Get Permission Sanjaya G, Reddy, Kumar, Anitha K S, Taklikar, and Gitte: Comparison of autonomic functions in moderate and heavy smokers using heart rate variability


Introduction

The causative factors responsible for various diseases of the cardiovascular system are many but cigarette smoking is considered a major preventable risk factor. Previous studies have shown that smoking a cigarette increases heart rate and blood pressure due to the increase in the plasma concentration of norepinephrine and epinephrine.1 Further studies confirmed smoking caused increase in sympathetic stimulation of the heart.2 It is also suggested that the incidence of arrhythmias3, 4 and cardiac arrest5 was more in cigarette smokers. Heart rate variability (HRV) has been used as a tool to measure cardiovascular dysfunction caused due to autonomic imbalance.6 In HRV analysis, low-frequency (LF) component, LF power expressed in normalized unit (LFnu) represent sympathetic function and total power (TP), high-frequency (HF) component, HF power expressed in normalized unit (HFnu) represent parasympathetic function, and ratio of LF to HF power (LF-HF ratio) gives the net result of autonomic functions.6 Many studies done earlier have established that HRV is decreased in smokers when compared to non-smokers.7 However not many studies have compared the autonomic functions in moderate smokers and heavy smokers assessed by pack years. Therefore this study is aimed to measure and compare autonomic functions in male moderate and heavy cigarette smokers.

Materials and Methods

The present study was conducted in our Physiology department. Permission to conduct the study was obtained from institutional research ethical committee. The study was conducted among male cigarette smokers in the age group between 20-50 years who were healthy. The subjects for the study were the residents of our District and selection was done by simple random sampling. After matching body mass index (BMI), detailed history was taken regarding smoking habit. The study group subjects were divided into moderate and heavy smokers taking into account the duration and amount of smoking calculated by pack years.8 Smokers having pack years between 20.1 and 40 were grouped as moderate smokers and smokers having pack years > 40 were grouped as heavy smokers, pack years was calculated using the formula.8

Figure 1
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50 smokers were selected in each group, the sample size being calculated by considering the prevalence of smoking. The prevalence of smoking being 42.4%9 with 14% acceptable error and 95% confidence interval, the sample size was calculated by using the formula, n=4pq/d2 where p is the prevalence, q is (1-p) and d being acceptable error. The sample size turned out to be 49.8 which was rounded to 50.

Smokers with history of hypertension, diabetes mellitus, active respiratory infection, other cardiovascular illness, thyroid disorders, renal and hepatic disorders, psychiatric illness, smokers taking drugs affecting autonomic nervous system and beedi smokers were excluded from the study

After explaining the procedure informed consent was taken from each subject. Detailed history and clinical examination of the subjects was done to make sure the subjects met the inclusion and exclusion criteria. On inquiring about the type of cigarettes smoked most of the smokers told they smoked filtered cigarettes. The height and weight of the subjects was measured and BMI was calculated. The subjects were instructed to have light breakfast at 8 AM and refrain from having coffee or tea. The parameters were recorded during 10 AM to 11 AM in the morning for all the subjects to minimize the circadian effects.

Before starting the procedure the subject was made to rest for 15 min in supine position. A lead II electrocardiogram was recorded for HRV analysis for duration of 5 minutes as per the recommendation of task force,6 with subject awake using the instrument Power lab 8/30 series with dual bio amplifier (Manufactured by AD instruments, Australia, with model no ML870). To record heart rate, the ECG signal which was analogus was obtained using lead II which had a QRS complex of good amplitude and stable base line. The gathered data was subjected to analysis of HRV. HRV analysis was done by inbuilt software using parameters total power (TP), high frequency power (HF), low frequency power (LF), ratio of low frequency power to high frequency power (LF/HF).

Statistical analysis and methods

Data was collected by using a structured proforma. Data entered in MS excel sheet and analysed by using EPI Info Version 7.0 software. Data was expressed in terms of Mean and Standard deviation. Comparison of mean and SD between groups was done by using Independent sample t test. A p value of <0.05 was considered as statistically significant whereas a p value <0.001 was considered as highly significant.

Results

No significant difference was observed for BMI between moderate smokers and heavy smokers. The HRV parameters namely Low frequency (LF) component, LF power expressed in normalized unit (LFnu) and LF-HF ratio which represent sympathetic activity were significantly higher in heavy smokers compared to moderate smokers. Other HRV parameters namely Total power, high frequency (HF) component and HF power expressed in normalized unit (HFnu) which represent parasympathetic activity were found significantly less in heavy smokers compared to moderate smokers.

