ABSTRACT Background: Smoking now is identified as a major cause of respiratory diseases, heart related ailments, cancer and a wide variety of other health problems. The total number of tobacco users in the world has been estimated at 1.2 billion, which is expected to rise 1.6 billion during 2020’s.At present, tobacco use causes death of    3.5 ­to 4 million people globally and expected to increase about 10 million during 2020’s. It is well known that the acute effects of smoking produce an increase in systolic and diastolic blood pressure, tachycardia, cardiac output and vasoconstriction, increase in carotid artery occlusion, and sometimes instantaneous MI.  The present study is being undertaken to study the effects of smoking on electrocardiogram and blood pressure among smokers and non-smokers.Objectiv   To study the variation of ECG wave forms in healthy young smokers compared to nonsmokersMethodology: The study was conducted in the Department of Physiology, Vijayanagar Institute of Medical Sciences, Bellary, Karnataka. The study included 100 apparently healthy males, 50 smokers and 50 non-smokers, between ages 20-35 years. Demographic data, history of smoking habit (quantity and duration) and detailed medical history were obtained from the subjects. Electrocardiogram was recorded during resting state in supine position. The ECG recordings were evaluated for different parameters like heart rate, PR interval, QRS complex, QRS axis, QT interval, QTc interval, ST segment, Q wave and T wave. Results were compared from the two groups using statistical tools.Results: There was statistically significant increase in heart rate, decrease in PR interval, decrease in QT interval, increase in QTc interval, decrease in QRS axis, decrease in T wave amplitude, occurrence of Q wave in smokers when compared to non-smokers.

 

Conclusion: The study shows that there were numerous ECG changes in the absence of any cardiac disease in smokers.

 

Key words: Smokers; Non-smokers; Electrocardiography, ECG changes

INTRODUCTION

 

According to U.S. Surgeon General, “It is safe to say that smoking represents the most extensively documented cause of disease ever investigated in the history of biomedical research.”1

 

The habit of smoking is extensively practiced among world population from time immemorial. Recent research has shown that the hazards of prolonged cigarette smoking are even greater than used to be supposed. Smoking now is justified as a major cause of respiratory diseases, heart related ailments, cancer and other wide variety of other health related problems. The total number of tobacco users in the world has been estimated at 1.2 billion, which is expected to rise to 1.6 billion during year 2020’s. At present, tobacco use causes death of 3.5 to 4 million people globally and expected to increase about 10 million during year 2020’s.2

 

In India, according to a nation wide survey, carried out showed 184 million used tobacco, of which 112 million smoked tobacco. It kills 8 lakh people every year according to Indian Council of Medical Research (ICMR) which amounts to 2200 people dying every day from tobacco related diseases. Also revealed that each patient suffering from tobacco related disease costs the country Rs.2.5 million through direct medicinal costs, absenteeism, for treatment & loss of income due to premature death.3 In Karnataka too, tobacco use has reached a prevalence of 41% among men & 14.9% among women which is now escalating to higher levels.

 

 

 

It is well known that the acute effects of smoking produce an increase in systolic and diastolic blood pressure, tachycardia, cardiac output and vasoconstriction, increase in carotid artery occlusion, and sometimes instantaneous MI.4,5

Nicotine, which is the main component of tobacco, causes sudden coronary death6. It also has propensity to provoke ventricular arrhythmias7,8. A longer retention of nicotine occurs in the blood and in other specific tissues including the heart via a constant exposure9. In the heart it can result in profound electrophysiological alterations.

The 12-lead electrocardiogram (ECG) is a routine, inexpensive tool for assessment of cardio-vascular disease and its risk in both clinical and research settings, and ECG changes powerfully predict future CVD events10,11.

Hence the present study is being undertaken to study the effects of smoking on electrocardiogram and thereby creating awareness among people.

 

 

OBJECTIVE OF THE STUDY

To evaluate variations in ECG waves, segments and intervals in apparently healthy young smokers and thus test whether smokers have significant ECG changes compared to non-smokers.

 

 

 

 

MATERIALS AND METHODS

The study was conducted at the Physiology department, VIMS, Bellary.

Source of data:

Cases were apparently healthy male smokers between ages 20-35 years, selected from among students and staff of the institute, and attendants of patients visiting outpatient departments at the hospital. Non-smoking male controls of the same age group were selected from the same pool. The nature and purpose of the study were described to the subjects and informed consent was obtained from those willing to participate in the study.

A pre-structured proforma was given to each subject to record personal details and pertinent medical history from both cases and controls. Details of smoking habit, that is duration and quantum of smoking, were obtained from cases. For each subject in the case group, number of pack years was calculated. One pack year = 20 cigarettes smoked per day for a duration of one year.

