Decreased heart rate variability and its association with increased mortality after acute myocardial infarction

A high degree of heart rate (HR) variability is found in compensated hearts with good function, whereas HR variability can be decreased with severe coronary artery disease, congestive heart failure, aging and diabetic neuropathy. To test the hypothesis that HR variability is a predictor of long-term survival after acute myocardial infarction (AMI), the Holter tapes of 808 patients who survived AMI were analyzed. Heart rate variability was defined as the standard deviation of all normal RR intervals in a 24-hour continuous electrocardiogram recording made 11 +/- 3 days after AMI. In all patients demographic, clinical and laboratory variables were measured at baseline. Mean follow-up time was 31 months. Of all Holter variables measured, HR variability had the strongest univariate correlation with mortality. The relative risk of mortality was 5.3 times higher in the group with HR variability of less than 50 ms than the group with HR variability of more than 100 ms. HR variability remained a significant predictor of mortality after adjusting for clinical, demographic, other Holter features and ejection fraction. A hypothesis to explain this finding is that decreased HR variability correlates with increased sympathetic or decreased vagal tone, which may predispose to ventricular fibrillation.     

Higher heart rate variability of smokers after acute myocardial infarction

Although cigarette smoking is known to be a strong risk factor for the development of coronary artery disease, several large clinical studies have demonstrated that current smokers had a favorable prognosis compared to nonsmokers after myocardial infarction. This study sought to evaluate the effect of smoking status on heart rate variability after onset of acute myocardial infarction. We studied 52 patients (34 smokers, 18 nonsmokers) with a first myocardial infarction within 24 h of onset. We recorded 24-h ambulatory ECG to calculate very low frequency power (VLF), low frequency power (LF) and high frequency power (HF) 14 days after onset. Although smokers had a tendency to be younger than nonsmokers (mean age 57 versus 62, P = 0.0812), clinical characteristics were not statistically different between smokers and nonsmokers. After adjustment for age, left ventricular ejection fraction, history of diabetes, acute revascularization and use of beta-blockers, VLF (P = 0.0183) of smokers 14 days after onset was significantly higher than for nonsmokers. In conclusion, although smoking reduces heart rate variability in the general population, higher heart rate variability was observed in smokers than nonsmokers after acute myocardial infarction under the condition of smoking cessation.     

Influence of heart rate on mortality after acute myocardial infarction

Elevated heart rate (HR) during hospitalization and after discharge has been predictive of death in patients with acute myocardial infarction (AMI), but whether this association is primarily due to associated cardiac failure is unknown. The major purpose of this study was to characterize in 1,807 patients with AMI admitted into a multicenter study the relation of HR to in-hospital, after discharge and total mortality from day 2 to 1 year in patients with and without heart failure. HR was examined on admission at maximum level in the coronary care unit, and at hospital discharge. Both in-hospital and postdischarge mortality increased with increasing admission HR, and total mortality (day 2 to 1 year) was 15% for patients with an admission HR between 50 and 60 beats/min, 41% for HR greater than 90 beats/min and 48% for HR greater than or equal to 110 beats/min. Mortality from hospital discharge to 1 year was similarly related to maximal HR in the coronary care unit and to HR at discharge. In patients with severe heart failure (grade 3 or 4 pulmonary congestion on chest x-ray, or shock), cumulative mortality was high regardless of the level of admission HR (range 61 to 68%). However, in patients with pulmonary venous congestion of grade 2, cumulative mortality for patients with admission HR greater than or equal to 90 beats/min was over twice as high as that in patients with admission HR less than 90 beats/min (39 vs 18%, respectively); the same trend was evident in patients with absent to mild heart failure (mortality 18 vs 10%, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)     

