Letters to the Editor
[27]
[28]
[29] [30] [31]
2 4 - we e k , r a n d o m i z e d , o p e n - l a b e l , p r o s p e c t i ve s t u d y. C l i n T h e r 2010;32:492–505. Sharma AM, Davidson J, Koval S, Lacourcière Y. Telmisartan/hydrochlorothiazide versus valsartan/hydrochlorothiazide in obese hypertensive patients with type 2 diabetes: the SMOOTH study. Cardiovasc Diabetol 2007;6:28. Hasegawa H, Takano H, Narumi H, et al. Effects of telmisartan and losartan on cardiovascular protection in Japanese hypertensive patients. Hypertens Res 2011;34:1179–84. Watanabe M, Inukai K, Sumita T, et al. Effects of telmisartan on insulin resistance in Japanese type 2 diabetic patients. Intern Med 2010;49:1843–7. Yamada S, Ano N, Toda K, et al. Telmisartan but not candesartan affects adiponectin expression in vivo and in vitro. Hypertens Res 2008;31:601–6. Yano Y, Hoshide S, Ishikawa J, et al. The differential effects of angiotensin II type 1 receptor blockers on microalbuminuria in relation to low-grade inflammation in metabolic hypertensive patients. Am J Hypertens 2007;20:565–72.
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[32] Dormandy JA, Charbonnel B, Eckland DJ, et al. Secondary prevention of macrovascular events in patients with type 2 diabetes in the PROactive Study (PROspective pioglitAzone Clinical Trial In macroVascular Events): a randomised controlled trial. Lancet 2005;366:1279–89. [33] Schupp M, Clemenz M, Gineste R, et al. Molecular characterization of new selective peroxisome proliferator-activated receptor gamma modulators with angiotensin receptor blocking activity. Diabetes 2005;54:3442–52. [34] von Eckardstein A, Nofer JR, Assmann G. High density lipoproteins and arteriosclerosis. Role of cholesterol efflux and reverse cholesterol transport. Arterioscler Thromb Vasc Biol 2001;21:13–27. [35] Repa JJ, Turley SD, Lobaccaro JA, et al. Regulation of absorption and ABC1-mediated efflux of cholesterol by RXR heterodimers. Science 2000;289:1524–9.
0167-5273/$ – see front matter © 2012 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2012.02.008
Adiponectin and arterial stiffness in hypertensive patients Tomoyuki Kawada ⁎ Department of Hygiene and Public Health, Nippon Medical School, Japan
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Article history: Received 6 March 2012 Accepted 10 March 2012 Available online 5 April 2012 Keywords: Adiponectin Hypertension Arterial stiffness
To the Editor Youn et al. conducted 2-year follow-up study on the influence of plasma adiponectin on the rate of change of the pulse wave velocity (PWV) in hypertensive patients [1]. Heart-to-femoral PWV, in particular, was affected by the plasma adiponectin, which was considered to be attributable to the adverse effect of plasma adiponectin on the central arterial stiffness. In contrast, resistin, an indicator of systemic vascular inflammation, did not significantly contribute to the arterial stiffness in their study. With reference to this article, Tsioufis et al. reported that the carotid-to-femoral PWV was independently associated with the age, waist circumference, 24-h systolic blood pressure, log-transformed serum adiponectin and logtransformed serum high-sensitivity C-reactive protein in previously never-treated patients of stages I–II essential hypertension [2]. I think that one of the advantages of the study conducted by Youn et al. was that they handled an indicator of insulin resistance, which is important for vascular atherosclerosis or arterial stiffness. In this letter, the author points out some of the methodological problems in the study conducted by Youn et al. First of all, there were no significant differences in the mean values of the obesity indices, such as the body mass index, waist circumference, waist hip ratio and body fat percent between the
⁎ Department of Hygiene and Public Health, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-Ku, Tokyo 113-8602, Japan. Tel.: +81 3 3822 2131; fax: +81 3 5685 3065. E-mail address:
[email protected].
progressors and non-progressors. These data are only recorded in the baseline study. As the plasma adiponectin was measured twice, the obesity indices should also have been measured twice. The relationship between the changes in the plasma adiponectin and obesity may prove informative to check the validity of a review that reports the lack of any association between the BMI and plasma adiponectin [3]. Secondly, the authors handled the homeostasis model assessment of insulin resistance (HOMA-IR) as a normally distributed variable. However, it is generally log-normally distributed, and logarithmic transformation of the values is needed for multiple linear regression analysis. The same is the case for the serum triglyceride. In addition, HOMA-IR does not reliably reflect the degree of insulin resistance in subjects with plasma glucose levels exceeding 140 mg/dL. Especially in the progressor group of subjects, there seems to be a lack of validation of the HOMA-IR. Although HOMA-IR was selected as a significant predictor of the brachial-to-ankle PWV, re-analysis is needed by the previously mentioned procedures. Third, the authors measured serum total adiponectin rather than serum high-molecular-weight adiponectin, which is actually the parameter that is considered as a more useful marker of cardiovascular risk than the serum total adiponectin [4]. Therefore, in a future study, serum high-molecular-weight adiponectin should be evaluated as a marker of progression on arterial stiffness. Finally, the authors concluded that there were no relationships between the changes in the plasma adiponectin levels and the changes of the PWV, without providing any clear explanation. In view of the study limitations in relation to the number of study subjects and the follow-up period, further study is needed to understand the net effect of adiponectin on the arterial stiffness in hypertensive patients. I wish to express my appreciation to the members of Hygiene and Public Health, Nippon Medical School, for the preparation of this study. The author of this manuscript has certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology. References [1] Youn JC, Kim C, Park S. Adiponectin and progression of arterial stiffness in hypertensive patients. Int J Cardiol 2011, doi:10.1016/j.ijcard.2011.06.061.