Physical examination included measurement of height in centimeters, weight in kilograms, recording resting pulse rate by palpating radial artery and blood pressure recording with a mercury sphygmomanometer. Clinical examination of cardiovascular and respiratory systems was done in detail.

Persons with diagnosed hypertension, history of cardiac, respiratory, renal and endocrine disorders, abuse of alcohol and other psychoactive substances, family history of hypertension and cardiac diseases, history of anxiety or depressive disorders, were excluded. The final study group consisted of 50 smokers and 50 non-smokers.

The subjects were asked to visit the clinical physiology laboratory of the department of Physiology, in the morning hours between 9 AM to 12 noon. Each subject was allowed to rest in supine posture for 15 minutes before recording was done. After the period of rest, pulse rate was recorded in beats per minute by palpating Radial artery for one minute. Blood pressure was measured using mercury sphygmomanometer, from the left upper arm, with the subject in supine position.

 

Following the standard procedure, 12 lead electrocardiogram was recorded using Magic R 12 channel Electrocardiograph designed by Medline’s team of biomedical engineers.

 

The ECG was evaluated for different parameters like heart rate, PR interval, QRS complex, QRS axis, QT interval, QTc interval, ST segment, Q wave and T wave.

 

The data was compiled in Microsoft excel and analyzed using SPSS (Statistical Package for Social Sciences) version15. Level of significance was fixed at p < 0.05.

 

 

 

 

RESULTS

Mean age of study subjects was 27.94 +/- 4.25 years. Mean age of smokers: 28.06 +/- 4.01 years and mean age of non-smokers: 27.82 +/- 4.52 years. The two groups were age matched (p value- 0.97).

Mean weight of smokers was 54.5 +/- 4.13 kg and nonsmokers was 55.84 +/- 5.81 kg (p=0.084). Mean height of smokers and nonsmokers was 1.62+/-0.056m and 1.63+/-0.051m respectively (p=0.056). Mean BMI in the two groups was 20.58+/-1.03 kg/m2 and 20.89+/-1.46 kg/m2 (p+0.072). The two groups were matched in terms of weight, height and BMI.

Table 1: Comparison of BP and Pulse rate between smokers and non-smokers

Measurements

Smokers (N – 50)

Mean +/- Sd

Non-smokers ( N- 50)

Mean +/- Sd

P value*

Pulse rate (beats/min)

87.20 +/- 5.66

78.36 +/- 4.22

0.000

Systolic BP (mm Hg)

121.56 +/- 2.47

118.68 +/- 3.01

0.000

Diastolic BP (mm Hg)

80.60 +/- 1.29

79.32 +/- 2.04

0.000

* student‘t’ test

It is evident from the above table that resting pulse rate, Systolic BP and Diastolic BP were all significantly higher in smokers compared to non-smokers (p < 0.05).

 

 

 

 

 

 

Table 2: Comparison of PR and QRS interval between smokers and non-smokers

Measurements

Smokers (N – 50)

Mean +/- Sd

Non smokers ( N- 50)

Mean +/- Sd

P value*

PR interval (sec)

0.143 +/- 0.006

0.155 +/- 0.01

0.00

QRS interval (sec)

0.081 +/- 0.007

0.079 +/- 0.004

0.26

* student‘t’ test

 

PR interval (mean) was significantly shortened among smokers compared to non-smokers. But there was no statistically significant difference in QRS interval between the two groups.

 

Table 3: Comparison of QT interval, QTC interval and QRS axis between smokers and non smokers

Measurements

Smokers (N – 50)

Mean +/- Sd

Non smokers ( N- 50)

Mean +/- Sd

P value*

QT interval (sec)

0.34 +/- 0.03

0.36 +/- 0.02

0.04

QTC interval (sec)

0.39 +/- 0.016

0.38 +/- 0.012

0.00

QRS  axis (degrees)

42.62 +/- 12.16

65.44 +/- 7.22

0.00

* student‘t’ test

 

QT interval (mean) was significantly lesser among smokers compared to non-smokers. But QTC interval was slightly higher among smokers than non smokers and also this was found to be statistically significant. There was significant difference in mean QRS axis in the two groups.

Table 4: Comparison of ‘T’ wave configuration between smokers and non- smokers.

