International Journal of Cardiology 134 (2009) 401 – 434 www.elsevier.com/locate/ijcard
Letters to the Editor
Hypertension in Kazaks is more than just gene polymorphism Tsung O. Cheng The George Washington University, Washington, D.C. 20037, United States Received 12 November 2007; accepted 12 November 2007 Available online 10 January 2008
Keywords: Hypertension; Gene polymorphism; Kazaks; Sodium intake
To the Editor: The recent report that the +491C/T polymorphism of β2-adrenergic receptor gene is a risk factor for hypertension in Kazaks in Xinjiang [1] is interesting. But the authors did not mention the urinary sodium excretion in their subjects. A large nationwide survey of blood pressure, hypertension and sodium intake in 950,356 men and women carried out in China in 1991 [2] showed a positive correlation between blood pressure and sodium intake. In general, blood pressure and urinary sodium excretion tended to be higher in northern China, e.g., Beijing, than in southern China, e.g., Guangzhou (Fig. 1) [3,4]. The high blood pressure readings in inhabitants in Urumqi, Xinjiang, most of whom were Kazaks, corresponded to their high urinary sodium excretion. This ethnic difference in the prevalence of hypertension in China was again confirmed in a recent national survey carried out in China in 2002, being highest in the Tibetans and lowest in the Miaos in southern China [5]. Of particular interest was the observation that in Guangzhou, a 1989 study showed a gradual rise of both systolic and diastolic blood pressures as compared with a 1985 study, associated with a corresponding increase in urinary sodium excretion. The increase in sodium intake between these two surveys coincided with the rise in the number of American fastfood restaurants, such as MacDonald's and Kentucky Fried Chicken, that had opened in Guangzhou during that period [3,4].
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Therefore, hypertension in Kazaks is more than just gene polymorphism. Increased sodium intake is another important etiology.
Fig. 1. Linear relation between sodium intake as expressed in daily urinary sodium chloride excretion (NaCl g/d) on the abscissa and systolic (top) and diastolic (bottom) blood pressures on the ordinate in people from different cities in China. The numbers in parentheses after the city of Guangzhou denote the different years, i.e., 85 for 1985 and 89 for 1989. From Refs. [3] and [4].
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Letters to the Editor
References [1] Li N-f, Zhou L, Li T, Wang H-m, Liu H, Hu J-l. Association between the +491C/T polymorphism of β2-adrenergic receptor gene and risk of essential hypertension in Kasakns of Xinjiang. Chin J Cardiol 2007;35:706–9. [2] Tao SC, Zhou BF. Epidemiology of hypertension in China. Chin Med J 1999;112:878–82.
[3] Cheng TO. Diets play a major role in heart disease in China. Lipids 2004;39:291–2. [4] Cheng TO. Systolic and diastolic blood pressures and urinary sodium excretion in mainland China. Q J Med 2000;93:557–8. [5] Hu YS, Yao CH, Wang WZ, Hu JP, He YN, Zhai FY. Survey on the prevalence of hypertension in different ethnic groups in China in 2002. Wei Sheng Yan Jiu 2006;35:573–5.
0167-5273/$ - see front matter © 2007 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2007.11.051
Matrix metalloproteinases in acute coronary syndromes: A new therapeutic target? Turgay Celik a,⁎, Atila Iyisoy a , Ejder Kardesoglu b , Baris Bugan a , Ersoy Isik a b
a Gulhane Military Medical Academy, School of Medicine, Department of Cardiology, Etlik-Ankara, Turkey Gulhane Military Medical Academy, Haydarpasa Training Hospital, Department of Cardiology, Kadikoy-Istanbul, Turkey
Received 16 September 2007; accepted 11 December 2007 Available online 30 January 2008
Abstract Although matrix metalloproteinase (MMP) expression is found to be elevated after acute coronary syndrome (ACS), the slow elevation of MMP levels and the lack of clinical outcome data do not currently make MMPs useful biomarkers for therapeutic decision making or risk stratification in ACS. They do, however, remain an active area of investigation as a therapeutic target. © 2007 Elsevier Ireland Ltd. All rights reserved. Keywords: Matrix metalloproteinases; Acute coronary syndromes; Atherosclerosis
We have enjoyed reading the article by Fiotti and coworkers entitled ‘Metalloproteinases-2, -9, and TIMP-1 expression in stable and unstable coronary plaques undergoing PCI’ [1]. In that study, MMP-2, -9 and TIMP-1 expressions were assessed by real-time PCR from the debris collected into distal protective vascular guards from patients with stable angina (SA), acute coronary syndrome (ACS) undergoing percutaneous coronary interventions (PCI). MMP-2 and -9 activities were also evaluated by gelatin-substrate zymography on plasma samples collected immediately before PCI, and compared to those of healthy subjects. They found that the expression of MMP-2 was similar in ACS and SA-Groups. More importantly, MMP-9, but not TIMP-1, expression was
⁎ Corresponding author. Department of Cardiology, Gulhane School of Medicine, 06018 Etlik-Ankara, Turkey. Tel.: +90 312 3044268; fax: +90 312 3044250. E-mail address:
[email protected] (T. Celik).
higher in debris samples from patients in the ACS-Group than in SA-Group. Besides, in both groups, the expression of MMP-2 and MMP-9 was inversely correlated. Zymography data indicated that pro and active MMP-9 were higher in ACS than in SA-Group, while no difference in MMP-2 was found. They concluded that MMP-9, but not TIMP-1 or MMP-2 expression is increased in plaques causing ACS. Disruption of atherosclerotic plaque in the coronary arteries is the final common pathophysiology of most cases of sudden ischemic cardiac death, acute myocardial infarction (MI), and unstable angina [2,3]. Sites of plaque rupture are characterized macroscopically by a rent or erosion in the shoulder of the fibrous cap overlying the atheroma with superimposed thrombus. At the microscopic level, plaque vulnerable to rupture demonstrates intense inflammation with infiltration by macrophages, lymphocytes, and mast cells [2,3]. In an inflammatory environment, macrophages secrete matrix metalloproteinases (MMPs) that progressively degrade the collagenous components of the fibrous cap [4].