Korean Diabetes J.  2008 Dec;32(6):522-528. 10.4093/kdj.2008.32.6.522.

The Changes of Central Aortic Pulse Wave Analysis in Metabolic Syndrome

• Lee JI
• Sohn TS
• Kwon HS
• Lee JM
• Chang SA
• Cha BY
• Son HS

• KMID: 2222460
• DOI: http://doi.org/10.4093/kdj.2008.32.6.522

Abstract

The metabolic syndrome (MS) has been characterized as a cluster of risk factors that includes dyslipidemia, hypertension, glucose intolerance and central obesity. This syndrome increases the risk of cardiovascular disease. Augmentation index (AIx), a composite of wave reflection form medium-sized muscular arteries is related to the development of coronary artery disease. The aim of this study is to examine the change on central aortic waveforms in subjects between patients with metabolic syndrome and normal subjects. Using the non-invasive technique of pulse wave analysis by applantation tonometry, we investigated central aortic waveforms in 45 patients with MS and 45 matched controls. The MS was defined by NCEP-ATP III criteria. Age did not differ between the two groups. AIx was significantly elevated in patinets with MS compared with controls (21.91 +/- 11.41% vs 18.14 +/- 11.07%; P < 0.01). Subendocardial viability ratio (SEVR) (158.09 +/- 28.69 vs 167.09 +/- 30.06; P < 0.01) was significantly decreased in patients with MS compared with controls. Only the fasting glucose (r = 0.317, P = 0.03) among the components of MS and age (r = 0.424, P = 0.004) had a positive correlation with AIx. AIx increased as the number of MS components increased. These results show that the MS increased systemic arterial stiffness. Age and fasting blood glucose are independent risk factors of arterial stiffness in MS. The individual MS components, except for fasting blood glucose, do not affect arterial stiffness independently. But the clustering of MS components might interact to synergistically affect arterial stiffness.

Keyword

Arterial stiffness; Augmentation index; Metabolic syndrome; Pulse wave analysis

MeSH Terms

Arteries
Blood Glucose
Cardiovascular Diseases
Coronary Artery Disease
Dyslipidemias
Fasting
Glucose
Glucose Intolerance
Humans
Hypertension
Manometry
Obesity, Abdominal
Pulse Wave Analysis
Risk Factors
Vascular Stiffness
Blood Glucose
Glucose

Figure

• 

  Fig. 1 Augmentation index according to the number of the components of the metabolic syndrome. * P < 0.05.

Reference

1. Eckel RH, Grundy SM, Zimmet PZ. The metabolic syndrome. Lancet. 2005. 365:1415–1428.

2. Grundy SM. A constellation of complications: the metabolic syndrome. Clin Cornerstone. 2005. 7:36–45.

3. Stamler J, Vaccaro O, Neaton JD, Wentworth D. Diabetes, other risk factors, and 12-yr cardiovascular mortality for men screened in the Multiple Risk Factor Intervention Trial. Diabetes Care. 1993. 16:434–444.

4. Hanley AJ, Karter AJ, Williams K, Festa A, D'Agostino RB Jr, Wagenknecht LE, Haffner SM. Prediction of type 2 diabetes mellitus with alternative definitions of the metabolic syndrome: the Insulin Resistance Atherosclerosis Study. Circulation. 2005. 112:3713–3721.

5. Zieman SJ, Melenovsky V, Kass DA. Mechanisms, pathophysiology, and therapy of arterial stiffness. Arterioscler Thromb Vasc Biol. 2005. 932–943.

6. Hirata K, Kawakami M, O'Rourke MF. Pulse wave analysis and pulse wave velocity: a review of blood pressure interpretation 100 years after Korotkov. Circ J. 2006. 70:1231–1239.

7. Nichols WW, O'Rourke MF. Mcdonald's blood flow in arteries. Theoretical, experimental and clinical principles. 1998. 4th ed. London: Arnold.

