International Journal of Cardiology 192 (2015) 9–10
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
The influence of autonomic nervous system on the conduction system and heart muscle. Do different inhaled bronchodilators cause different tachyarrhythmias? Tamer Kırat a,⁎, Nuri Köse b, İbrahim Altun b, Fatih Akın b a b
Yücelen Hospital, Department of Cardiology, Muğla, Turkey Sıtkı Koçman University, Faculty of Medicine, Department of Cardiology, Muğla, Turkey
a r t i c l e
i n f o
Article history: Received 3 May 2015 Accepted 6 May 2015 Available online 8 May 2015 Keywords: Autonomic nervous system Bronchodilator therapy Tachyarrhythmia
We read with great interest the manuscript by Chang-Hoon Lee et al. [1]. They studied and found significantly increased risk of important tachyarrhythmias with the use of various inhaled bronchodilator therapies in patients with pulmonary diseases. This is an invaluable, large cohort study. We would like to make some comments about this study. The autonomic nervous system has an important role in the regulation of cardiac electrophysiology and arrhythmogenesis. The cardiac sympathetic nerves innervate the atria, including the sinoatrial (SA) node and atrioventricular (AV) node, and richly the ventricles. To our classical physiological knowledge, the parasympathetic system also innervates the atria with the SA and AV nodes but has little effect on the ventricles because of the sparse parasympathetic innervation of the ventricles [2]. However, modern histologic techniques revealed dense and intricate parasympathetic nerve network in the epi-endocardial surfaces of both the right and left ventricles of the various animal types and humans [3]. So, both the sympathetic and parasympathetic systems have influences on both the atriums and ventricles. It should be noted that autonomic nervous system behaves somewhat differently in the conduction system and in the cardiac myocytes. In the conduction system, sympathetic system accelerates sinus rhythm, AV conduction and speeds up the conduction in the rest, whereas,
parasympathetic activation has the opposite effects [2]. Although the sympathetic system has similar effects on the atrial and ventricular myocytes, however, the parasympathetic system has different effects. In the atrial mycotes, vagal activation reduces the atrial effective refractory period and promotes early after depolarizations, whereas in the ventricular myocytes, it prolongs action potential duration and effective refractory period. So, parasympathetic stimulation is proarrhythmic in the atrial myocytes, but it is antiarrhythmic in the ventricles [4]. On the other hand, sympathetic stimulation is proarrhythmic for both chambers [4]. In the study, inhaled long-acting β2 agonists (LABAs) (sympatheticomimetics) and long-acting muscarinic antagonists (LAMAs) (parasympatheticolytics) were found to be significantly associated with tachyarrhythmias. However, the types and subtypes of tachyarrhythmias (i.e. supraventricular, ventricular and subtypes) weren't mentioned in the manuscript. In light of the above data and for prognostic information, we think that it would be of value and interesting to see the association between the incidences of tachyarrhythmia types with subtypes and LAMAs or LABAs or both in the study. Heart failure, valvular heart disease and hyperthyroidism, which are not mentioned in the article, are potential and frequent causes of supraventricular and ventricular tachyarrhythmias. The differences of these diseases between the groups might affect the results. In addition, although calcium channel blockers (CCB) were taken as a whole group in the manuscript, we think that it would be better to mention the selectivity status separately because, as is known, cardioselective CCBs (diltiazem and verapamil) can prevent some supraventricular tachycardias, or can slow the ventricular rate in atrial fibrillation or flutter in which palpitations may not be sensed by the patient that might preclude the diagnosis. Finally, because the severeness of the lung disease and hence hypoxemia status might play an important role in tachyarrhythmias, we think that the stages of the pulmonary diseases (for example GOLD stages of COPD) in the groups might be better to be declared for comparison.
Conflict of interest ⁎ Corresponding author at: Yücelen Hospital Kötekli Mevkii, 48000 Muğla, Turkey. E-mail address: [email protected] (T. Kırat).
http://dx.doi.org/10.1016/j.ijcard.2015.05.021 0167-5273/© 2015 Elsevier Ireland Ltd. All rights reserved.
The authors report no relationships that could be construed as a conflict of interest.
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T. Kırat et al. / International Journal of Cardiology 192 (2015) 9–10
References [1] C.-H. Lee, S. Choi, E.J. Jang, H.-M. Yang, H.I. Yoon, Y.J. Kim, J. Kim, J.-J. Yim, D.K. Kim, Inhaled bronchodilators and the risk of tachyarrhythmias, Int. J. Cardiol. 190 (2015) 133–139. [2] L. Sherwood, Cardiac physiology, Fundamentals of Human Physiology, 4th ed.Cengage Learning, UK 2011, pp. 228–259.
[3] K.E. Brack, J. Winter, G.A. Ng, Mechanisms underlying the autonomic modulation of ventricular fibrillation initiation—tentative prophylactic properties of vagus nerve stimulation on malignant arrhythmias in heart failure, Heart Fail. Rev. 18 (2013) 389–408. [4] M.J. Shen, D.P. Zipes, Role of the autonomic nervous system in modulating cardiac arrhythmias, Circ. Res. 114 (2014) 1004–1021.
