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Smoking impairs vagal modulation in old persons: the more we age, the more we learn
Hellenic Journal of Cardiology 58 (2017) 289e290
Contents lists available at ScienceDirect
Hellenic Journal of Cardiology journal homepage: http://www.journals.elsevier.com/ hellenic-journal-of-cardiology/
Editorial
Smoking impairs vagal modulation in old persons: the more we age, the more we learn The pathogenic mechanisms underlying the relationships between smoking and cardiovascular disease (CVD) have been the subject of innumerous investigations. Among these is the fact that smoking impairs baroreflex sensitivity, which may contribute to the smoking-induced increase in blood pressure and heart rate
and to the concomitant alterations in their variability. Moreover, the autonomic neurohumoral response that is evoked by smoking results in the downregulation of the beta-adrenergic receptors in long-term smokers1. On the positive side, it is well documented that smoking cessation can restore CVD health, both by reducing
Fig. 1. Acute effects of tobacco smoking on the sympathetic nerve activity (SNA) depend on the net balance of the sympathetic excitatory effect of cigarette smoke on the central neural outflow and the sympathetic inhibitory effect of the baroreflex, activated by the increase in blood pressure from smoking. When the baroreflex is intact, SNA is suppressed, but when the baroreflex is chronically impaired, as it is in many vulnerable populations, SNA increases. BP: blood pressure; BR: baroreflex sensitivity; SNS: sympathetic nervous system. With permission from Middlekauff HR, Park J, Moheimani RS. J Am Coll Cardiol. 20148.
Peer review under responsibility of Hellenic Society of Cardiology. https://doi.org/10.1016/j.hjc.2017.10.001 1109-9666/© 2017 Hellenic Society of Cardiology. Publishing services by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons. org/licenses/by-nc-nd/4.0/).
290
Editorial / Hellenic Journal of Cardiology 58 (2017) 289e290
sympathetic hyperactivity and by the re-establishment of parasympathetic modulation (i.e., vagal activity2). Furthermore, smoking cessation may improve blood pressure control and decrease the risk of an acute coronary event3. However, current knowledge regarding the restoration of autonomic activation after smoking cessation is restricted to results obtained from younger individuals4. Pereira et al in this issue of the Hellenic Journal of Cardiology5 address the topic of smoking effects on heart autonomic control (HAC) in older individuals with and without smoking habit. The study was done in 210 older (60 years) adults divided into 2 groups: nonsmokers or those who had stopped smoking (n¼190) and current smokers (n¼20). All participants were submitted to measurement of HAC parameters. The striking findings of the study provide clear evidence for the poor sympathovagal modulation in older adults who continue to smoke. The findings also provide further support for the benefit of smoking cessation in elders, which should be investigated in future studies with longitudinal design and/or intervention methods. The impairment of baroflex sensitivity by smoking should trigger a search for the impact of tobacco smoking in “vulnerable populations,” such as older long-term smokers. The acute effects of tobacco smoke on the sympathetic nerve activity (SNA) depend on the net balance of the sympathetic excitatory effect of cigarette smoke on the central neural outflow and the sympathetic inhibitory effect of the baroreflex, activated by the increase in blood pressure from smoking. When the baroreflex is intact, the SNA is suppressed, but when the baroreflex is chronically impaired, as it is in many “vulnerable populations” such as older individuals, the SNA increases8 (Fig. 1). In older long-term smokers with relatively impaired baroreflex function, acute smoking produces an increase in muscle SNA due to a lack of baroreflex restraint9. A question arises as to whether smoking per se rather than the age of the smoker is the cause of the impaired autonomic modulation; in other words, is smoking in older smokers merely a bystander or a causal factor? Certainly, the findings of the study indicate that both sympathetic and parasympathetic nervous systems are affected by the habit of smoking. It is important to note that, differently from previous studies6,7, the study is restricted to older adults, which could explain the wide impairment in the autonomic nervous system, owing to the additive effect of aging and smoking habit. Moreover, the adjustment of HAC parameters for potential confounders is an essential step to clarify relationships, especially regarding data obtained from older adults, considering the complex interactions between aging, CVD, metabolic diseases, cardiovascular drugs (i.e., b-blockers), lifestyle, and HAC. Cigarette smoking induces an inflammatory reaction, which has been associated with heart rate variability in middle-aged and older subjects with no apparent heart disease10. Nicotine is a chemotactic agent for the attraction and extravasation of neutrophils into the subendothelium.11 Expanding the “realm” of smoking, electronic cigarettes (ECs) have gained unprecedented popularity, but only little, and surely not enough, is known about their CVD risks12. We have recently demonstrated that EC smoking for 30 min exerts a similar unfavorable effect as that of smoking one conventional cigarette on blood pressure and aortic stiffness13. In a recent study, habitual EC use
was associated with a shift in cardiac autonomic balance toward SNA predominance in young individuals14. Preliminary data also indicate that EC smoking has a detrimental effect on sympathetic nerve activity regulation similar to tobacco smoking in healthy subjects15. An interesting question to be answered would be whether ECs induce a differential effect in HAC in older smokers.
