ACTA FAC. MED. NAISS. 2003; 20 (3): 169-173

Original article

THE CORRELATION BETWEEN VENTRICULAR ARRHYTHMIAS, HEART RATE VARIABILITY AND LEFT VENTRICULAR SYSTOLIC FUNCTION IN PATIENTS AFTER MYOCARDIAL INFARCTION
 

Dragan Đorđević, Stevan Ilić, Marina Deljanin Ilić, Branko Lović, Ivan Tasić, Dejan Petrović, Aleksandar Nikolić Institute for prevention, treatment and rehabilitation of rheumatic and cardiovascular diseases, Niška Banja
 

INTRODUCTION
Efforts to assess the risk of sudden cardiac death have been made since the middle of the last century when it was recognized that frequent ventricular ectopy was associated with an increased mortality rate during the first year after myocardial infarction. Subsequent studies showed that both frequency and complexity of ventricular ectopy are important risk factors following myocardial infarction (1, 2).
The mortality rate during the first year after myocardial infarction is inversely related to the left ventricular systolic function. The risk for death increases dramatically in patients with ejection fraction of less then 30% and is usually determined with the presence of ventricular arrhythmias. The left ventricular ejection fraction is the single, most powerful predictor of mortality and the risk for life-threatening ventricular arrhythmias after myocardial infarction (2). Both left ventricular dysfunction and frequent ventricular premature complexes (VPCs) roughly double the risk of death.
Several studies have implicated the autonomic nervous system as a trigger of sudden cardiac death (3, 4). Reduced vagal activity, resulting in sympathetic dominance, is associated with an increased risk for life-threatening arrhythmias during myocardial ischemia and following myocardial infarction. The two autonomic markers that have received most attention are heart rate variability and baroreflex sensitivity. The simplest measure of heart rate variability expresses the reciprocal of heart rate (RR intervals) and calculates the standard deviation of all normal beats (SDNN).
 

OBJECTIVE
The aim of this study was to examine the relationship between ventricular arrhythmias and heart rate variability in patients with reduced left ventricular systolic function.
 

MATERIAL AND METHODS
Sixty-six patients (pts) after myocardial infarction (ł10 days after the onset of the simptoms) with the frequency of premature ventricular beats higher then 10 per hour were examined. The patients were divided in two groups: the first group had 37 patients with left ventricular ejection fraction (LVEF) greater than 40% and the second group had 29 patients with LVEF Ł 40% (table 1). There was no significant difference in frequency of VPCs per hour between these two groups of patients. The frequency of use of beta blockers, ACE inhibitors and Amiodarone was similar in both groups.
Both groups of patients were compared with 20 healthy persons without significant arrhythmias, mean age 59,1 ± 5,9 years. The average number of VPCs per hour was 28,2 ± 57,5 (p < 0.001) and EF was 69,8 ± 3,7% in the control group. They didn't undergo any treatment.
In all patients and healthy persons the clinical examination and echocardiographic research (Sequoia C256) were carried out and 24 hour Holter recording (Del-Mar Avionics) was obtained with heart rate variability analyses. The following parameters of heart rate variability were analysed: standard deviation of the normal-to-normal RR (NN) intervals (SDNN), standard deviation of average NN intervals calculated over a short period - 5 minutes (SDANN), the square root of the mean squared differences of successive NN intervals (RMS-SD), the number of interval differences of successive NN intervals greater than 50 ms (N-N' > 50 ms), their 24 hours values, daily and night values and daily minus night values (D/N delta).
The folowing statistical methods were used: Student's t-test, c2 test and Pearson's correlation


