Relationship between hyperinsulinemia and pulse wave velocity in moderately hyperglycemic patients
ABSTRACT Arterial stiffness assessed by pulse wave velocity (PWV) reflects early stage arteriosclerosis. The influence of hyperinsulinemia on peripheral vascular disease (PVD) is still unknown. We determined the influences of hyperinsulinemia on PVD assessed by PWV in moderately hyperglycemic patients.
Thirty-six moderately hyperglycemic, outcoming patients were recruited in this study. All subjects were divided into two groups by fasting immunoreactive insulin (F-IRI) concentrations; group A; F-IRI> or =5 microU/ml, group B; F-IRI<5 microU/ml. Both hbPWV (from heart to brachial artery) and baPWV (brachial to artery to ankle) were evaluated by using Form PWV/ABI, in addition to ankle-brachial pressure index (ABPI).
In group A, both hbPWV and baPWV showed significantly higher values than in group B. ABPIs were not different between two groups. Although age, FPG, plasma HbA1c, serum total-cholesterol, HDL-cholesterol concentrations, and systolic and diastolic blood pressure were at same levels in group A as group B, body mass index, HOMA-R, serum triglyceride concentrations were significantly higher in group A, indicating the existence of insulin resistance in group A.
Hyperinsulinemia may be involved in the development of PVD in moderately hyperglycemic patients.
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ABSTRACT: Background and Objectives:Aging is a major factor related to a relaxation abnormality of the left ventricle. Increased arterial stiffness and central distribution of body fat are common physiologic changes observed in the elderly. To further elucidate the relationship between aging and a relaxation abnormality of the left ventricle, we investigate the relationship between the pulse wave velocity, abdominal obesity and diastolic function parameters of the left ventricle. Subjects and Methods:In 490 subjects (153 normotensive, 128 prehypertensive, 120 un- treated hypertensive and 89 hypertensive on anti-hypertensive drugs, aged 59.8±12.6 (21-88) years), the brachial-ankle pulse wave velocity (baPWV) and echocardiographic indices for a relaxation abnormality, i.e. transmitral E, A, E/A, DT, IVRT, were measured. A relaxation abnormality was defined by an E/A 240 ms in the young (Korean Circulation Journal 01/2006; 36(3). DOI:10.4070/kcj.2006.36.3.221
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ABSTRACT: In order to diagnose arteriosclerosis in any part of the body, pulse wave velocity (PWV) measurement is a useful approach. However, it is considered that the technique of PWV measurement should be simplified. A new method for measuring PWV has therefore been proposed in Japan. The PWV of the brachial artery (ba) and the ankle was measured by applying air pressure with the aid of a volume plethysmograph. Comparisons between the baPWV measurement method and the conventional method are currently being performed. Since satisfactory results have been obtained to date, baPWV has gained popularity throughout Japan. Since this method measures PWV in the arm and foot, it may be said that aortic PWV is not reflected though a large amount of past PWV measurements. BaPWV is influenced by blood pressure. With the baPWV technique, blood pressure compensation is not carried out. Furthermore, the pulse pressure is measured by air pressure; therefore any stimulus that exerts pressure on an artery may influence these results. Due to these reasons, a cardie-ankle vascular index (CAVI) has been proposed in which the pressure wave form indicating the closing of the aortic valve appears in the form of an arterial pressure wave after a fixed delay time. This delay is the time difference between the actual closing of the aortic valve and the measuring point. Prior to the introduction of baPWV, PWV was measured in the carotid artery and foot. As in traditional PWV, baPWV uses the delay time, but between the brachial artery and the ankle artery. However, the carotid artery differs from the brachial artery, and the measured value differs depending on whether the arteriosclerosis is present in the carotid artery or the brachial artery. CAVI is calculated from the ECG, PCG, brachial artery waveform and ankle artery waveform using a special algorithm. This new method represents a breakthrough in the diagnosis of atherosclerosis.Biomedecine [?] Pharmacotherapy 11/2004; 58 Suppl 1(Suppl 1):S95-8. DOI:10.1016/S0753-3322(04)80015-5 · 2.11 Impact Factor
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ABSTRACT: Obesity is characterized by insulin resistance and hyperinsulinemia that may elevate arterial pressure due to sympathetic overactivity and volume overload. The aim of the study is to measure hemodynamic parameters and metabolic variables in obese normotensive subjects. Twenty-four normotensive, overweight subjects from our medical staff were enrolled. They had personal and group meetings with a physician, dietician, and psychologist to improve their compliance with regard to physical activity and personal low-calorie diet. In addition, each subject was given orlistat 120 mg three times daily for 12 weeks. Noninvasive hemodynamic parameters including arterial compliance were measured using radial artery pulse wave analysis, at the beginning and 1 month after taking the last dose of Orlistat, and insulin resistance was calculated using HOMA score. At the end of the 3-month period, the average weight was reduced from 89.5 +/- 12 kg to 81.5 +/- 9 kg. The systolic arterial pressure was reduced from 128 +/- 12 mm Hg to 121 +/- 10 mm Hg and diastolic arterial pressure was reduced from 75.4 +/- 9 mm Hg to 69.6 +/- 7 mm Hg. Arterial compliance measurements showed significant improvement in large artery compliance from 13 +/- 4 to 15.8 +/- 3.6 while no change occurred in small arteries. The insulin sensitivity assessed by HOMA score improved significantly from 6.5 +/- 4.5 to 4.8 +/- 3.1 with weight reduction. Our data show that weight loss is accompanied by lowering of blood pressure, even in normotensive obese patients. This weight loss brings about an improvement in insulin resistance and a rise in large artery compliance, whereas no change occurs in small artery compliance.The American Journal of the Medical Sciences 11/2005; 330(4):157-60. DOI:10.1097/00000441-200510000-00001 · 1.52 Impact Factor