References 1. Mancia G, Groppelli A, Di Rienzo M, Castiglioni P, Parati G. Smoking impairs baroreflex sensitivity in humans. Am J Physiol. 1997;273(3 Pt 2):H1555eH1560. 2. Clair C, Rigotti NA, Porneala B, et al. Association of Smoking Cessation and Weight Change With Cardiovascular Disease Among Adults With and Without Diabetes. JAMA. 2013;309(10):1014. 3. Bullen C. Impact of tobacco smoking and smoking cessation on cardiovascular risk and disease. Expert Rev Cardiovasc Ther. 2008;6(6):883e895. 4. Girard D, Delgado-Eckert E, Schaffner E, et al. Smoking cessation and heart rate variability: Is it possible to fully recover? Eur Respir J. 2014;44(Suppl 58):P319. 5. Pereira E, Ribeiro I, Freire I, Passos R, Casotti C, Pereira R. Smoking habit influences negatively the autonomic heart control in community-dwelling old adults. Hellenic J Cardiol. 2017;58:283e288. 6. Hayano J, Yamada M, Sakakibara Y, et al. Short- and long-term effects of cigarette smoking on heart rate variability. Am J Cardiol. 1990;65(1):84e88. 7. Harte CB, Meston CM. Effects of smoking cessation on heart rate variability among long-term male smokers. Int J Behav Med. 2014;21(2):302e309. 8. Middlekauff HR, Park J, Moheimani RS. Adverse effects of cigarette and noncigarette smoke exposure on the autonomic nervous system: mechanisms and implications for cardiovascular risk. J Am Coll Cardiol. 2014;64(16):1740e1750. 9. Hering D, Somers VK, Kara T, et al. Sympathetic neural responses to smoking are age dependent. J Hypertens. 2006;24(4):691e695. 10. Sajadieh A, Nielsen OW, Rasmussen V, Hein HO, Abedini S, Hansen JF. Increased heart rate and reduced heart-rate variability are associated with subclinical inflammation in middle-aged and elderly subjects with no apparent heart disease. Eur Heart J. 2004;25(5):363e370. 11. Benowitz N, Burbank A. Cardiovascular toxicity of nicotine: Implications for electronic cigarette use. Trends in Cardiovasc Med. 2016;26(6):515e522. 12. Ioakeimidis N, Vlachopoulos C, Tousoulis D. Efficacy and Safety of Electronic Cigarettes for Smoking Cessation: A Critical Approach. Hellenic J Cardiol. 2016;57(1):1e6. 13. Vlachopoulos C, Ioakeimidis N, Abdelrasoul M, et al. Electronic Cigarette Smoking Increases Aortic Stiffness and Blood Pressure in Young Smokers. J Am Coll Cardiol. 2016;67(23):2802e2803. 14. Moheimani RS, Bhetraratana M, Yin F, et al. Increased Cardiac Sympathetic Activity and Oxidative Stress in Habitual Electronic Cigarette Users: Implications for Cardiovascular Risk. JAMA Cardiol. 2017;2(3):278e284. 15. Tsioufis C, Dimitriadis K, Kasiakogias, et al. Acute detrimental effects of electronic cigarette and tobacco cigarette smoking on blood pressure and sympathetic nerve activity in healthy subjects. Eur Heart J.38. https://doi.org/10.1093/ eurheartj/ehx504.P4429.
Nikolaos Ioakeimidis, Charalambos Vlachopoulos*, Dimitrios Tousoulis Hypertension and Cardiometabolic Syndrome Unit, 1st Department of Cardiology, Medical School, National and Kapodistrian University of Athens, Hippokration Hospital, Athens, Greece * Corresponding author: Charalambos Vlachopoulos, 1st Cardiology Department, Athens Medical School, National and Kapodistrian University of Athens, Hippokration Hospital, Profiti Elia 24, Athens 14575, Greece. Tel: þ30 697 227 2727; fax: þ30 210 747 3374. E-mail address: [email protected] (C. Vlachopoulos).
