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 Table of Contents  
ORIGINAL ARTICLE
Year : 2017  |  Volume : 7  |  Issue : 3  |  Page : 109-112

Effect of cigarette smoking on myocardial workload in young adults


Department of Physiology, Veer Surendra Sai Institute of Medical Sciences and Research, Burla, Odisha, India

Date of Web Publication15-Sep-2017

Correspondence Address:
Sunil Kumar Jena
Department of Physiology, Veer Surendra Sai Institute of Medical Sciences and Research, Burla - 768 017, Odisha
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/AIHB.AIHB_6_17

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  Abstract 


Background: Cigarette smoking is a major independent risk factor for coronary artery disease and other cardiovascular (CV) events. Cigarette smoking causes sympathovagal imbalance leading to various CV events. Thus, this study was proposed to evaluate the status of smoking in young adults and its effect on myocardial workload. Materials and Methods: This case–control study was conducted among 60 smokers (case) and 48 non-smokers (control). Participants selected for this study (both cases and controls) were MBBS students of a health university in Odisha. Cigarette smoking status was quantified by pack year (PY). Recordings of blood pressure (BP) and heart rate (HR) were done between 7.30 and 8.30 am after taking 10 min rest. HR was calculated by carotid pulsation. Recording of BP was done in the right arm sitting position, auscultatory method. Two parameters i.e., systolic BP (SBP) and HR were used to calculate rate pressure product (RPP). Results: Smoking status suggested that the smokers recruited were of low intensity of smoking or light smokers. HR, SBP and RPP of smokers were more than that of non-smokers. This variation was found to be significant at P < 0.0001. A quantitative analysis suggested that smokers had 19.25 times more risk to develop CV disease than non-smokers which was also significant at P < 0.0001. Conclusion: Various studies suggested that heavy chronic smokers are suffered from CV diseases. This study suggested that short duration of smoking as well as smoking history of low PY increases myocardial workload and risk of heart disease.

Keywords: Cardiovascular risk, cigarette smoking, myocardial workload


How to cite this article:
Jena SK. Effect of cigarette smoking on myocardial workload in young adults. Adv Hum Biol 2017;7:109-12

How to cite this URL:
Jena SK. Effect of cigarette smoking on myocardial workload in young adults. Adv Hum Biol [serial online] 2017 [cited 2020 Apr 7];7:109-12. Available from: http://www.aihbonline.com/text.asp?2017/7/3/109/214897




  Introduction Top


Cigarette smoking is reported as one of the well-established strongest risk factors for cardiovascular (CV) disease including coronary artery disease, stroke, sudden death, peripheral artery disease and aortic aneurysm.[1] There are several proposed physiological mechanisms involved in CV events because of cigarette smoking, sympathetic overactivity is one of the most important mechanisms among them.[2] It has also been reported that there is a strong relationship between cigarette smoking and decreased cardiac vagal activity with increased cardiac death.[3] There is also evidence that decreased cardiac vagal activity and sympathetic overactivity have also been observed as short-term effects of cigarette smoking.[4]

It has been proved that myocardial oxygen consumption (MVO2) is a major haemodynamic indicator of cardiac economy. The MVO2 is determined primarily by heart rate (HR), left ventricular mass and volume, myocardial contractility and also by external work of heart and blood pressure (BP).[5] In clinical practice, MVO2 can be very well estimated by the measurement of the double product or rate pressure product (RPP), since the latter is highly correlated with myocardial oxygen demands.[5],[6],[7] Therefore, RPP is a good indicator of myocardial work and is inversely related to cardiac economy.[5] The components of RPP, i.e., HR and systolic BP (SBP), are important indicators of CV health and fitness. Lower HR at rest and during exercise indicates physical status of individuals and is related with improved physical fitness.[8],[9],[10],[11],[12],[13] Higher values of HR and SBP at rest, as well as their increased variability and response during exercise, are important risk factors for future CV morbidity and prognostic indicators of cardiac disease.[14],[15],[16] Chronic smokers usually exhibit elevated myocardial workload and reduced exercise capacity, and thus, lower overall CV fitness.[5],[17],[18] Few studies have examined the chronic effects of smoking on resting values of BP, HR and RPP in young healthy adults and they have yielded conflicting results. A very few studies have been done to observe the effect of low intensity of smoking on BP, HR and RPP. The aim and objective of this study was:

  1. To assess smoking status of young adults
  2. To evaluate the effect of cigarette smoking on HR, SBP and RPP
  3. To quantify the association between cigarette smoking and risk of heart disease.