心肌梗死前后心率变异性的变化及意义

目的　了解心肌梗死前后心率变异性（ＨＲＶ）的变化及心肌梗死前的ＨＲＶ对心肌梗死后心脏猝死的预测价值。方法　２７ 只兔随机分为对照组和心梗组,术前和术后２ 周分别测量ＨＲＶ一次,并行电刺激诱发室颤。结果　梗死组按电刺激能否诱发心室颤动（ＶＦ） 再分为ＶＦ 组和无ＶＦ组,心肌梗死前三组ＨＲＶ无差异,心肌梗死后ＶＦ组ＨＲＶ较心肌梗死前明显降低,无ＶＦ组和对照组无明显变化。结论　心肌梗死后ＨＲＶ 的降低与心脏猝死的发生有关,心肌梗死前ＨＲＶ对心肌梗死后的心脏猝死可能无预测价值。     

急性心肌梗死后心率变异性的特点及其临床意义

目的　探讨急性心肌梗死 ( AMI)早期心率变异性 ( HRV)特点及其临床意义。方法　 AMI病人 5 2例入院 48小时内进行 2 4小时动态心电图检查 ,应用计算机软件进行 HRV的时域分析 ,并观察 HRV与心脏事件的关系。结果　所有 AMI患者的 HRV时域值均较正常对照组 32例明显降低 ( P<0 .0 1) ,发生心脏事件组的 HRV时域值更进一步降低。结论　早期检测 AMI后的 HRV指标可预测心脏事件的发生。     

急性心肌梗塞早期的心率变异性测定

目的 研究急性心肌梗塞（ＡＭＩ）较早期的心率变异性（ＨＲＶ）改变及其预后意义，探讨不同梗塞部位，心功能，溶栓与再通过ＨＲＶ的影响。方法 ＡＭＩ患５０例，Ｈｏｌｔｅｒ记录在胸痛发作２４小时之内开始进行，平均（１３．６±７．９）小时，健康对照组５０例。结果 （１）ＡＭＩ组ＨＲＶ各项指标均低于正常对照组，统计学达显意义，并且正常ＲＲ间期的标准差，低频等成分失去了昼夜间的差异。ＡＭＩ患２４小时ＨＲＶ     

Personality traits and heart rate variability predict long-term cardiac mortality after myocardial infarction.

AIMS: To investigate personality traits and sympatho-vagal modulation of heart rate variability (HRV) during acute myocardial infarction (AMI), assessing their relationships and their long-term prognostic value. METHODS AND RESULTS: Psychological traits and 24 h HRV were prospectively investigated in 246 patients at discharge of an AMI. Patients were followed-up to 8 years for the occurrence of cardiac death and non-fatal reinfarction. Low coping and anxiety traits associated with reduced HRV characterized the study population. At univariate analysis, low emotional sensitivity and insecurity, relative tachycardia, reduced high frequency (HF), and low frequency power and pNN50 were predictive of cardiac death at 8-year follow-up. At multivariable analysis, low emotional sensitivity and low HF power remained predictive, with a relative risk of 4.18 (P=0.003) and 2.76 (P=0.007), respectively; also the type of infarction (Q vs. non-Q) and hospital length of stay were independent predictive variables. CONCLUSION: Anxiety and emotional sensitivity were significant predictors of 8-year cardiac mortality after AMI. Reduced HF power, a recognized marker of vagal withdrawal, increased the risk.     

Traditional and nonlinear heart rate variability are each independently associated with mortality after myocardial infarction

