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Hypertension. 1998;31:1200-1201

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(Hypertension. 1998;31:1200-1201.)
© 1998 American Heart Association, Inc.


Letters to the Editor

Noninvasive Assessment of Flow-Mediated Vasodilation With 30-MHz Transducer in Pregnant Women

Atsushi Yoshida; Shinji Nakao; Hisaaki Kobayashi; ; Mitsunao Kobayashi

Department of Perinatal and Maternal Medicine, National Defense Medical College, Saitama, Japan

To the Editor:

Cockell and Poston (April 1997)1 reported that flow-mediated vasodilation is enhanced in pregnant women but reduced in preeclampsia. They assessed the vasodilation using biopsies of small arteries. Therefore, their assessment was not in vivo but in vitro study. We assessed flow-mediated vasodilation in pregnant women noninvasively. Noninvasive assessment of flow-mediated vasodilation in nonpregnant subjects was first reported by Celermajer et al,2 who measured the brachial artery with high-resolution ultrasound (7.5-MHz transducer). We previously reported that with a 30-MHz transducer it is possible to detect endothelial dysfunction more accurately by measuring the radial artery.3

We examined 60 Japanese women including 20 nonpregnant normotensive healthy women (28.7±5.0 years old), 18 normal pregnant women (31.3±5.0 years old, 35.8±3.1 weeks of pregnancy), and 22 pregnant women with preeclampsia (29.8±3.8 years old, 36.0±3.3 weeks of pregnancy). The diagnosis of preeclampsia was made according to the criteria of the Committee on Terminology of the American Collage of Obstetricians and Gynecologists.4 All 60 subjects were nonsmokers.

Images of the radial artery in 60 women were obtained longitudinally with a 30-MHz mechanical linear probe and an SSD-550 system (Aloka, Tokyo, Japan). In each study, we confirmed the clear visualization of the three layers of the vessel wall, including the "m" lines (the interface between media and adventitia) in both near and far walls. When the clear visualization of these layers was confirmed, the probe was fixed with a steel flexible arm. Adequate scans were obtained in all cases. A cuff of 140 mm in width placed on the upper arm was inflated to 30 mm Hg above the systolic pressure for 5 minutes. The radial artery diameter was measured before inflation (baseline) and after deflation of the cuff. Imaging of the artery was performed for 6 minutes after cuff deflation. The radial artery diameter was defined as the distance from the near side of the "m" line in the near wall to the near side of the "m" line in the far wall. Measurements were taken within 1 minute before cuff inflation (baseline) and 30, 60, 90, 120, 180, 240, 300, and 360 seconds after cuff deflation at end diastole. Flow-mediated vasodilation was determined by calculating the change in the radial artery diameter (percent increase for the baseline diameters). Student's t test was used for statistical analysis, and a value of P<.01 was considered significant.

Baseline radial artery diameters in nonpregnant women, normal pregnant women, and preeclamptic women were 2.26±0.42, 2.41±0.38, and 2.22±0.35 mm, respectively. No significant differences were seen among these groups. Maximum dilation was obtained 1 minute after cuff deflation. The percent increases of radial artery diameter during reactive hyperemia in nonpregnant women, normal pregnant women, and preeclamptic women were 11.8±3.6%, 18.9±3.4%, and 7.9±3.0%, respectively. In normal pregnant women, vasodilation was significantly greater than that in nonpregnant women (P<.001). Vasodilation in preeclamptic women was significantly less than that in normal pregnant women (P<.001) or nonpregnant women (P<.001).

Our results indicate that peripheral vascular endothelial function in pregnant women was improved, but in preeclamptic women endothelial function was impaired. Our conclusions were in accordance with the findings of Cockell and Poston. Using our method, we can asses the endothelial function in pregnant women noninvasively. Because Cockell and Poston used biopsies obtained at cesarean section, their assessment was limited to subjects at or near term, but our method is applicable to subjects even in early pregnancy. Further work is in progress to evaluate the usefulness of our method as a predictor of preeclampsia.

References

1. Cockell AP, Poston L. Flow-mediated vasodilation is enhanced in normal pregnancy but reduced in preeclampsia. Hypertension. 1997;30:247–251.[Abstract/Free Full Text]

2. Celermajer DS, Sorensen KE, Gooch VM, Spiegelhalter DJ, Miller OI, Sullivan ID, Lloyd DJ, Deanfield JE. Non-invasive detection of endothelial dysfunction in children and adults at risk of atherosclerosis. Lancet. 1992;340:1111–1115.[Medline] [Order article via Infotrieve]

3. Kobayashi H, Yoshida A, Kobayashi M, Nakao S. Non-invasive detection of endothelial dysfunction with 30 MHz transducer. Lancet. 1996;347:1336–1337.

4. American College of Obstetricians and Gynecologists. Hypertension in Pregnancy. Technical Bulletin No. 219. Washington, DC: ACOG; 1996.

Response

Lucilla Poston; ; Anna Cockell

Fetal Health Research Group, Division of Obstetrics and Gynaecology, St Thomas' Hospital, London, UK

We read with interest the letter of Yoshida et al describing a study of the reactive hyperemic response in radial arteries of nonpregnant and pregnant women and of patients with preeclampsia. Using ultrasonography, the authors have shown blunted dilatation after cuff inflation on the upper arm in women with preeclampsia when compared with findings in normal pregnant women. These data would appear to confirm our in vitro findings described in Hypertension,1 in which we showed blunted endothelium-dependent, nitric oxide–mediated dilatation to shear stress in small arteries obtained during caesarean section from women with preeclampsia. However, some degree of caution should be applied when ascribing endothelium dependence to the abnormal dilatory response in the radial arteries, since vasodilation induced by hyperemia of the upper arm will undoubtedly lead to endothelium-independent elements of relaxation unrelated to increased flow per se2 in the lower arm. Previous studies have circumvented this problem by applying the cuff to the lower arm, thus evoking an increase in shear stress in the upper arm but precluding any influence of locally acting metabolites.3 Nonetheless, Yoshida et al have shown clearly that vasodilator responses are significantly increased in pregnant women compared with nonpregnant and are blunted in women with preeclampsia. Together with our observations in resistance-sized arteries in vitro, these data add further strength to the hypothesis that impairment of vasodilatory responses may contribute to elevation of the blood pressure in women with preeclampsia.

References

1. Cockell AP, Poston L. Flow-mediated vasodilation is enhanced in normal pregnancy but reduced in preeclampsia. Hypertension. 1997;30:247–251.

2. Meredith IT, Currie KE, Roddy MA, Ganz P, Creager MA. Postischemic vasodilation in human forearm is dependent on endothelium-derived nitric oxide. Am J Physiol. 1996;270:H1435–H1440.[Abstract/Free Full Text]

3. Celermajer DS, Adams MR, Clarkson P, Robinson J, McCredie R, Donald A, Deanfield JE. Passive smoking and impaired endothelium-dependent arterial dilatation in healthy young subjects. N Engl J Med. 1996;334:150–154.[Abstract/Free Full Text]




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