  Materials and Methods Top


This study was conducted in the department of physiology in an medical college of Odisha. This study was approved by the institutional ethical committee and institutional review board of a local institution. This study was accomplished between January 2016 and December 2016. In this case–control study, researchers hypothesised to prove the effect of cigarette smoking on myocardial workload in young adults. For this study, MBBS students were selected as the participants. A total of 108 male medical students were selected and categorised according to case (smoker) and control (non-smoker) groups. Case group included 60 smokers while control group included 48 non-smokers. A case means an apparently healthy young male medical student who was a current cigarette smoker having a minimum of 1 year of smoking history. A control means an apparently healthy young male medical student who has not smoked any cigarette or consumed any nicotine product. Students having any CV disease, respiratory disease, endocrine disease, renal disease, neural disease, hypertension, family history of diabetes mellitus and occasional smokers were excluded from the study. For selection of participants, an information sheet was prepared which included name, age, smoking history, disease history and family history of disease. The information sheets were distributed among 200 male medical students and they were instructed to answer the questions honestly. They were given confidence that their name would not be disclosed. Out of 200 information sheets, 178 were returned. After analysis of returned information sheets, 108 students were selected for this study. On the basis of selection criteria of cases and controls, 60 students were included in the case group and 48 were included in the control group. Severity of smoking was evaluated by calculating pack year (PY). Two parameters i.e., years of smoking and number of cigarettes smoked per day were used to calculate PY by the formula given below.[19]

No. of PYs = No. of cigarettes smoked per day × No. of years smoked/20.

From PY estimation, we found that all the smokers were low intensity smokers or light smokers. Participants were clarified about the purpose and output of the study. An informed written consent was obtained from each participant. All participants, both case and control groups, were subjected to the measurement of HR and BP. All recordings were done between 7.30 a.m. and 8.30 a.m. after 10 min rest. HR was calculated by palpating carotid pulsation for 30 s and rate per minute was calculated. Similarly, carotid pulsation was recorded thrice at an interval of 1 min, and the average of three was taken as the average HR. BP was recorded by auscultatory method using Elkometer sphygmomanometer. Recording of BP was done in the right arm sitting position. RPP was calculated by the following formula.[20]

RPP = (SBP × HR) × 10−2

Statistical analysis was done by statistical software Statistical Package for the Social Sciences, version 16 (IBM Corporation, Armonk, New York, USA). Unpaired t-test was used to compare data between cases and controls. Odds ratio (OR) was used to quantify the association between cigarette smoking and risk of CV events. P < 0.05 was considered statistically significant. Generation of tables and graphs was done by Microsoft Word and Excel.


  Results Top


This study was performed by recruiting 108 apparently healthy individuals distributed in case and control groups. Case group included 60 (56%) smokers and control group included 48 (44%) non-smokers. All the participants were young adult male and were within a narrow age range of 19–24 years.

[Table 1] depicts the basic variables of smokers and data expressed in minimum, maximum and mean ± standard deviation (SD) form. Minimum and maximum duration of cigarette smoking was 1 year and 13 years, respectively; with mean duration of 3.6 years and SD of 2.95. Minimum and maximum number of cigarettes smoked per day was 2 and 12, respectively; with the mean number of cigarettes smoked per day was 3.8 and SD was 2.1. Minimum and maximum PY was 0.1 and 3.3, respectively; mean PY was 0.677 with SD of 0.671. These data suggested that smokers selected in this study were low intensity smokers or can say light smokers.
Table 1: Smoking history of cases

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[Table 2] depicts the comparison of haemodynamic variables between cases and controls. Mean HR of case group was 84/min with SD of 9.1, while in control group, it was 75/min with SD of 5.24. This variation of HR between cases and controls was statistically significant at P < 0.0001. Mean SBP of case group was 133 mmHg with SD of 10.5 while that of control group was 117 mmHg with SD of 7.5. This variation was statistically significant at P < 0.0001. Mean RPP of cases was 113.9 with SD of 1.94 while mean RPP in control group was 88.6 with SD of 1.19. This variation was statistically significant at P < 0.0001.
Table 2: Comparison of haemodynamic variables

