Associated With Subclinical Coronary and Aortic Calcification in Postmenopausal Women Psychosom Med, July 1, 2005; 67(4): 553 - 560. [Abstract] [Full Text] [PDF]
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L. F. Berkman Tracking Social and Biological Experiences: The Social Etiology of Cardiovascular Disease Circulation, June 14, 2005; 111(23): 3022 - 3024. [Full Text] [PDF]
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H. Hemingway, M. Shipley, E. Brunner, A. Britton, M. Malik, and M. Marmot Does Autonomic Function Link Social Position to Coronary Risk?: The Whitehall II Study Circulation, June 14, 2005; 111(23): 3071 - 3077. [Abstract] [Full Text] [PDF]
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 J N Townend The way to dusty death? Thorax, June 1, 2005; 60(6): 441 - 442. [Full Text] [PDF]
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J Schwartz, A Litonjua, H Suh, M Verrier, A Zanobetti, M Syring, B Nearing, R Verrier, P Stone, G MacCallum, et al. Traffic related pollution and heart rate variability in a panel of elderly subjects Thorax, June 1, 2005; 60(6): 455 - 461. [Abstract] [Full Text] [PDF]
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 F. Holguin, M. M. Tellez-Rojo, M. Lazo, D. Mannino, J. Schwartz, M. Hernandez, and I. Romieu Cardiac Autonomic Changes Associated With Fish Oil vs Soy Oil Supplementation in the Elderly Chest, April 1, 2005; 127(4): 1102 - 1107. [Abstract] [Full Text] [PDF]
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R. P Sloan, M.-H. Huang, S. Sidney, K. Liu, O D. Williams, and T. Seeman Socioeconomic status and health: is parasympathetic nervous system activity an intervening mechanism? Int. J. Epidemiol., April 1, 2005; 34(2): 309 - 315. [Abstract] [Full Text] [PDF]
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S. A. Neumann, E. C. Lawrence, J. R. Jennings, R. E. Ferrell, and S. B. Manuck Heart Rate Variability Is Associated With Polymorphic Variation in the Choline Transporter Gene Psychosom Med, March 1, 2005; 67(2): 168 - 171. [Abstract] [Full Text] [PDF]
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|
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N. Tahara, H. Takaki, A. Taguchi, K. Suyama, T. Kurita, W. Shimizu, S. Miyazaki, T. Kawada, and K. Sunagawa Pronounced HR variability after exercise in inferior ischemia: evidence that the cardioinhibitory vagal reflex is invoked by exercise-induced inferior ischemia Am J Physiol Heart Circ Physiol, March 1, 2005; 288(3): H1179 - H1185. [Abstract] [Full Text] [PDF]
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 |
|
 S. M. Caples, A. S. Gami, and V. K. Somers Obstructive Sleep Apnea Ann Intern Med, February 1, 2005; 142(3): 187 - 197. [Full Text] [PDF]
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|
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|
M. Buchheit, C. Simon, F. Piquard, J. Ehrhart, and G. Brandenberger Effects of increased training load on vagal-related indexes of heart rate variability: a novel sleep approach Am J Physiol Heart Circ Physiol, December 1, 2004; 287(6): H2813 - H2818. [Abstract] [Full Text] [PDF]
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N. H.M. Kupper, G. Willemsen, M. van den Berg, D. de Boer, D. Posthuma, D. I. Boomsma, and E. J.C. de Geus Heritability of Ambulatory Heart Rate Variability Circulation, November 2, 2004; 110(18): 2792 - 2796. [Abstract] [Full Text] [PDF]
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 A. M. Makikallio, T. H. Makikallio, J. T. Korpelainen, K. A. Sotaniemi, H. V. Huikuri, and V. V. Myllyla Heart rate dynamics predict poststroke mortality Neurology, May 25, 2004; 62(10): 1822 - 1826. [Abstract] [Full Text] [PDF]