INTRODUCTION: Decreased heart rate variability (HRV) and abnormal nonlinear HRV shortly after myocardial infarction (MI) are risk factors for mortality. Traditional HRV predicts mortality in patients with a range of times post-MI, but the association of nonlinear HRV and outcome in this population is unknown. METHODS AND RESULTS: HRV was determined from 740 tapes recorded before antiarrhythmic therapy in Cardiac Arrhythmia Suppression Trial patients with ventricular premature contractions (VPCs) suppressed on the first randomized treatment. Patients were 70 +/- 121 days post-MI. Follow up was 362 +/- 241 days (70 deaths). The association between traditional time and frequency-domain HRV and mortality and nonlinear HRV and mortality were compared for the entire population (ALL), those without coronary artery bypass graft post-MI (no CABG), and those without CABG or diabetes (no CABG, no DIAB) using univariate and multivariate Cox regression analysis. Strength of association was compared by P values and Wald Chi-square values. Nonlinear HRV included short-term fractal scaling exponent, power law slope, and SD12 (Poincare dimension). For ALL and for no CABG, increased daytime SD12 had the strongest association with mortality (P=0.002 ALL and P <0.001 no CABG). For no CABG, no DIAB increased 24-hour SD12 hours had the strongest association (P <0.001) with mortality. Upon multivariate analysis, increased SD12, decreased ln ULF (ultra low frequency), and history of prior MI and history of congestive heart failure each remained in the model. CONCLUSION: Nonlinear HRV is associated with mortality post-MI. However, as with traditional HRV, this is diluted by CABG surgery post-MI and by diabetes. Results suggest that decreased long-term HRV and increased randomness of heart rate are each independent risk factors for mortality post-MI.     

Circadian rhythm of heart rate variability after acute myocardial infarction and its influence on the prognostic value of heart rate variability

This study examined heart rate (HR) variability in patients surviving acute myocardial infarction (AMI) to find the optimum time and duration of recording of the ambulatory electrocardiogram for the prediction of the risk of sudden cardiac death, or serious arrhythmic events, or both. Twenty patients (group I) who initially survived an AMI but later experienced serious events (death or symptomatic sustained ventricular tachycardia) during a 6-month follow-up were compared with 20 patients (group II) who remained free of complications for greater than 6 months after discharge. Groups I and II were matched with regard to age, gender, infarct site, ejection fraction, and beta-blocker treatment. HR variability was assessed in the 24-hour electrocardiograms recorded during the first 2 weeks after an AMI and in various portions of the complete 24-hour recording, with both the beginning and the length of the analyzed portion varied by 20 minutes (a total of 5,113 possibilities). The maximum reduction of HR variability in group I patients was systematically found when assessing HR variability in recordings starting approximately at 6 A.M. and lasting for approximately 8 hours. In the low-risk patient, the diurnal rhythm of HR variability is more marked than in the high-risk patient and the long-term components of HR variability due to the diurnal variation must be included in the measurement of HR variability when using it as a long-term predictor of risk from arrhythmic events after an AMI.     

Low frequency spectral component of heart rate variability and myocardial beta-adrenoceptor density after acute myocardial infarction

Objective The low frequency spectral component (LF; 0.04–0.15 Hz) of heart rate variability (HRV) is considered to be an index of sympathetic modulation of sinus node activity under physiological conditions, although the relationship is less clearly defined in non-physiological conditions. Several cardiovascular diseases are characterized by an absent or blunted 24-h pattern of the LF spectral component. The aim of the present study was to investigate the relationship between chronically increased neural sympathetic efferent drive to the heart, quantified in terms of downregulation of myocardial β-receptors, and the 24-h power of the LF spectral component in patients after acute myocardial infarction. Methods In 24 patients, HRV was analyzed for a 24-h period, one month after an uncomplicated Q wave myocardial infarction. The following time domain measures and spectral components were calculated: mean RR, SDNN, SDANN, RMSSD, SDNN index, pNN50, and very low frequency (VLF), low frequency (LF) and high frequency (HF) spectral components. The density of β-adrenoceptors was measured in vivo by positron emission tomography (PET) with ¹¹C-CGP-12177. Results Post-AMI patients had normal plasma levels of adrenaline and noradrenaline (respectively 1.48 ± 0.18 and 0.28 ± 0.03 IU/L) but reduced myocardial β-adrenoceptor density (6.86 ± 0.24 pmol/g). Patients had similar heart rates but lower values of SDNN and SDANN compared with control subjects. The absolute and normalized power of the spectral components were similar in the two groups, but the usual day-night oscillation was blunted in patients. Moreover, the day-night change in the power of the LF spectral component was positively related (r = 0.51; p < 0.001) to the myocardial β-adrenoceptor density. Conclusions The loss of the day-night oscillation of the LF spectral component appears to be a significant marker of sustained sympathetic over-activity in post-AMI patients. Received: 6 June 2001, Returned for revision: 26 June 2001, Revision received: 8 August 2001, Accepted: 28 August 2001     