Table 1

Group Statistics

Group

N

Mean

Std. Deviation

Std. Error Mean

BMI

Moderate Smokers

50

28.8248

4.05917

.57405

Heavy Smokers

50

29.2214

4.15548

.58767

TP

Moderate Smokers

50

2772.5278

154.02450

21.78235

Heavy Smokers

50

2359.4596

157.24279

22.23749

LF

Moderate Smokers

50

818.4040

23.30667

3.29606

Heavy Smokers

50

963.6450

7.69742

1.08858

HF

Moderate Smokers

50

448.0810

16.62493

2.35112

Heavy Smokers

50

371.5658

17.81130

2.51890

Lfnu

Moderate Smokers

50

64.6788

.99755

.14107

Heavy Smokers

50

72.1818

.94128

.13312

Hfnu

Moderate Smokers

50

35.3734

.84767

.11988

Heavy Smokers

50

27.8052

.93829

.13269

LF/HF

Moderate Smokers

50

1.8246

.06938

.00981

Heavy Smokers

50

2.5946

.12218

.01728

Table 2

t-test for Equality of Means

t

df

Sig.

(2-tailed)

Mean Difference

Std. Error Difference

95% Confidence Interval of the Difference

Lower

Upper

BMI

-.483

98

.630

-.39660

.82152

-2.02688

1.2337

TP

13.270

98

.000

413.06820

31.12839

351.29492

474.8415

LF

-41.842

98

.000

-145.24100

3.47117

-152.12942

-138.3527

HF

22.206

98

.000

76.51520

3.44567

69.67739

83.3530

Lfnu

-38.682

98

.000

-7.50300

.19396

-7.88792

-7.1181

Hfnu

42.322

98

.000

7.56820

.17883

7.21333

7.9231

LF/HF

-38.752

98

.000

-.77000

.01987

-.80943

-.7306

Discussion

The main purpose of the present study was to measure and compare autonomic functions in moderate and heavy smokers. It was observed that parameters representing sympathetic fuction such as LF, LFnu and LF/HF ratio were significantly increased in heavy smokers compared to moderate smokers. This suggests that the cardiac sympathetic activity was increased in heavy smokers compared to moderate smokers. It was observed that parameters representing parasympathetic function such a HF, HFnu and TP were significantly decreased in heavy smokers compared to moderate smokers. This suggests that the parasympathetic activity was less in heavy smokers compared to moderate smokers. The imbalance observed in autonomic functions in smokers has been attributed to the effects of nicotine and other substances present in cigarette.10, 11, 12, 13 The possible explanation for changes in HRV parameters observed in heavy smokers compared to moderate smokers is because of the higher dose and long duration of exposure to nicotine and other substances found in cigarettes.

The effects of smoking of conventional cigarettes on autonomic control of cardiovascular system was studied by George K. Ndrikopoulos, Dimitrios J. Richter, Polychronis E. Dilaveris et al,14 the study concluded smoking causes an increase in sympathetic control and decrease in parasympathetic control of cardiovascular system. The effect of the intensity of smoking on cardiac autonomic functions measured by using HRV was studied by Ana Paula Soares dos Santos, Dionei Ramos, Gabriela Martins de Oliveira.15 The study concluded that the intensity of smoking had an influence over the autonomic regulation of cardiac functions, it was seen that autonomic regulation was less functional in heavy smokers than in moderate smokers.15 In our study same observations were made. Sultana Ferdousi, Mehboba Ferdous, Md. Saiful Islam16 studied influence of smoking on autonomic functions considering different intensity of exposure, they used HRV as a measuring tool and concluded that smoking causes an increased sympathetic stimulation leading to autonomic dysfunction of cardiovascular system,16 similar observations were made in our study also.

The strength of our study was we compared autonomic functions in smokers by classifying them taking into account both the dose and duration of smoking exposure. The limitations of the study were we relied on the history given by smokers for classifying smokers, and there is a possibility that the information given may not be accurate. Studies in future can be done by considering the plasma nicotine level of each smoker.

Conclusion

Autonomic imbalance characterized by increased sympathetic function with associated decrease in the cardiac vagal modulation was seen in heavy smokers compared to moderate smokers. Taking into account the high prevalence of smoking, also knowing that various diseases are associated with smoking, health education of general population should be done to decrease the cardiovascular morbidity.

Source of Funding

None.

Conflict of Interest

The authors declare no conflict of interest.

References

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S Ferdousi M Ferdous MS Islam Impact of smoking status on autonomic functions assessed by spectral analysis of heart rate variabilityInt J Clin Exp Physiol2014115762



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Article History

Received : 21-01-2022

Accepted : 29-01-2022


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https://doi.org/ 10.18231/j.ijcap.2022.007


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