International Journal of Cardiology 176 (2014) 1078–1079
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
The relationship between epicardial fat thickness and arterial stiffness; role of antihypertensive drugs and statins Ercan Varol ⁎ Department of Cardiology, Suleyman Demirel University, Faculty of Medicine, Isparta, Turkey
a r t i c l e
i n f o
Article history: Received 28 May 2014 Accepted 26 July 2014 Available online 2 August 2014 Keywords: Arterial stiffness Epicardial fat thickness Antihypertensive drugs Statins
Dear Sir, I read the article by Kim et al. with great interest [1]. They investigated the relationship between epicardial fat thickness (EFT) and brachialankle pulse wave velocity (baPWV). They classified the subjects into two groups according to baPWV value, group I with baPWVs ≤ 1366 cm/s and group II with baPWVs N 1366 cm/s. The EFT in group II was significantly higher than that in group I. The baPWV also increased with increasing quartile of EFT. Moreover, EFT was an independent determinant of baPWV. As a result, they concluded that echocardiographic EFT is independently associated with arterial stiffness, irrespective of confounding factors suggesting that echocardiographic EFT measurements could provide additional information on assessing subclinical target organ damage. I congratulate the authors for this well presented study. However, I want to make minor criticism from methodological aspect. Arterial stiffness is a complex process and associated with confounding factors. Cecelja et al. published a systematic review which showed that the contribution of cardiovascular risk factors other than age and blood pressure to aortic stiffness measured by carotid-femoral PWV is small or insignificant and age and blood pressure were consistently independently associated with aortic stiffness [2]. It has also been shown that antihypertensive drug classes may have different effects on arterial stiffness [3,4]. While angiotensin converting enzyme inhibitors, calcium channel blockers, and mineralocorticoid antagonists are beneficial in reducing arterial stiffness ⁎ Suleyman Demirel Univesitesi, Tip Fakultesi, Isparta, Turkey. Tel.: +90 5323468258; fax: +90 24623245. E-mail address: [email protected].
http://dx.doi.org/10.1016/j.ijcard.2014.07.131 0167-5273/© 2014 Published by Elsevier Ireland Ltd.
and central blood pressure, some beta blockers may have the opposite effects while lowering peripheral blood pressure [4]. On the other hand, majority of studies on beta blockers have investigated the effects of atenolol and there are insufficient data available regarding the effects of vasodilating beta blockers. Recent study showed that aliskiren, a direct renin inhibitor, appears to be as effective as quinapril, an angiotensin-converting enzyme inhibitor, in reducing arterial stiffness [5]. In addition, atenolol exerts less beneficial effects on markers of arterial stiffness not only against quinapril or aliskiren but also against nebivolol, despite similar reductions in peripheral blood pressure [5]. Finally, renin–angiotensin–aldosterone system inhibitors appear to exert a more persistent reduction in carotid to femoral pulse wave velocity than beta-blockers [5]. The authors did not mention about the antihypertensive drug classes which can greatly influence arterial stiffness parameters. The authors did not also mention about the statin use. Recent studies showed that statin therapy reduced EFT and arterial stiffness [3,6]. And although intensive therapy was more effective than moderate-intensity therapy, this effect of statin does not seem to link to low-density lipoprotein lowering and may be secondary to other actions of statins such as anti-inflammatory effects. It would have been useful if the authors had provided information about these factors. A growing amount of evidence suggests that epicardial adipose tissue plays an important role in cardiovascular diseases. Because of its anatomic and functional proximity to the myocardium and its intense metabolic activity, some interactions between the heart and its visceral fat depot have been suggested [7]. Epicardial adipose tissue is regarded as a metabolically active endocrine and paracrine organ which secretes an array of pro-inflammatory and proatherogenic cytokines [7]. Echocardiographic EFT measurement is an inexpensive, reproducible, and direct measure of visceral fat. It may have an important role in predicting and stratifying cardiovascular risk in both clinical care and the research setting. On the other hand, EFT has a significant relationship with cardiovascular risk factors and statin use. Antihypertensive drugs and statins should be considered in EFT and arterial stiffness evaluation. Conflict of interest The authors have no declaration of interest. References [1] Kim BJ, Kim BS, Kang JH. Echocardiographic epicardial fat thickness is associated with arterial stiffness. Int J Cardiol 2013;167(5):2234–8.
E. Varol / International Journal of Cardiology 176 (2014) 1078–1079 [2] Cecelja M, Chowienczyk P. Dissociation of aortic pulse wave velocity with risk factors for cardiovascular disease other than hypertension: a systematic review. Hypertension 2009;54(6):1328–36. [3] Cavalcante JL, Lima JA, Redheuil A, Al-Mallah MH. Aortic stiffness: current understanding and future directions. J Am Coll Cardiol 2001;57(14):1511–22. [4] Dudenbostel T, Glasser SP. Effects of antihypertensive drugs on arterial stiffness. Cardiol Rev 2012;20(5):259–63. [5] Koumaras C, Tziomalos K, Stavrinou E, et al. Effects of renin–angiotensin–aldosterone system inhibitors and beta-blockers on markers of arterial stiffness. J Am Soc Hypertens 2014;8(2):74–82.
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[6] Alexopoulos N, Melek BH, Arepalli CD, et al. Effect of intensive versus moderate lipid-lowering therapy on epicardial adipose tissue in hyperlipidemic post-menopausal women: a substudy of the BELLES trial (Beyond Endorsed Lipid Lowering with EBT Scanning). J Am Coll Cardiol 2013;61(19):1956–61. [7] Iacobellis G, Willens HJ. Echocardiographic epicardial fat: a review of research and clinical applications. J Am Soc Echocardiogr 2009;22(12):1311–9.
