ISSN: 1223-1533

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HRV IN HEART FAILURE – HOW TO INTERPRET DATA


Authors: Costel Matei




 

Heart rate variability (HRV), the variation over time of the period between consecutive heartbeats, is predominantly dependent on the extrinsic regulation of the heart rate (HR). HRV is thought to reflect the heart’s ability to adapt to changing circumstances by detecting and quickly responding to unpredictable stimuli.

The normal variability in HR is due to autonomic neural regulation of the heart and the circulatory system. The balancing action of the sympathetic nervous system (SNS) and parasympathetic nervous system (PNS) branches of the ANS controls the HR.

HRV analysis demonstrates to be an important tool for prognostic stratification in patients with cardiovascular disease with high mortality, i.e. post myocardial infarction, heart failure (HF). Studies coming from 1990 investigated this analysis in different conditions and now it is a common sense to consider decreased HRV as predictor for bad prognosis: high mortality rate, high incidence of malignant ventricular arrhythmias.

Potential confunding factors can influence the interpretation and the significance of data in specific population. HRV can independently be modified by volume overload, age, exercise training, drugs as common conditions in HF. Also co-morbidities associated to heart failure can modify HRV data (depression, sleep disorders, thyroid dysfunction).

 

Volume overload. Some small studies showed there is a statistically significant improvement in HRV with diuresis, which closely correlated with volume loss. This is the reason it is better to avoid HRV evaluation during acute decompensation  of  chronic  HF  as  it  can  give  false information if you think HRV is a predictor of survival.

 

Age. The influence of age on HRV was analyzed in healthy subjects  showing a shift towards parasympathetic dominance with aging that leads to conclusion that healthy longevity depends on preservation of autonomic function, in   particular,   HRV–parasympathetic   function.   Other studies  showed  in  older  adults  there  is  an  increasing prevalence of sinus arrhythmia (“erratic rhythm”) that is not of respiratory origin nor of autonomic influences. Thus, increased values of beat-to-beat HRV measures are completely confounded in the elderly and cannot be taken as   measures   of   parasympathetic dominance without verifying this is truly due to respiratory sinus arrhythmia rather than erratic rhythm.

 

Exercise.  It  is  very  well  known  that  regular  exercise training  produces  a  shift  of  autonomic  balance  toward higher parasympathetic activity which is consistent with improved cardiac health. This finding could explain effects of exercise training in patients with HF and the potential benefits of regular training programs in this category of patients.  Also,  the  effort  intensity  produces  different responses on HRV. Moderate intensity effort seems not to produce a significant change in HRV, but severe intensity effort  showed  an  increase  of  sympathetic  tone  both immediately and after 24 hours after exercise cessation.

 

Drugs. HRV can be influenced by various groups of drugs, so the influence of medication should be considered, while interpreting HRV. Beta-blockers and ACE-I are commonly used in HF, so their influence is important. Also, HRV can be used to quantify the efficacy of these drugs in HF.

 

Depression. Depression is frequently found in HF patients. Depression  is  associated  with  changes  in  autonomic activity  and  this  imbalance  seems  to  correlate  with increased morbidity and mortality in chronic HF patients, independent of disease severity. The decreased HRV in patients  with  major  depression  could  be  a  potential explanation  for  the  association  of  a  worse  outcome  in patients with major depression.

 

Thyroid dysfunction. Overt or subclinically hyperthyroidism can be associated with heart failure, especially in elderly or in patients with arrhythmogenic cardiomyopathy. There were some studies that have examined cardiac autonomic function in untreated and treated hyperthyroidism. Overall measures of HRV and those specific for cardiac vagal modulation are attenuated in patients with overt hyperthyroidism compared with normal subjects; measurements of HRV remained low in those with low levels of serum thyrotropin but returned to normal in patients with biochemical euthyroidism.

Also studies in patients with hypothyroidism demonstrated that   hypothyroidism   is   associated   with   a   decreased sympatho-vagal modulation of the heart rate and with an increased in-homogeneity of ventricular recovery times. Sleep deprivation and sleep disorders. A number of HRV studies  showed  the  heart  rate  and  HRV  progressively decrease during non-REM sleep and increase during REM sleep. Results are consistent with increased vagal control of HRV in non-REM sleep and increased SNS control during REM sleep.

HRV can be influenced by various sleep disorders.

There were few studies comparing HRV between insomniacs and good sleepers. A reduced HRV in insomniacs compared with control was observed across all sleep stages (REM or non-REM). Different categories of subjects were assessed in several studies (college students, drivers, nurses night shift vs. day-shift) and there was a significant increase of sympathetic vs. parasympathetic tonus in all categories mentioned.

Obstructive sleep apnea (OSA) influences also HRV. Both normalized LF and HF are significantly higher at the end of respiratory events during sleep, compared with baseline sleep, even there was no change in heart rate. HRV results are consistent with SNS enhancement during sleep due to sleep apneas and may help explain increased cardiac risk. Use of effective CPAP in patients with OSA is consistently associated with changes in both night-time and day-time HRV. CPAP-treatment in patients with dilated cardiomyopathy (ischemic or non-ischemic, LVEF <0.45) had significantly increased HF and decreased LF/HF ratio compared  to  non-CPAP  patients.  CPAP  also  improved LVEF by a significant 8%. This suggested CPAP improves PNS  modulation  of  HR  in  CHF  patients  with  OSA, improved LV function and reduced SNS activation. Further studies of HRV and CPAP in HF are needed.

 

Conclusion: HRV is an important tool for prognostic evaluation in patients with heart failure. Both time-domain and frequency-domain measurements are useful, with a slight advantage of frequency-domain analysis. Particular conditions in which this evaluation is performed should be taken into account when interpreting the results.