倍他乐克对急性心肌梗死患者心率变异性的影响

目的:探讨倍他乐克对急性心肌梗死患者早期的心率变异性的影响。方法:符合该研究入选标准的急性心肌梗死患者48例,其中未使用倍他乐克者19例为对照组,使用倍他乐克1周以上者24例为治疗组,于发病第2周末或第3周行24小时动态心电图检查,比较两组24小时最大心率(HRmax)、最小心率(HRmin)、心脏缺血总负荷(TIB)和HKV各项时域指标。结果:治疗组和对照组间HRV的HR、SDNN、SDANN、PNNS0均有显著性差异(P<0.05或P<0.01)。结论:急性心肌梗死患者早期使用β受体阻滞剂(倍他乐克)不仅能减少心脏缺血的发生而且可升高HRV,改善失衡的自主神经功能。     

Heart rate variability as an index of sympathovagal interaction after acute myocardial infarction

By analysis of spectral components of heart rate variability, sympathovagal interaction was assessed in patients after acute myocardial infarction (AMI). At 2 weeks after AMI (n = 70), the low-frequency component was significantly greater (69 +/- 2 vs 53 +/- 3 normalized units [NU], p less than 0.05) and the high-frequency component was significantly smaller (17 +/- 1 vs 35 +/- 3 NU) than in 26 age-matched control subjects. This difference was likely to reflect an alteration of sympathovagal regulatory outflows with a predominance of sympathetic activity. At 6 (n = 33) and 12 (n = 29) months after AMI, a progressive decrease in the low- (62 +/- 2 and 54 +/- 3 NU) and an increase in the high-frequency (23 +/- 2 and 30 +/- 2 NU) spectral components was observed, which suggested a normalization of sympathovagal interaction. An increase in sympathetic efferent activity induced by tilt did not further modify the low-frequency spectral component (78 +/- 3 vs 74 +/- 3 NU) in a subgroup of 24 patients at 2 weeks after AMI. Instead, 1 year after AMI, this maneuver was accompanied by an increase in the low-frequency component (77 +/- 3 vs 53 +/- 3 NU, p less than 0.05) of a magnitude similar to the one observed in control subjects (78 +/- 3 vs 53 +/- 3 NU). These data indicate that the sympathetic predominance that is detectable 2 weeks after AMI is followed by recovery of vagal tone and a normalization of sympathovagal interaction, not only during resting conditions, but also in response to a sympathetic stimulus.     

急性心肌梗塞患者心率变异性的分析

目的 探讨急性心肌梗塞患者的心纺变异性。方法 对３４例急性心肌梗塞（ＡＭＩ）患者及３０例正常对照者２４小时动态心电图进行分析,通过计算机人工确认窦性心博后,经计算机处理,算出心率变异（ＨＲＶ）的时域和频域的各项指标。结果 ＡＭＩ组与对照组的平均心动周期标准差（ＳＤＮＮ）、相邻Ｒ－Ｒ间期之差的均方根值（rＭＳＳＤ）、相邻 Ｒ－Ｒ间期差值〉５ｍｓ的百分比（ＰＮＮ５０）、低频（ＬＦ）、高频（ＨＦ）及ＬＦ／     

Heart rate versus heart rate variability in risk prediction after myocardial infarction