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[Table 3] depicts the quantitative association between cigarette smoking and risk of CV disease. Out of the 60 smokers, RPP of 44 was more than 100. Out of the 48 non-smokers, RPP of 6 was more than 100. OR determined that the smokers had 19.25 times more risk to develop CV disease than non-smokers.
Table 3: Quantitative association between smoking and risk of heart disease

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  Discussion Top


The present study evaluated the effect of cigarette smoking on myocardial workload in young adults. All smokers in this study were of low intensity smokers or light smokers. For estimation of MVO2 and workload, various invasive and imaging techniques are implemented. However, this study evaluated MVO2 and workload by implementing simple non-invasive methods to measure HR, BP and RPP. To avoid gender variation of different haemodynamic variables, participants selected were of a single gender i.e., male. Similarly, to avoid age variation, participants selected were within a narrow range of age i.e., between 20 and 24 years. In this study, the major suggestive findings were the mean HR, SBP and RPP of case group (young smokers) which were more than the control group (young non-smokers). Furthermore, we found that smokers had 19.25 times more risk to develop CV disease than non-smokers. Gidding et al. in a study reported that male smokers had more resting HR and increased resting MVO2 which was similar to the result found in our study.[9] Czernin et al. in a study reported that young male smokers had more RPP and myocardial blood flow at rest which was similar to the result found in our study.[7] Some other studies reported that SBP of young smokers was higher than that of non-smokers which was similar to the result obtained in this study.[21]

It was suggested by various researchers that a number of autonomic changes are seen in smokers which is due to the effect of nicotine and other substances found in cigarette smoke.[3],[19],[22] Autonomic imbalance in smokers can be linked to the effect of nicotine-mediated stimulation of autonomic ganglia and adrenal medulla, resulting in increased discharge in cardiac sympathetic fibres.[23],[24],[25] This enhanced sympathetic activity increases HR, BP and myocardial contractility by acting on β1 adrenergic receptor and also increases coronary vasomotor tone by acting on α2 adrenoceptor.[23],[24],[25],[26] In chronic nicotinic abuse, baroreflex centres are directly affected in brain stem that reduces afferent baroreceptor sensitivity and results in elevated sympathetic tone.[27] Smoking causes impaired sympathovagal balance due to high nicotine concentration that impairs baroreceptor sensitivity which is also a known CV risk. In addition to direct nicotine effect, the increased release of neuropeptide Y as a part of physiological adjustment for autonomic balance might cause suppression of cardiac vagal tone contributing to the reduced vagal modulation in smokers.[27] Increased RPP is a known predictor of CV risk that reflects increased myocardial oxygen demand and stress.[28] Increased RPP in smokers could explain the nicotinic-induced sympathetic overactivity, causing increased coronary vasomotor tone by acting on α2 adrenoceptor.[24] Under resting condition, safe RPP should vary within 70–90. When the RPP is higher than 100, it indicates the increased risk of heart disease.[29],[30] In this study, 44 smokers and 6 non-smokers were detected whose RPP was more than 100. OR determined that the smokers had 19.25 times more risk to develop CV disease than non-smokers.


  Conclusion Top


A lot of studies had been done on chronic smokers and it has been suggested that chronic long-term smoking increases myocardial workload and risk of cardiovascular disease. This study suggested that short duration of smoking as well as smoking history of low PY increases myocardial workload and risk of heart disease. Thus, young adults should be counselled to avoid smoking so that they will remain fit and healthy.

Limitations of this study

There was a mismatch of body mass index of the participants. Could not exclude the sleep habit and stress level of the participants. HR was calculated by carotid pulsation, not by ECG because ECG is the most accurate method of HR calculation. These limitations provide further scope of future study.

Acknowledgment

It gives me immense pleasure to express my heartiest thanks to Dr. Palas Kumar Majhisamanta, intern, VIMSAR, for substantial contribution for this study.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
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