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
The relationship between epicardial fat thickness and arterial stiffness; role of antihypertensive drugs and statins Ercan Varol ⁎ Department of Cardiology, Suleyman Demirel University, Faculty of Medicine, Isparta, Turkey
a r t i c l e
i n f o
Article history: Received 28 May 2014 Accepted 26 July 2014 Available online 2 August 2014 Keywords: Arterial stiffness Epicardial fat thickness Antihypertensive drugs Statins
Dear Sir, I read the article by Kim et al. with great interest [1]. They investigated the relationship between epicardial fat thickness (EFT) and brachialankle pulse wave velocity (baPWV). They classified the subjects into two groups according to baPWV value, group I with baPWVs ≤ 1366 cm/s and group II with baPWVs N 1366 cm/s. The EFT in group II was significantly higher than that in group I. The baPWV also increased with increasing quartile of EFT. Moreover, EFT was an independent determinant of baPWV. As a result, they concluded that echocardiographic EFT is independently associated with arterial stiffness, irrespective of confounding factors suggesting that echocardiographic EFT measurements could provide additional information on assessing subclinical target organ damage. I congratulate the authors for this well presented study. However, I want to make minor criticism from methodological aspect. Arterial stiffness is a complex process and associated with confounding factors. Cecelja et al. published a systematic review which showed that the contribution of cardiovascular risk factors other than age and blood pressure to aortic stiffness measured by carotid-femoral PWV is small or insignificant and age and blood pressure were consistently independently associated with aortic stiffness [2]. It has also been shown that antihypertensive drug classes may have different effects on arterial stiffness [3,4]. While angiotensin converting enzyme inhibitors, calcium channel blockers, and mineralocorticoid antagonists are beneficial in reducing arterial stiffness ⁎ Suleyman Demirel Univesitesi, Tip Fakultesi, Isparta, Turkey. Tel.: +90 5323468258; fax: +90 24623245. E-mail address: [email protected].
http://dx.doi.org/10.1016/j.ijcard.2014.07.131 0167-5273/© 2014 Published by Elsevier Ireland Ltd.
and central blood pressure, some beta blockers may have the opposite effects while lowering peripheral blood pressure [4]. On the other hand, majority of studies on beta blockers have investigated the effects of atenolol and there are insufficient data available regarding the effects of vasodilating beta blockers. Recent study showed that aliskiren, a direct renin inhibitor, appears to be as effective as quinapril, an angiotensin-converting enzyme inhibitor, in reducing arterial stiffness [5]. In addition, atenolol exerts less beneficial effects on markers of arterial stiffness not only against quinapril or aliskiren but also against nebivolol, despite similar reductions in peripheral blood pressure [5]. Finally, renin–angiotensin–aldosterone system inhibitors appear to exert a more persistent reduction in carotid to femoral pulse wave velocity than beta-blockers [5]. The authors did not mention about the antihypertensive drug classes which can greatly influence arterial stiffness parameters. The authors did not also mention about the statin use. Recent studies showed that statin therapy reduced EFT and arterial stiffness [3,6]. And although intensive therapy was more effective than moderate-intensity therapy, this effect of statin does not seem to link to low-density lipoprotein lowering and may be secondary to other actions of statins such as anti-inflammatory effects. It would have been useful if the authors had provided information about these factors. A growing amount of evidence suggests that epicardial adipose tissue plays an important role in cardiovascular diseases. Because of its anatomic and functional proximity to the myocardium and its intense metabolic activity, some interactions between the heart and its visceral fat depot have been suggested [7]. Epicardial adipose tissue is regarded as a metabolically active endocrine and paracrine organ which secretes an array of pro-inflammatory and proatherogenic cytokines [7]. Echocardiographic EFT measurement is an inexpensive, reproducible, and direct measure of visceral fat. It may have an important role in predicting and stratifying cardiovascular risk in both clinical care and the research setting. On the other hand, EFT has a significant relationship with cardiovascular risk factors and statin use. Antihypertensive drugs and statins should be considered in EFT and arterial stiffness evaluation. Conflict of interest The authors have no declaration of interest. References [1] Kim BJ, Kim BS, Kang JH. Echocardiographic epicardial fat thickness is associated with arterial stiffness. Int J Cardiol 2013;167(5):2234–8.
E. Varol / International Journal of Cardiology 176 (2014) 1078–1079 [2] Cecelja M, Chowienczyk P. Dissociation of aortic pulse wave velocity with risk factors for cardiovascular disease other than hypertension: a systematic review. Hypertension 2009;54(6):1328–36. [3] Cavalcante JL, Lima JA, Redheuil A, Al-Mallah MH. Aortic stiffness: current understanding and future directions. J Am Coll Cardiol 2001;57(14):1511–22. [4] Dudenbostel T, Glasser SP. Effects of antihypertensive drugs on arterial stiffness. Cardiol Rev 2012;20(5):259–63. [5] Koumaras C, Tziomalos K, Stavrinou E, et al. Effects of renin–angiotensin–aldosterone system inhibitors and beta-blockers on markers of arterial stiffness. J Am Soc Hypertens 2014;8(2):74–82.
1079
[6] Alexopoulos N, Melek BH, Arepalli CD, et al. Effect of intensive versus moderate lipid-lowering therapy on epicardial adipose tissue in hyperlipidemic post-menopausal women: a substudy of the BELLES trial (Beyond Endorsed Lipid Lowering with EBT Scanning). J Am Coll Cardiol 2013;61(19):1956–61. [7] Iacobellis G, Willens HJ. Echocardiographic epicardial fat: a review of research and clinical applications. J Am Soc Echocardiogr 2009;22(12):1311–9.