INTRODUCTION: The aim of this study was to evaluate and compare heart rate and heart rate variability (HRV) in risk prediction after acute myocardial infarction (MI) and to evaluate the effect of beta-blocker treatment on the prognostic performance of heart rate and HRV. METHODS AND RESULTS: Three hundred sixty-six patients underwent 24-hour Holter recording 1 to 6 days after an MI. HRV was expressed as the standard deviation of all normal-to-normal intervals. Left ventricular systolic function was evaluated using the wall motion index. Half of the patients were taking a beta-blocker at the time of Holter recording. Mean follow-up was 44 months (median 34) after MI. By the end of follow-up, 82 patients had died. Mortality at 1 and 3 years was 12.5% and 22.6%, respectively. HRV, heart rate, wall motion index, number of ventricular premature beats per hour, and ventricular tachycardia were all significantly (P < 0.05) associated with mortality in univariate analysis, independent of beta-blocker therapy. In multivariate Cox analysis, only heart rate, wall motion index, number of ventricular premature beats per hour, and age had independent prognostic value (P < 0.001). In any model, including heart rate, HRV had no predictive value. CONCLUSION: The prognostic information of HRV is contained completely in heart rate, which carries prognostic information further than that of HRV. This result was independent of beta-blocker treatment.     

Influence of residual ischaemia on heart rate variability after myocardial infarction

Despite the growing evidence for the positive predictive valueof depressed baroreflex sensitivity and/or reduced heart ratevariability after myocardial infarction, the mechanisms involvedin these autonomic alterations are not fully understood. Specifically,the possible influence of residual ischaemia has not been assessed. To address this problem we studied the spectral analysis ofheart rate variability in 21 patients with a first myocardialinfarction in whom the only clinical correlate was the presenceof residual ischaemia, as documented by the positive responseto both an exercise stress test and an echocardiographic stresstest. Data from these patients were compared with those obtainedin a group of postmyocardial infarction patients similar forseveral risk factors, age, site of myocardial infarction, butwithout residual ischaemia. Patients positive for residual ischaemiahad lower power in the whole spectrum (1146±158 vs 1631±159ms², P=0—032) as well as in the low and high frequencybands of heart rate variability. A nocturnal increase in highfrequency was observed in those without residual ischaemia (from167 ± 35 to 242 ± 51 ms², +45%, P0·034),but not in those with residual ischaemia (from 111 ±19 to 141 ± 29 ms², +27%, ns). Thus, residual ischaemia reduces heart rate variability aftermyocardial infarction. The autonomic effects of residual ischaemiaprobably contribute to its negative prognostic value after myocardialinfarction.     

Frequency domain measures of heart period variability and mortality after myocardial infarction.

BACKGROUND. We studied 715 patients 2 weeks after myocardial infarction to establish the associations between six frequency domain measures of heart period variability (HPV) and mortality during 4 years of follow-up. METHODS AND RESULTS. Each measure of HPV had a significant and at least moderately strong univariate association with all-cause mortality, cardiac death, and arrhythmic death. Power in the lower-frequency bands--ultra low frequency (ULF) and very low frequency (VLF) power--had stronger associations with all three mortality end points than power in the higher-frequency bands--low frequency (LF) and high frequency (HF) power. The 24-hour total power also had a significant and strong association with all three mortality end points. VLF power was the only variable that was more strongly associated with arrhythmic death than with cardiac death or all-cause mortality. In multivariate Cox regression models using a step-up approach to evaluate the independent associations between frequency domain measures of heart period variability and death of all causes, ULF power was selected first (i.e., was the single component with the strongest association). Adding VLF or LF power to the Cox regression model significantly improved the prediction of outcome. With both ULF and VLF power in the Cox regression model, the addition of the other two components, LF and HF power, singly or together, did not significantly improve the prediction of all-cause mortality. We explored the relation between the heart period variability measures and all-cause mortality, cardiac death, and arrhythmic death before and after adjusting for five previously established postinfarction risk predictors: age, New York Heart Association functional class, rales in the coronary care unit, left ventricular ejection fraction, and ventricular arrhythmias detected in a 24-hour Holter ECG recording. CONCLUSIONS. After adjustment for the five risk predictors, the association between mortality and total, ULF, and VLF power remained significant and strong, whereas LF and HF power were only moderately strongly associated with mortality. The tendency for VLF power to be more strongly associated with arrhythmic death than with all-cause or cardiac death was still evident after adjusting for the five covariates. Adding measures of HPV to previously known predictors of risk after myocardial infarction identifies small subgroups with a 2.5-year mortality risk of approximately 50%.