 

Lead Smokers Non smokers P value*
N F I N F I
Lead I 50 (100%) 00 00 50(100%) 00 00 ——
Lead II 50 (100%) 00 00 50(100%) 00 00 ——
Lead III 12 (24%) 9 (18%) 29(58%) 23 (46%) 6(12%) 21(42%) 0.02
Lead aVR 50 (100%) 00 00 50(100%) 00 00 ——
Lead aVL 50 (100%) 00 00 50(100%) 00 00 ——
Lead aVF 48 (96%) 00 2 (4%) 50(100%) 00 00 0.49
Lead V1 12 (24%) 4(8%) 34(68%) 22 (44%) 00 28(56%) 0.03
Lead V2 39 (78%) 00 11(22%) 50(100%) 00 00 0.00
Lead V3 39 (78%) 00 11(22%) 50(100%) 00 00 0.00
Lead V4 45 (90%) 1(2%) 4 (8%) 50(100%) 00 00 0.02
Lead V5 50(100%) 00 00 50(100%) 00 00 —–
Lead V6 50(100%) 00 00 50(100%) 00 00 —–

* chi square test          N – normal,  F – flat, I – inverted

In Lead III, smaller percentage of smokers had normal wave and larger percentage had flat or inverted wave compared to non-smokers. This difference was found to be statistically significant. Leads V1 to V4 showed significantly greater proportion of smokers having inverted T waves compared to non-smokers.        

 

 

Table 5: Comparison of occurrence of ‘Q’ wave in limb leads between smokers and nonsmokers

Lead

Smokers

Non smokers

P value*

Present

Absent

Present

Absent

Lead I

7 (14%)

43 (86%)

2 (4%)

48 (96%)

0.04

Lead II

21(42%)

29 (58%)

12(24%)

38 (76%)

0.03

Lead III

27(54%)

23 (46%)

21(42%)

29 (58%)

0.23

Lead aVR

3 (6%)

47 (94%)

00

50(100%)

0.24

Lead aVL

13(26%)

37 (74%)

4 (8%)

46 (92%)

0.04

Lead aVF

19(48%)

31 (62%)

15(30%)

35(70%)

0.39

Lead V1

00

50(100%)

2 (4%)

48 (96%)

0.15

Lead V2

00

50(100%)

00

50(100%)

—–

Lead V3

00

50(100%)

00

50(100%)

—–

Lead V4

7(14%)

43 (86%)

6 (12%)

44 (88%)

0.76

Lead V5

27(54%)

23 (46%)

26(52%)

24 (48%)

0.84

Lead V6

30(60%)

20 (40%)

26(52%)

24 (48%)

0.42

 

In recordings from Leads I, II and aVL, statistically significant proportion of smokers had Q wave, compared to nonsmokers.

 

 

 

 

 

 

Table 6: Comparison of ECG parameters among smokers based on pack-years

Parameters 1 – 3 pack yrs 4 – 6 yrs 7 – 9 yrs P value*
P wave amplitude 1.07 1.02 1.01 0.13
P wave duration 0.080 0.082 0.082 0.58
PR interval 0.163 0.163 0.165 0.72
QRS 0.076 0.081 0.081 0.25
QT 0.33 0.34 0.34 0.62
QTC 0.38 0.39 0.40 0.00
QRS axis 42.67 43.46 42.26 0.95

* ANOVA test            (above values are mean values)

There was no statistically significant difference in ECG parameters among smokers with different number of pack-years.

 

DISCUSSION

In this case control study, it was found that resting heart rate, systolic and diastolic blood pressure were higher among smokers compared to controls matched for age, gender and BMI. High resting heart rate is an indicator of high sympathetic tone12. The increase in heart rate and blood pressures could be due to stimulation of sympathetic ganglia and discharge of catecholamines from adrenal medulla.13

 

Changes in ECG parameters:

PR interval:

In this study, PR interval (mean) was shortened among smokers compared to nonsmokers. This result finding was in agreement with Baden L et al14 and Khan IS et al15

Cigarette smoking increases the velocity of conduction and shortens the effective refractory period at the AV node.13 This could predispose to greater incidence of cardiac rhythm disorders in smokers16.

 

QRS Axis:

In this study, the mean QRS axis showed statistically significant decrease in smokers when compared to nonsmokers. Venkatesh G and Swamy RM13 found decreased QRS axis in smokers when compared to nonsmokers but the difference was not significant, whereas Chatterjee S, et al17 found QRS and P axes differed significantly between smokers and non-smokers. The rate of shifting of these axes to the left with increasing age was relatively higher in non-smokers. These results indicate that aging affects electrocardiographic wave patterns and that this aging effect is modified by long term smoking.

 

QT and QTc  interval:

QT interval was less among smokers compared to nonsmokers while            QTC interval was slightly higher among smokers than nonsmokers. Similar finding was reported by Dilaveris P et al18

 

The Ventricular repolarization is altered in young male cigarette smokers. The differences in the heterogeneity of ventricular repolarization between smokers and nonsmokers are mainly due to heart rate differences between the 2 study groups. 18

Shortened QT and ST intervals indicate shortened duration of ventricular repolarization. The cardio-mechanical correlate of this finding is that there could be shortening of ventricular filling phase during which major coronary flow occurs. Insufficient myocardial perfusion may predispose to ischeamic cardiac disease19.