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
The influence of autonomic nervous system on the conduction system and heart muscle. Do different inhaled bronchodilators cause different tachyarrhythmias? Tamer Kırat a,⁎, Nuri Köse b, İbrahim Altun b, Fatih Akın b a b
Yücelen Hospital, Department of Cardiology, Muğla, Turkey Sıtkı Koçman University, Faculty of Medicine, Department of Cardiology, Muğla, Turkey
a r t i c l e
i n f o
Article history: Received 3 May 2015 Accepted 6 May 2015 Available online 8 May 2015 Keywords: Autonomic nervous system Bronchodilator therapy Tachyarrhythmia
We read with great interest the manuscript by Chang-Hoon Lee et al. [1]. They studied and found significantly increased risk of important tachyarrhythmias with the use of various inhaled bronchodilator therapies in patients with pulmonary diseases. This is an invaluable, large cohort study. We would like to make some comments about this study. The autonomic nervous system has an important role in the regulation of cardiac electrophysiology and arrhythmogenesis. The cardiac sympathetic nerves innervate the atria, including the sinoatrial (SA) node and atrioventricular (AV) node, and richly the ventricles. To our classical physiological knowledge, the parasympathetic system also innervates the atria with the SA and AV nodes but has little effect on the ventricles because of the sparse parasympathetic innervation of the ventricles [2]. However, modern histologic techniques revealed dense and intricate parasympathetic nerve network in the epi-endocardial surfaces of both the right and left ventricles of the various animal types and humans [3]. So, both the sympathetic and parasympathetic systems have influences on both the atriums and ventricles. It should be noted that autonomic nervous system behaves somewhat differently in the conduction system and in the cardiac myocytes. In the conduction system, sympathetic system accelerates sinus rhythm, AV conduction and speeds up the conduction in the rest, whereas,
parasympathetic activation has the opposite effects [2]. Although the sympathetic system has similar effects on the atrial and ventricular myocytes, however, the parasympathetic system has different effects. In the atrial mycotes, vagal activation reduces the atrial effective refractory period and promotes early after depolarizations, whereas in the ventricular myocytes, it prolongs action potential duration and effective refractory period. So, parasympathetic stimulation is proarrhythmic in the atrial myocytes, but it is antiarrhythmic in the ventricles [4]. On the other hand, sympathetic stimulation is proarrhythmic for both chambers [4]. In the study, inhaled long-acting β2 agonists (LABAs) (sympatheticomimetics) and long-acting muscarinic antagonists (LAMAs) (parasympatheticolytics) were found to be significantly associated with tachyarrhythmias. However, the types and subtypes of tachyarrhythmias (i.e. supraventricular, ventricular and subtypes) weren't mentioned in the manuscript. In light of the above data and for prognostic information, we think that it would be of value and interesting to see the association between the incidences of tachyarrhythmia types with subtypes and LAMAs or LABAs or both in the study. Heart failure, valvular heart disease and hyperthyroidism, which are not mentioned in the article, are potential and frequent causes of supraventricular and ventricular tachyarrhythmias. The differences of these diseases between the groups might affect the results. In addition, although calcium channel blockers (CCB) were taken as a whole group in the manuscript, we think that it would be better to mention the selectivity status separately because, as is known, cardioselective CCBs (diltiazem and verapamil) can prevent some supraventricular tachycardias, or can slow the ventricular rate in atrial fibrillation or flutter in which palpitations may not be sensed by the patient that might preclude the diagnosis. Finally, because the severeness of the lung disease and hence hypoxemia status might play an important role in tachyarrhythmias, we think that the stages of the pulmonary diseases (for example GOLD stages of COPD) in the groups might be better to be declared for comparison.
Conflict of interest ⁎ Corresponding author at: Yücelen Hospital Kötekli Mevkii, 48000 Muğla, Turkey. E-mail address: [email protected] (T. Kırat).
http://dx.doi.org/10.1016/j.ijcard.2015.05.021 0167-5273/© 2015 Elsevier Ireland Ltd. All rights reserved.
The authors report no relationships that could be construed as a conflict of interest.
10
T. Kırat et al. / International Journal of Cardiology 192 (2015) 9–10
References [1] C.-H. Lee, S. Choi, E.J. Jang, H.-M. Yang, H.I. Yoon, Y.J. Kim, J. Kim, J.-J. Yim, D.K. Kim, Inhaled bronchodilators and the risk of tachyarrhythmias, Int. J. Cardiol. 190 (2015) 133–139. [2] L. Sherwood, Cardiac physiology, Fundamentals of Human Physiology, 4th ed.Cengage Learning, UK 2011, pp. 228–259.
[3] K.E. Brack, J. Winter, G.A. Ng, Mechanisms underlying the autonomic modulation of ventricular fibrillation initiation—tentative prophylactic properties of vagus nerve stimulation on malignant arrhythmias in heart failure, Heart Fail. Rev. 18 (2013) 389–408. [4] M.J. Shen, D.P. Zipes, Role of the autonomic nervous system in modulating cardiac arrhythmias, Circ. Res. 114 (2014) 1004–1021.