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L. S. Kinder, M. R. Carnethon, L. P. Palaniappan, A. C. King, and S. P. Fortmann Depression and the Metabolic Syndrome in Young Adults: Findings From the Third National Health and Nutrition Examination Survey Psychosom Med, May 1, 2004; 66(3): 316 - 322. [Abstract] [Full Text] [PDF]
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D. Liao, Y. Duan, E. A. Whitsel, Z.-j. Zheng, G. Heiss, V. M. Chinchilli, and H.-M. Lin Association of Higher Levels of Ambient Criteria Pollutants with Impaired Cardiac Autonomic Control: A Population-based Study Am. J. Epidemiol., April 15, 2004; 159(8): 768 - 777. [Abstract] [Full Text] [PDF]
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A. Sajadieh, O. W. Nielsen, V. Rasmussen, H. O. Hein, S. Abedini, and J. F. Hansen Increased heart rate and reduced heart-rate variability are associated with subclinical inflammation in middle-aged and elderly subjects with no apparent heart disease Eur. Heart J., March 1, 2004; 25(5): 363 - 370. [Abstract] [Full Text] [PDF]
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 C. S. Fox, L. Sullivan, R. B. D'Agostino Sr, and P. W.F. Wilson The Significant Effect of Diabetes Duration on Coronary Heart Disease Mortality: The Framingham Heart Study Diabetes Care, March 1, 2004; 27(3): 704 - 708. [Abstract] [Full Text] [PDF]
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R J Winsley, N Armstrong, K Bywater, and S G Fawkner Reliability of heart rate variability measures at rest and during light exercise in children Br. J. Sports Med., December 1, 2003; 37(6): 550 - 552. [Abstract] [Full Text] [PDF]
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R. Krittayaphong, G. Veerakul, K. Nademanee, and C. Kangkagate Heart rate variability in patients with Brugada syndrome in Thailand Eur. Heart J., October 1, 2003; 24(19): 1771 - 1778. [Abstract] [Full Text] [PDF]
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K.-i. Iwasaki, R. Zhang, J. H. Zuckerman, and B. D. Levine Dose-response relationship of the cardiovascular adaptation to endurance training in healthy adults: how much training for what benefit? J Appl Physiol, October 1, 2003; 95(4): 1575 - 1583. [Abstract] [Full Text] [PDF]
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N. Hakansson, P. Gustavsson, A. Sastre, and B. Floderus Occupational Exposure to Extremely Low Frequency Magnetic Fields and Mortality from Cardiovascular Disease Am. J. Epidemiol., September 15, 2003; 158(6): 534 - 542. [Abstract] [Full Text] [PDF]
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R. Virtanen, A. Jula, J. K. Salminen, L.-M. Voipio-Pulkki, H. Helenius, T. Kuusela, and J. Airaksinen Anxiety and Hostility Are Associated With Reduced Baroreflex Sensitivity and Increased Beat-to-Beat Blood Pressure Variability Psychosom Med, September 1, 2003; 65(5): 751 - 756. [Abstract] [Full Text] [PDF]
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K. L. Rennie, H. Hemingway, M. Kumari, E. Brunner, M. Malik, and M. Marmot Effects of Moderate and Vigorous Physical Activity on Heart Rate Variability in a British Study of Civil Servants Am. J. Epidemiol., July 15, 2003; 158(2): 135 - 143. [Abstract] [Full Text] [PDF]
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M. R. Carnethon, S. H. Golden, A. R. Folsom, W. Haskell, and D. Liao Prospective Investigation of Autonomic Nervous System Function and the Development of Type 2 Diabetes: The Atherosclerosis Risk In Communities Study, 1987-1998 Circulation, May 6, 2003; 107(17): 2190 - 2195. [Abstract] [Full Text] [PDF]