21 August 2017 Available online 19 October 2017
Contents lists available at ScienceDirect
Hellenic Journal of Cardiology journal homepage: http://www.journals.elsevier.com/ hellenic-journal-of-cardiology/
Editorial
Smoking impairs vagal modulation in old persons: the more we age, the more we learn The pathogenic mechanisms underlying the relationships between smoking and cardiovascular disease (CVD) have been the subject of innumerous investigations. Among these is the fact that smoking impairs baroreflex sensitivity, which may contribute to the smoking-induced increase in blood pressure and heart rate
and to the concomitant alterations in their variability. Moreover, the autonomic neurohumoral response that is evoked by smoking results in the downregulation of the beta-adrenergic receptors in long-term smokers1. On the positive side, it is well documented that smoking cessation can restore CVD health, both by reducing
Fig. 1. Acute effects of tobacco smoking on the sympathetic nerve activity (SNA) depend on the net balance of the sympathetic excitatory effect of cigarette smoke on the central neural outflow and the sympathetic inhibitory effect of the baroreflex, activated by the increase in blood pressure from smoking. When the baroreflex is intact, SNA is suppressed, but when the baroreflex is chronically impaired, as it is in many vulnerable populations, SNA increases. BP: blood pressure; BR: baroreflex sensitivity; SNS: sympathetic nervous system. With permission from Middlekauff HR, Park J, Moheimani RS. J Am Coll Cardiol. 20148.
Peer review under responsibility of Hellenic Society of Cardiology. https://doi.org/10.1016/j.hjc.2017.10.001 1109-9666/© 2017 Hellenic Society of Cardiology. Publishing services by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons. org/licenses/by-nc-nd/4.0/).
290
Editorial / Hellenic Journal of Cardiology 58 (2017) 289e290
sympathetic hyperactivity and by the re-establishment of parasympathetic modulation (i.e., vagal activity2). Furthermore, smoking cessation may improve blood pressure control and decrease the risk of an acute coronary event3. However, current knowledge regarding the restoration of autonomic activation after smoking cessation is restricted to results obtained from younger individuals4. Pereira et al in this issue of the Hellenic Journal of Cardiology5 address the topic of smoking effects on heart autonomic control (HAC) in older individuals with and without smoking habit. The study was done in 210 older (60 years) adults divided into 2 groups: nonsmokers or those who had stopped smoking (n¼190) and current smokers (n¼20). All participants were submitted to measurement of HAC parameters. The striking findings of the study provide clear evidence for the poor sympathovagal modulation in older adults who continue to smoke. The findings also provide further support for the benefit of smoking cessation in elders, which should be investigated in future studies with longitudinal design and/or intervention methods. The impairment of baroflex sensitivity by smoking should trigger a search for the impact of tobacco smoking in “vulnerable populations,” such as older long-term smokers. The acute effects of tobacco smoke on the sympathetic nerve activity (SNA) depend on the net balance of the sympathetic excitatory effect of cigarette smoke on the central neural outflow and the sympathetic inhibitory effect of the baroreflex, activated by the increase in blood pressure from smoking. When the baroreflex is intact, the SNA is suppressed, but when the baroreflex is chronically impaired, as it is in many “vulnerable populations” such as older individuals, the SNA increases8 (Fig. 1). In older long-term smokers with relatively impaired baroreflex function, acute smoking produces an increase in muscle SNA due to a lack of baroreflex restraint9. A question arises as to whether smoking per se rather than the age of the smoker is the cause of the impaired autonomic modulation; in other words, is smoking in older smokers merely a bystander or a causal factor? Certainly, the findings of the study indicate that both sympathetic and parasympathetic nervous systems are affected by the habit of smoking. It is important to note that, differently from previous studies6,7, the study is restricted to older adults, which could explain the wide impairment in the autonomic nervous system, owing to the additive effect of aging and smoking habit. Moreover, the adjustment of HAC parameters for potential confounders is an essential step to clarify relationships, especially regarding data obtained from older adults, considering the complex interactions between aging, CVD, metabolic diseases, cardiovascular drugs (i.e., b-blockers), lifestyle, and HAC. Cigarette smoking induces an inflammatory reaction, which has been associated with heart rate variability in middle-aged and older subjects with no apparent heart disease10. Nicotine is a chemotactic agent for the attraction and extravasation of neutrophils into the subendothelium.11 Expanding the “realm” of smoking, electronic cigarettes (ECs) have gained unprecedented popularity, but only little, and surely not enough, is known about their CVD risks12. We have recently demonstrated that EC smoking for 30 min exerts a similar unfavorable effect as that of smoking one conventional cigarette on blood pressure and aortic stiffness13. In a recent study, habitual EC use
was associated with a shift in cardiac autonomic balance toward SNA predominance in young individuals14. Preliminary data also indicate that EC smoking has a detrimental effect on sympathetic nerve activity regulation similar to tobacco smoking in healthy subjects15. An interesting question to be answered would be whether ECs induce a differential effect in HAC in older smokers.