 

T wave:

Occurrence of   T wave abnormalities was different in recordings from different leads. But on the whole, it was observed with greater frequency in smokers than in nonsmokers. Baden L et al14,Dilaveris P et al18,Chatterjee S et al17.and Khan IS et al15  found that R, S and T wave amplitudes were decreased at higher rates in smokers than non-smokers. The mechanism for the decrease in R, S and T wave amplitude is unknown. It might be that smoking has a direct effect on ventricular electrical activity. An alternative explanation is that smoking results in acceleration of atherosclerosis, which in turn leads to non-specific R, S and T wave changes14.

 

Q wave:

Q wave was seen more often in smokers than in nonsmokers.

Gupta R et al20  found there was higher frequency of ECG-Q waves in smokers. Similar findings have emerged in other major studies as well21.   This finding has been considered to be indicative of myocardial scarring by some workers. Also it has been found from prospective studies that the age-independent association between baseline major Q-waves and smoking burden in pack-years supports the idea that increased lifetime smoking burden increases CVD risk and that increased CVD risk related to long-term smoking can be detected by the 12-lead ECG22.

In the present study, we could not establish a relationship between presence of ECG changes and the number of pack years. Possible reason for this is less number of subjects in each pack-year group. However, such correlation has been found by other workers22. Such a correlation may emerge from long term prospective follow up study involving larger number of subjects.

Though at the current stage, it is not possible to explain all the ECG changes caused by smoking, it has been proposed that Nicotine, which is the main component of tobacco, may be the causative agent. The cardiac effects of nicotine are attributed to the release of catecholamines23, which are released due to the binding of nicotine to the nicotinic cholinergic gate on the cation channels in receptors throughout the body. Nicotine also facilitates a conduction block and a re-entry and it increases the vulnerability to a ventricular fibrillation24. Nicotine is a potent inhibitor of the cardiac A type potassium channels, which contributes to the changes in the electrophysiology which manifest as ECG changes25.

In the general population, major and minor ECG changes predict increased mortality11,26. Individuals who smoke are more likely to have ECG findings consistent with ischemic heart disease27, structural heart disease28, and cardiac rhythm disorders16. Such changes have been found even in young individuals with lesser number of pack years.

As ECG is a very inexpensive diagnostic technique available even in basic health care facilities, and its application and analysis is easy for health care professionals, it can be made use of to detect early changes in smokers to evaluate possible risk of cardiovascular morbidity, and also to counsel smokers and motivate them to quit smoking. As smoking is one of the most important modifiable risk factors in cardiovascular disease, early intervention in young smokers will go a long way in decreasing the overall burden of the said disease in the community.

CONCLUSION

The following conclusions can be drawn from the results of this study:

  • Smoking induces significant alteration in cardiac electrophysiology and heamodynamics in apparently healthy young individuals, which may predispose to cardiovascular morbidity and mortality in the long run.
  • Smoking induced alterations manifest as significant variation in waveforms in ECG recordings of even asymptomatic smokers when compared to nonsmokers.
  • ECG can be a used as a simple and inexpensive tool to assess smoking induced damage, and to counsel and motivate smokers to quit cigarettes.

 

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First Author :

Name                                       Dr.V MALLIKARJUNA

Designation                             Associate Professor

Department                             Dept. of Physiology

Address                                   Vijayanagar Institute of Medical Sciences, Bellary

Email                                       mercury003@gmail.com

Phone                                      9844958455

Fax                                                      —

 

Corresponding Author :

Name                                       Dr.V MALLIKARJUNA

Designation                             Associate Professor

Department                             Dept. of Physiology

Address                                   Vijayanagar Institute of Medical Sciences, Bellary

Email                                       mercury003@gmail.com

Phone                                      9844958455

Fax                                                      —

 

Coauthor – 2

Names                                     Dr. PRASHANTH BABU G

Designation                             Taluka Medical Officer, Yelburga

Department                             Health & Family Welfare

Address/email/phone/ Fax      THO, Yelburga, Koppal Dist.

 

 

 

 

 

Coauthor – 3

Names                                     Dr. ARUN KUMAR S

Designation                             Professor

Department                             Dept. of Physiology

Address/email/phone/ Fax      Vijayanagar Institute of Medical Sciences, Bellary

 

 

Coauthor – 4

Names                                     Dr. PRASHANTH KS

Designation                             Assistant Professor

Department                             Dept. of Physiology

Address/email/phone/ Fax      Bangalore Medical College & Research Institute, Bengaluru.

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