8. O'Rourke MF, Kelly RP, Avolio AP. The arterial pulse. 1992. London: Lea & Febiger.

9. Buckberg GD, Towers B, Paglia DE. Experimental subendocardial ischaemia in dogs with normal coronary arteries. Circ Res. 1972. 30:67–81.

10. Kylin E. Studien ueber das Hypertonie-hyperglykamie-hyperurikamie syndrome. Zentralblatt fur innere medizin. 1923. 44:105–127.

11. Vageu J. La differenciation sexuelle. facteur determinant des formes de l'obesite. Press Med. 1947. 30:339–340.

12. Reaven GM. Banting lecture 1988. Role of insulin resistance in human disease. Diabetes. 1988. 37:1595–1607.

13. Executive Summary of The Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol In Adults (Adult Treatment Panel III). JAMA. 2001. 285:2486–2497.

14. Lakka HM, Laaksonen DE, Lakka TA. The metabolic syndrome and total and cardiovascular disease mortality in middle aged men. JAMA. 2002. 288:2709–2716.

15. Girman CJ, Rhodes T, Mercuri M. The metabolic syndrome and risk of major coronary events in the Scandinavian Simvastatin Survival Study (4S) and the Air Force/Texas Coronary Atherosclerosis Prevention Study (AFCAPS/TexCAPS). Am J Cardiol. 2004. 93:136–141.

16. Malik S, Wong ND, Franklin SS. Impact of the metabolic syndrome on mortality from coronary heart disease, cardiovascular disease, and all causes in United States adults. Circulation. 2004. 110:1245–1250.

17. Grundy SM, Hansen B, Smith SC Jr, Cleeman JI, Kahn RA. Clinical management of metabolic syndrome: Report of the American Heart Association/National Heart, Lung, and Blood Institute/American Diabetes Association conference on scientific issues related to management. Circulation. 2004. 109:551–556.

18. Ferro G, Diulio C, Spinelli L. Relation between diastolic perfusion time and coronary artery stenosis during stress-induced myocardial ischaemia. Circulation. 1995. 92:342–347.

19. Kannel WB, Gordon T, Schwartz MJ. Systolic versus diastolic blood pressure and risk of coronary heart disease: the Framingham study. Am J Cardiol. 1971. 27:335–346.

20. Franklin SS, Larson MG, Khan SA, Wong ND, Leip EP, Kannel WB, Levy D. Does the relation of blood pressure to coronary heart disease risk change with aging? The Framingham Heart study. Circulation. 2001. 103:1245–1249.

21. O'Rourke MF, Seward JB. Central arterial pressure and arterial pressure pulse: new views entering the second century after Korotkov. Mayo Clin Proc. 2006. 81:1057–1068.

22. Nichols WW. Clinical measurement of arterial stiffness obtained from noninvasive pressure waveforms. AJH. 2005. 18:3S–10S.

23. Oliver JJ, Webb DJ. Noninvasive assessment of arterial stiffenss and risk of atherosclerotic events. Arterioscler Thromb Vasc Biol. 2003. 23:554–566.

24. London GM, Asmar RG, O'Rourke MF, Safar ME. REASON project Investigators. Mechanism(s) of selective systolic blood pressure reduction after a low-dose combination of perindopril/indapamide in hypertensive subjects: comparison with atenolol. J Am Coll Caridl. 2004. 43:92–99.

25. Wlliams B, Lacy PS, Thom SM. CAFE investigators. Anglo-Scandinavian Cardiac Outcomes Trial Investigators. Cafe Stering Committee and Writing Committee. Differential impact of blood pressure-lowering drugs on central aortic pressure and clinical outcomes: principal results of the Conduit Artery Function Evaluation (CAFE) study. Circulation. 2006. 113:1213–1225.

26. Kang JY, Choi HA, Yoon HS, Yu SH, Song MJ, Chang EG, Kim HS, Shin HH, Park JB, Lee WR. Reversal of arterial stiffness by treatment with the angiotensin receptor antagonist irbesartan in essential hypertension. Korean J Med. 2004. 67:241–248.