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[2] Tsioufis C, Kyvelou S, Dimitriadis K, et al. The diverse associations of uric acid with low-grade inflammation, adiponectin and arterial stiffness in never-treated hypertensives. J Hum Hypertens 2011;25:554–9. [3] Kuo SM, Halpern MM. Lack of association between body mass index and plasma adiponectin levels in healthy adults. Int J Obes (Lond) 2011;35:1487–94.
[4] Kawada T, Hasegawa M. Predictive ability of serum high-molecular-weight adiponectin in combination with serum insulin and serum C-reactive protein for the presence of metabolic syndrome. Ann Hum Biol 2012;39:108–12.
0167-5273/$ – see front matter © 2012 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2012.03.122
Effect of single or dual blockade of renin-angiotensin system in acute myocardial infarction patients according to renal function Hae Chang Jeong a, Ji Min Jeong a, Myung Ho Jeong a,⁎, Youngkeun Ahn a, Shung Chull Chae b, Seung Ho Hur c, Taek Jong Hong d, Young Jo Kim e, In Whan Seong f, Jei Keon Chae g, Jay Young Rhew h, In Ho Chae i, Myeong Chan Cho j, Jang Ho Bae k, Seung Woon Rha l, Chong Jin Kim m, Donghoon Choi n, Yang Soo Jang n, Junghan Yoon o, Wook Sung Chung p, Jeong Gwan Cho a, Ki Bae Seung p, Seung Jung Park q and Other Korea Acute Myocardial Infarction Registry Investigators a
Chonnam National University Hospital, Gwangju, Republic of Korea Kyungpuk National Univ. Hosp., Daegu, Republic of Korea Keimyung University Dongsan Medical Center, Daegu, Republic of Korea d Busan National Univ. Hosp., Busan, Republic of Korea e Yeungnam Univ. Hosp., Daegu, Republic of Korea f Chungnam National Univ. Hosp., Daejon, Republic of Korea g Chunbuk National Univ. Hosp., Jeonju, Republic of Korea h Jeonju Presbyterian Medical Center, Jeonju, Republic of Korea i Seoul National University Bundang Hospital, Republic of Korea j Chungbuk National University Hospital, Cheongju, Republic of Korea k Konyang University, Daejon, Republic of Korea l Korea University Guro Hospital, Seoul, Republic of Korea m Kyung Hee Univ. Hosp., Seoul, Republic of Korea n Yonsei University Hospital, Seoul, Republic of Korea o Wonju University Hospital, Wonju, Republic of Korea p Catholic University Hospital, Seoul, Republic of Korea q Asan Medical Center, Seoul, Republic of Korea b c
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Article history: Received 14 March 2012 Accepted 15 March 2012 Available online 16 April 2012 Keywords: Angiotensin Kidney Myocardial infarction Prognosis
Recent studies have demonstrated that the angiotensin-II receptor blocker (ARB) was as effective as angiotensin converting enzyme inhibitor (ACEI) in patients at high risk for cardiovascular events, but the combination treatment of ACEI and ARB has been a controversy. The kidney is both an endocrine organ and target organ of the reninangiotensin system (RAS) [1]. Therefore, the effects of ACEI or ARB can be varied according to renal function. We therefore investigated to assess the effect of ARB, ACEI, and combination of the two drugs for the improvement of long term clinical outcomes in acute myocardial infarction (AMI) patients according to renal function.
⁎ Corresponding author at: Professor, principal investigator of Korea Acute Myocardial Infarction Registry, director of Heart Research Center nominated by Korea Ministry of Health and Welfare, Chonnam National University Hospital, 8 Hak-dong, Dong-gu, Gwangju 501-757, Republic of Korea. Tel.: +82 62 220 6243; fax: +82 62 228 7174. E-mail address:
[email protected] (M.H. Jeong).
Between November 2005 and June 2010, eligible 10,083 patients who were successfully treated by percutaneous coronary intervention (PCI) with stent implantation, had completed 12 months clinical follow-up, and without cardiogenic shock were analyzed in the Korea Acute Myocardial Infarction Registry (KAMIR) [2]. We divided the population by estimated glomerular filtration rate (e-GFR) [3]. And each renal function group was then broken into subgroups according to ACEI or ARB treatment (Fig. 1). The primary endpoint was the summation of in-hospital death and composite major adverse cardiac events (MACEs) during 12 months. The methods of unpaired Student's t-test, chi-square test, and multivariate Cox proportional regression analysis were used (SPSS for Window 17.0). During the 12-month follow-up period, the incidences of composite of MACEs were not significantly different between the ACEI group and the ARB group (11.7% vs. 11.7%, p = 0.948). However, the incidence of composite of MACEs was significantly higher in the combination group and the control group than in the ACEI group (17.3% vs. 11.7%, p b 0.001, 16.9% vs. 11.7%, p b 0.001, respectively). And, the incidence of primary end point was showed tendency that the incidence of primary end point had increased, as e-GFR had decreased (Fig. 2). Adjusted cumulative incidences of total MACEs at 12 months according to the different therapeutic strategy in the different renal function groups by multivariable Cox regression analysis are presented in Fig. 3. In the normal renal function and mild, moderated renal dysfunction group, the incidence of MACEs was not significantly different between the ACEI group and the ARB group, and the combination group, however it was significantly higher in the control group than in the ACEI group. Whereas, in the severe renal dysfunction group, it was significantly higher in the combination group and the control group than in the ACEI