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Atherosclerosis. 2010 May;210(1):268-73. doi: 10.1016/j.atherosclerosis.2009.11.003. Epub 2009 Nov 10.

Dysfunctional central hemodynamic regulation after daily meal intake in metabolic syndrome.

Author information

1
Department of Cardiology, NHO Ehime National Hospital, 366 Yokogawara, Toon, Ehime, Japan. jfunada@ehime-nh.go.jp

Abstract

OBJECTIVE:

Postprandial hyperlipidemia and insulin resistance play roles in the development of atherosclerosis in metabolic syndrome (MetS); however, the clinical significance of postprandial hemodynamic variables in this condition is still in question. The aim of this study was to investigate hemodynamic and metabolic indicators related to MetS after a mixed meal (Calorie mate, 500 kcal).

METHODS:

Of 107 participants undergoing this investigation, 24 fulfilled ATPIII criteria for MetS. The remaining 83 subjects were controls. Both the augmentation index (AI) and late systolic blood pressure in the radial artery (rSBP2) as an index of central blood pressure were monitored using HEM-9000AI (Omron Healthcare, Kyoto, Japan) until 240 min after meal intake.

RESULTS:

Both AI and rSBP2 showed significant decreases after meal intake in both groups. Changes in postprandial AI showed a similar trend in the groups. rSBP2 reduction 60 min after meal ingestion was also comparable, -7.5+/-2.3 mmHg in MetS; -7.8+/-0.9 mmHg in control; however, delta rSBP2-120, the degree of rSBP2 reduction 120 min after meal ingestion comparing the fasting level, showed a significant difference between 2 groups, -0.5+/-2.0 mmHg in MetS; -5.3+/-0.9 mmHg in control, P<0.02. Stepwise regression analysis revealed low-density-lipoprotein cholesterol (beta=0.333, P=0.001), high-density-lipoprotein cholesterol (beta=-0.209, P<0.05) and systolic blood pressure (beta=-0.377, P<0.001) as independent variables for determining delta rSBP2-120.

CONCLUSION:

Subjects with MetS exhibit signs of blunted rSBP2 (=central blood pressure) regulation after food intake. Dysfunctional postprandial hemodynamic regulation is another feature of MetS that may contribute to the progression of cardiovascular disease.

[Indexed for MEDLINE]

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