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 R.B. Devlin, A.J. Ghio, H. Kehrl, G. Sanders, and W. Cascio Elderly humans exposed to concentrated air pollution particles have decreased heart rate variability Eur. Respir. J., May 1, 2003; 21(40_suppl): 76S - 80s. [Abstract] [Full Text] [PDF]
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E. G. Lakatta and D. Levy Arterial and Cardiac Aging: Major Shareholders in Cardiovascular Disease Enterprises: Part II: The Aging Heart in Health: Links to Heart Disease Circulation, January 21, 2003; 107(2): 346 - 354. [Full Text] [PDF]
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A. R. Schwartz, W. Gerin, K. W. Davidson, T. G. Pickering, J. F. Brosschot, J. F. Thayer, N. Christenfeld, and W. Linden Toward a Causal Model of Cardiovascular Responses to Stress and the Development of Cardiovascular Disease Psychosom Med, January 1, 2003; 65(1): 22 - 35. [Abstract] [Full Text] [PDF]
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 |
|
 D. Liao, M. Carnethon, G. W. Evans, W. E. Cascio, and G. Heiss Lower Heart Rate Variability Is Associated With the Development of Coronary Heart Disease in Individuals With Diabetes: The Atherosclerosis Risk in Communities (ARIC) Study Diabetes, December 1, 2002; 51(12): 3524 - 3531. [Abstract] [Full Text] [PDF]
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J. Sahl, G. Mezei, R. Kavet, A. McMillan, A. Silvers, A. Sastre, and L. Kheifets Occupational Magnetic Field Exposure and Cardiovascular Mortality in a Cohort of Electric Utility Workers Am. J. Epidemiol., November 15, 2002; 156(10): 913 - 918. [Abstract] [Full Text] [PDF]
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C. Johansen, M. Feychting, M. Moller, P. Arnsbo, A. Ahlbom, and J. H. Olsen Risk of Severe Cardiac Arrhythmia in Male Utility Workers: A Nationwide Danish Cohort Study Am. J. Epidemiol., November 1, 2002; 156(9): 857 - 861. [Abstract] [Full Text] [PDF]
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 |
|
 J E Mietus, C-K Peng, I Henry, R L Goldsmith, and A L Goldberger The pNNx files: re-examining a widely used heart rate variability measure Heart, October 1, 2002; 88(4): 378 - 380. [Abstract] [Full Text] [PDF]
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|
 J. Davies and A. Struthers Review: The potential benefits of aldosterone antagonism in Type 2 diabetes mellitus Journal of Renin-Angiotensin-Aldosterone System, September 1, 2002; 3(3): 150 - 155. [Abstract] [PDF]
|
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M. R. Carnethon, D. Liao, G. W. Evans, W. E. Cascio, L. E. Chambless, W. D. Rosamond, and G. Heiss Does the Cardiac Autonomic Response to Postural Change Predict Incident Coronary Heart Disease and Mortality? : The Atherosclerosis Risk in Communities Study Am. J. Epidemiol., January 1, 2002; 155(1): 48 - 56. [Abstract] [Full Text] [PDF]
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|
 B. M. Curtis and J. H. O'Keefe Jr Autonomic Tone as a Cardiovascular Risk Factor: The Dangers of Chronic Fight or Flight Mayo Clin. Proc., January 1, 2002; 77(1): 45 - 54. [Abstract] [PDF]
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|
|
 |
|
 H. V. Huikuri, A. Castellanos, and R. J. Myerburg Sudden Death Due to Cardiac Arrhythmias N. Engl. J. Med., November 15, 2001; 345(20): 1473 - 1482. [Full Text] [PDF]
|
|
|
|
 |
|
 L G P M van Amelsvoort, E G Schouten, A C Maan, C A Swenne, and F J Kok Changes in frequency of premature complexes and heart rate variability related to shift work Occup. Environ. Med., October 1, 2001; 58(10): 678 - 681. [Abstract] [Full Text] [PDF]