RESULTS
There were 8/37 (21.6%) patients with nonsustained ventricular tachycardia (3 or more ventricular premature beats) in the first group and 7/29 (24.1%) patients in the second group. Sustained ventricular tachycardia was not found. There were no statistically significant differences among the groups according to the average number of VPCs and the degree of ventricular arrhythmias according Lown's classification. There was no statistically significant correlation between the heart rate variability and ventricular arrhythmias.
Patients from the second group had statistically significant lower average values of all parameters of heart rate variability during the period of 24 hours in comparison to the patients from the first group (SDNN 85.4 ± 26.5 ms vs. 103.5 ± 23.2 ms; p < 0.01; SDANN 74.1 ± 17.6 ms vs. 84.5 ± 21.4 ms; p < 0,05; RMS-SD 20.2 ± 8.3 ms vs. 24.9 ± 9.1 ms; p < 0,05; N-N' > 50 ms 2.1 ± 2.4 % vs. 6.4 ± 9.3 %; p < 0,05; Figure 1).
In the control group all the parameters of heart rate variability (SDNN 142.3 ± 36.7; SDANN 126.6 ± 33.1; RMS-SD 32.3±11.3; N-N'>50 ms 13.3 ± 15.7 %) were significantly greater than the values of some parameters in both groups of patients (p < 0.0001 for all examined parameters, in both groups).
Daily and nightly values of heart rate variability in the examined groups of patients are shown in table 2. All daily and nightly values of heart rate variability were significantly lower in the first group than in the second group (p < 0.05). There were no statistically significant differences between these groups of patients referring to daily minus night values. In the control group daily values of heart rate variability were: SDNNd 119.0 ± 30.7 ms, RMS-SDd 29.6 ± 10.9 ms and night values were SDNNn 102.6 ± 23.5 ms and RMS-SDn 37.4 ± 14.3 ms, and those values were significantly greater than in both groups of patients separately (p < 0.001).
There were no statistically significant correlations between LVEF and the parameters of heart rate variability in the examined groups (I and II) of patients. However, we found out weak but statistically significant correlations between left ventricular ejection fraction and the folowing parameters of heart rate variability in all the examined patients: SDNN r = 0,322 (p < 0,05); SDANN r = 0,318 (p < 0,05); RMS-SD r = 0,266 (p < 0,05); N-N' > 50 ms r = 0,258 (p < 0,05).
 

DISCUSSION
Lethal arrhythmias cause approximately half of the deaths in the first year after the miocardial infarction. Therapies designed to prevent sudden cardiac death have proved to be very effective but some are costly and not without risk. Therefore, it remains important to identify individuals who are at the greatest risk to experience sudden cardiac death after myocardial infarction and who can benefit most from therapy (5, 2).
Bilchick et al. demonstrated that SDNN has a strong and independent assotiation with mortality in patients with moderate to severe heart failure of predominatly ischemic origin, as well as a significant association with a sudden death. In that study, in a multivariate analysis, patients with SDNN < 65.3 ms had a risk ratio of 2.4 for suddan death. In our study we found out statistically significant positive correlation between parameters of heart rate variability and left ventricular ejection fraction (6).
The main predictor for sudden cardiac death in patients with myocardial infarction is left ventricular ejection fraction lower than 35%. The second important predictor for sudden cardiac death, without myocardial ischemia are VPCs. We did not find any statistically significant correlation between VPCs and the parameters of heart rate variability, as the markers for autonomic nervous system activation. Such a result may be explained by multifactorial origin of ventricular arrhythmias. Sympathetic dominance is an important trigger for life-threatening arrhythmias and a suddan cardiac death. The Autonomic Tone and Reflexes After Myocardial infarction (ATRAMI) trial showed that SDNN < 70 ms carried a significant multivariate risk of cardiac mortality. The predictive value of baroreflex sensitivity or SDNN in combination with left ventricular ejection fraction was greater than each parameter considered alone. The combination of all three risk factors increased the risk of death 22-fold (3).
In our study we have examined daily and nightly values of all parameters but we found out the best correlation for SDNN with left ventricular ejection fraction. However, only 24 hour SDNN from time domain heart rate variability may be used as a parameter with greater importance for risk stratification.
 

CONCLUSION
Patients with the reduced left ventricular ejection fraction had lower parameter values of heart rate variability than the patients with preserved left ventricular ejection fraction. There was weak but statistically significant correlation between heart rate variability and left ventricular ejection fraction in patients after myocardial infarction. No correlation between heart rate variability and ventricular arrhythmias was found. In patients after myocardial infarction SDNN may be used as an additional parameter for both risk stratification and prognosis.
 

REFERENCES

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