References 1. Mancia G, Groppelli A, Di Rienzo M, Castiglioni P, Parati G. Smoking impairs baroreflex sensitivity in humans. Am J Physiol. 1997;273(3 Pt 2):H1555eH1560. 2. Clair C, Rigotti NA, Porneala B, et al. Association of Smoking Cessation and Weight Change With Cardiovascular Disease Among Adults With and Without Diabetes. JAMA. 2013;309(10):1014. 3. Bullen C. Impact of tobacco smoking and smoking cessation on cardiovascular risk and disease. Expert Rev Cardiovasc Ther. 2008;6(6):883e895. 4. Girard D, Delgado-Eckert E, Schaffner E, et al. Smoking cessation and heart rate variability: Is it possible to fully recover? Eur Respir J. 2014;44(Suppl 58):P319. 5. Pereira E, Ribeiro I, Freire I, Passos R, Casotti C, Pereira R. Smoking habit influences negatively the autonomic heart control in community-dwelling old adults. Hellenic J Cardiol. 2017;58:283e288. 6. Hayano J, Yamada M, Sakakibara Y, et al. Short- and long-term effects of cigarette smoking on heart rate variability. Am J Cardiol. 1990;65(1):84e88. 7. Harte CB, Meston CM. Effects of smoking cessation on heart rate variability among long-term male smokers. Int J Behav Med. 2014;21(2):302e309. 8. Middlekauff HR, Park J, Moheimani RS. Adverse effects of cigarette and noncigarette smoke exposure on the autonomic nervous system: mechanisms and implications for cardiovascular risk. J Am Coll Cardiol. 2014;64(16):1740e1750. 9. Hering D, Somers VK, Kara T, et al. Sympathetic neural responses to smoking are age dependent. J Hypertens. 2006;24(4):691e695. 10. Sajadieh A, Nielsen OW, Rasmussen V, Hein HO, Abedini S, Hansen JF. Increased heart rate and reduced heart-rate variability are associated with subclinical inflammation in middle-aged and elderly subjects with no apparent heart disease. Eur Heart J. 2004;25(5):363e370. 11. Benowitz N, Burbank A. Cardiovascular toxicity of nicotine: Implications for electronic cigarette use. Trends in Cardiovasc Med. 2016;26(6):515e522. 12. Ioakeimidis N, Vlachopoulos C, Tousoulis D. Efficacy and Safety of Electronic Cigarettes for Smoking Cessation: A Critical Approach. Hellenic J Cardiol. 2016;57(1):1e6. 13. Vlachopoulos C, Ioakeimidis N, Abdelrasoul M, et al. Electronic Cigarette Smoking Increases Aortic Stiffness and Blood Pressure in Young Smokers. J Am Coll Cardiol. 2016;67(23):2802e2803. 14. Moheimani RS, Bhetraratana M, Yin F, et al. Increased Cardiac Sympathetic Activity and Oxidative Stress in Habitual Electronic Cigarette Users: Implications for Cardiovascular Risk. JAMA Cardiol. 2017;2(3):278e284. 15. Tsioufis C, Dimitriadis K, Kasiakogias, et al. Acute detrimental effects of electronic cigarette and tobacco cigarette smoking on blood pressure and sympathetic nerve activity in healthy subjects. Eur Heart J.38. https://doi.org/10.1093/ eurheartj/ehx504.P4429.
Nikolaos Ioakeimidis, Charalambos Vlachopoulos*, Dimitrios Tousoulis Hypertension and Cardiometabolic Syndrome Unit, 1st Department of Cardiology, Medical School, National and Kapodistrian University of Athens, Hippokration Hospital, Athens, Greece * Corresponding author: Charalambos Vlachopoulos, 1st Cardiology Department, Athens Medical School, National and Kapodistrian University of Athens, Hippokration Hospital, Profiti Elia 24, Athens 14575, Greece. Tel: þ30 697 227 2727; fax: þ30 210 747 3374. E-mail address: [email protected] (C. Vlachopoulos).
21 August 2017 Available online 19 October 2017