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H. M. Colhoun, D. P. Francis, M. B. Rubens, S. R. Underwood, and J. H. Fuller The Association of Heart-Rate Variability With Cardiovascular Risk Factors and Coronary Artery Calcification: A study in type 1 diabetic patients and the general population Diabetes Care, June 1, 2001; 24(6): 1108 - 1114. [Abstract] [Full Text]
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R. P. Sloan, E. Bagiella, P. A. Shapiro, J. P. Kuhl, D. Chernikhova, J. Berg, and M. M. Myers Hostility, Gender, and Cardiac Autonomic Control Psychosom Med, May 1, 2001; 63(3): 434 - 440. [Abstract] [Full Text] [PDF]
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T. H. Makikallio, H. V. Huikuri, A. Makikallio, L. B. Sourander, R. D. Mitrani, A. Castellanos, and R. J. Myerburg Prediction of sudden cardiac death by fractal analysis of heart rate variability in elderly subjects J. Am. Coll. Cardiol., April 1, 2001; 37(5): 1395 - 1402. [Abstract] [Full Text] [PDF]
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O. Baltatu, B. J. Janssen, G. Bricca, R. Plehm, J. Monti, D. Ganten, and M. Bader Alterations in Blood Pressure and Heart Rate Variability in Transgenic Rats With Low Brain Angiotensinogen Hypertension, February 1, 2001; 37(2): 408 - 413. [Abstract] [Full Text] [PDF]
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M. Kornitzer Predictive value of electrocardiographic markers for autonomic nervous system dysfunction in healthy populations: more studies needed Eur. Heart J., January 2, 2001; 22(2): 109 - 112. [PDF]
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 H. Tasaki, T. Serita, A. Irita, O. Hano, I. Iliev, C. Ueyama, K. Kitano, S. Seto, M. Hayano, and K. Yano A 15-Year Longitudinal Follow-Up Study of Heart Rate and Heart Rate Variability in Healthy Elderly Persons J. Gerontol. A Biol. Sci. Med. Sci., December 1, 2000; 55(12): 744M - 749. [Abstract] [Full Text]
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A. Loimaala, H. Huikuri, P. Oja, M. Pasanen, and I. Vuori Controlled 5-mo aerobic training improves heart rate but not heart rate variability or baroreflex sensitivity J Appl Physiol, November 1, 2000; 89(5): 1825 - 1829. [Abstract] [Full Text] [PDF]
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M. Kikuya, A. Hozawa, T. Ohokubo, I. Tsuji, M. Michimata, M. Matsubara, M. Ota, K. Nagai, T. Araki, H. Satoh, et al. Prognostic Significance of Blood Pressure and Heart Rate Variabilities : The Ohasama Study Hypertension, November 1, 2000; 36(5): 901 - 906. [Abstract] [Full Text] [PDF]
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J. M. Dekker, R. S. Crow, A. R. Folsom, P. J. Hannan, D. Liao, C. A. Swenne, and E. G. Schouten Low Heart Rate Variability in a 2-Minute Rhythm Strip Predicts Risk of Coronary Heart Disease and Mortality From Several Causes : The ARIC Study Circulation, September 12, 2000; 102(11): 1239 - 1244. [Abstract] [Full Text] [PDF]
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T. G. M. Vrijkotte, L. J. P. van Doornen, and E. J. C. de Geus Effects of Work Stress on Ambulatory Blood Pressure, Heart Rate, and Heart Rate Variability Hypertension, April 1, 2000; 35(4): 880 - 886. [Abstract] [Full Text] [PDF]
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D. R. Gold, A. Litonjua, J. Schwartz, E. Lovett, A. Larson, B. Nearing, G. Allen, M. Verrier, R. Cherry, and R. Verrier Ambient Pollution and Heart Rate Variability Circulation, March 21, 2000; 101(11): 1267 - 1273. [Abstract] [Full Text] [PDF]
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